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[ { "answer_id": 24915, "body": "<p>A tooth has two parts- crown and a root. Now going from outside to inside the crown portion has 3 layers- enamel, dentin and pulp. The root has 3 layers- cementum, dentin and pulp.\n<a href=\"https://en.wikipedia.org/wiki/Human_tooth\" rel=\"noreferrer\">Reference</a>\nNow among these only pulp is vascular and innervated.\nDentin has got dentinal tubules containing dentinal fluid. Whenever there is any stimulus which has not yet reached the pulp, but may have reached the dentin, eg of stimulus in the form of pressure, temperature change, sweet food, sour food etc, cause the fluid to move or get displaced. The displacement of dentinal fluid stimulates nerve endings in the pulp and hence generates a pain/sensitivity response to your brain.\n<img src=\"https://i.stack.imgur.com/oSvFm.jpg\" alt=\"enter image description here\" />\n<a href=\"https://www.deardoctor.com/inside-the-magazine/issue-23/treatment-of-tooth-sensitivity/\" rel=\"noreferrer\">Reference</a></p>\n<p><img src=\"https://i.stack.imgur.com/HW9AB.jpg\" alt=\"enter image description here\" />\n<a href=\"https://www.dentin.co/new-blog/2017/6/9/dentinal-hypersensitivity-hydrodynamic-theory\" rel=\"noreferrer\">Reference</a></p>\n<blockquote>\n<p>There are three main theories of dentine hypersensitivity: Direct Innervation (DI) Theory Odontoblast Receptor (OR) Theory Fluid Movement/Hydrodynamic Theory</p>\n</blockquote>\n<blockquote>\n<p>The Hydrodynamic or Fluid Movement theory is one of the main theories in dentistry to explain the mechanism by which a tooth perceives the sensation of pain. It is currently the most widely accepted theory used to explain tooth sensitivity.</p>\n</blockquote>\n<p><a href=\"https://en.wikipedia.org/wiki/Hydrodynamic_theory_dentistry\" rel=\"noreferrer\">Reference</a></p>\n<p>Now coming back to your question. As the tooth is cracked, the enamel in that area must have been chipped off and the dentinal tubules and/or pulp must have been exposed.\nAs mentioned earlier the sweet food also causes the dentinal fluid to be displaced causing a sharp shooting pain as perceived by your brain.\nThis is because of change is osmolarity. The sweets/sugars changes the osmolarity of dentinal fluid.</p>\n<blockquote>\n<p>Clinically, osmotic stimuli such as a wide variety of\nsweet food, particularly chocolate and sugar syrup, are\none of the main factors causing dentin hypersensitivity.\nPrevious studies showed that the different stimuli, including osmotic, when applied to dentin caused pain by a hydrodynamic mechanism that involves displacement of\nthe dentinal fluid and excites intradental nerve endings.\n<a href=\"http://www.quintpub.com/userhome/jad/jad_2010_02_s0103.pdf\" rel=\"noreferrer\">Reference</a></p>\n</blockquote>\n<p>Hope I have satisfactorily answered your question :)</p>\n", "score": 5 } ]

[ "dentistry", "pain", "sugar", "cracked-broken-tooth" ]

[ { "answer_id": 24923, "body": "<p><a href=\"https://dx.doi.org/10.5402/2012/132196\" rel=\"nofollow noreferrer\">Kassi et al. (2012)</a> does state that there is low yield in some cases as you pointed out in your quote and was highlighted in the Reddit cross-post.</p>\n<p>Again, pointed out in Reddit, you are sucking up individual cells and not taking a piece of tissue and therefore it can have an incredibly low yield and sometimes produce false negative results.</p>\n<p>With the figures on low yield, as you said in the comments, <a href=\"https://dx.doi.org/10.5402/2012/132196\" rel=\"nofollow noreferrer\">Kassi et al. (2012)</a> points out that:</p>\n<blockquote>\n<p>The limitation of the technique is low yield in some of the cases (5.7%).</p>\n</blockquote>\n<p>You may be correct that this points to 2 out of their 37 patient cohort, however when you consider that about 4.32 million basal cell skin cancers are diagnosed each year in the US alone,</p>\n<blockquote>\n<p>According to one estimate, about 5.4 million basal and squamous cell skin cancers are diagnosed each year in the US (occurring in about 3.3 million Americans, as some people have more than one). About 8 out of 10 of these are basal cell cancers (<a href=\"https://www.cancer.org/cancer/basal-and-squamous-cell-skin-cancer/about/key-statistics.html\" rel=\"nofollow noreferrer\">American Cancer Society, 2020</a>)</p>\n</blockquote>\n<p>that figure of 2 rises to a potential of a much larger number of false negatives.</p>\n<p>It is more accurate to <a href=\"https://www.cancer.org/treatment/understanding-your-diagnosis/tests/testing-biopsy-and-cytology-specimens-for-cancer/what-doctors-look-for.html\" rel=\"nofollow noreferrer\">look at the <strong>structure/organization</strong> of the cells</a> via a shave biopsy. An FNA does not allow you do do that. That is why <a href=\"https://dx.doi.org/10.5402/2012/132196\" rel=\"nofollow noreferrer\">Kassi et al. (2012)</a> only recommends FNA for:</p>\n<blockquote>\n<p><strong>the initial evaluation</strong> of a patient with suspected BCC or in cases of recurrence. The technique is cheap, quick, less invasive, and highly accurate for the diagnosis of BCC. However, “cytology does not give much information about tumor patterns or subtypes which can be related to aggressive behavior and can be very important in further therapeutic decisions” [(<a href=\"https://doi.org/10.1046/j.1365-4362.2000.00893.x\" rel=\"nofollow noreferrer\">Vega‐Memije, et al. 2000</a>)]. This should, thus, be followed by “histopathological confirmation before any therapeutic maneuver is considered” [(<a href=\"https://doi.org/10.1046/j.1365-4362.2000.00893.x\" rel=\"nofollow noreferrer\">Vega‐Memije, et al. 2000</a>)]. <strong>[emphasis mine]</strong>.</p>\n</blockquote>\n<h2>References</h2>\n<p>American Cancer Society (2020). Key Statistics for Basal and Squamous Cell Skin Cancers. <em>American Cancer Society</em>. <a href=\"https://www.cancer.org/cancer/basal-and-squamous-cell-skin-cancer/about/key-statistics.html\" rel=\"nofollow noreferrer\">https://www.cancer.org/cancer/basal-and-squamous-cell-skin-cancer/about/key-statistics.html</a></p>\n<p>Kassi, M., Kasi, P. M., Afghan, A. K., Marri, S. M., Kassi, M., &amp; Tareen, I. (2012). The role of fine-needle aspiration cytology in the diagnosis of basal cell carcinoma. <em>Isrn Dermatology, 2012</em>. <strong>Open Access</strong> <a href=\"https://dx.doi.org/10.5402/2012/132196\" rel=\"nofollow noreferrer\">https://dx.doi.org/10.5402/2012/132196</a></p>\n<p>Vega‐Memije, E., De Larios, N. M., Waxtein, L. M., &amp; Dominguez‐Soto, L. (2000). Cytodiagnosis of cutaneous basal and squamous cell carcinoma. <em>International journal of dermatology, 39</em>(2), 116-120. <a href=\"https://doi.org/10.1046/j.1365-4362.2000.00893.x\" rel=\"nofollow noreferrer\">https://doi.org/10.1046/j.1365-4362.2000.00893.x</a></p>\n", "score": 1 } ]

[ "dermatology", "diagnosis", "biopsy", "basal-cell-carcinoma" ]

[ { "answer_id": 24933, "body": "<p>My recollection of that time was not that <strong>doctors</strong> recommended being exposed to chickenpox but rather that <strong>parents</strong> sometimes chose to expose their children at a time they felt might be more convenient for the family, since everyone would catch it eventually. Some recommended times to get it: while you only had one child to look after (subsequent children then each getting it one at a time), while it was summer and they could play outside without clothes that might hurt on rashed skin, before they started school so they wouldn't miss class time, and so on.</p>\n<p>When the vaccine was new, there was uncertainty about how long the immunity lasted. My doctor recommended at that time that if a girl didn't get it by puberty, she should get the vaccine (chickenpox while you're pregnant is serious.) I believe the current recommendations are to get the vaccine and try to avoid catching the virus, which thanks to the vaccine is a strategy you can actually follow, since less kids now catch it.</p>\n<p><a href=\"https://en.wikipedia.org/wiki/Pox_party\" rel=\"nofollow noreferrer\">Wikipedia</a> says doctors have never recommended deliberately getting infected with anything, and it seems pretty easy for reporters doing a story on such parties to find a doctor who says it's a bad idea.</p>\n", "score": 2 } ]

[ "virus", "immune-system", "chickenpox" ]

[ { "answer_id": 24956, "body": "<p>OK. I'll tackle your question in two parts....</p>\n<p>The baking soda part:\nIf you've read the <a href=\"https://pubmed.ncbi.nlm.nih.gov/21042013/\" rel=\"nofollow noreferrer\">source article</a> cited by you till the end, you will understand that oral sodium bicarbonate, <strong>through correction of metabolic acidosis</strong>, improved thyroid function in CKD patients. So...the so called helpful effect which you've mentioned is seen only in patients with chronic kidney disease. It doesn't directly effect thyroid metabolism</p>\n<p>The Resveratrol part:\nAgain in the <a href=\"https://pubmed.ncbi.nlm.nih.gov/28668442/\" rel=\"nofollow noreferrer\">article</a> cited by you, the said 'negative' effects were seen only in in-vitro cell lines. Not in humans. Even the in-vivo rat study showed no clinical effects (only biochemical and histological evidence of goitrogenic potential). These kinds of anti-oxidants are prescribed by doctors only after weighing the risks and benifits (like in case of cancer patients).\nRemember:</p>\n<blockquote>\n<p>Only the right dose differentiates a drug from poison</p>\n</blockquote>\n", "score": 2 } ]

[ "supplement", "thyroid", "baking-soda" ]

[ { "answer_id": 24943, "body": "<p>I'm afraid it would be frowned you all if I answered it by myself and took my response as a solution, but...\nAs I mentioned in the comments section above, I found <a href=\"https://www.fda.gov/drugs/drug-information-consumers/fdas-drug-review-process-continued\" rel=\"nofollow noreferrer\">a very summarized resource</a> on the FDA's web site.</p>\n<p><strong>(1)FDA</strong> <br>\nAccording to the <a href=\"https://www.fda.gov/drugs/drug-information-consumers/fdas-drug-review-process-continued\" rel=\"nofollow noreferrer\">FDA</a>, Drug Review Steps Simplified is as follows.(This is a regular approve route. Not a <a href=\"https://medicalsciences.stackexchange.com/questions/24343/progress-of-the-fdas-review-of-rmat-products\">shortcut-way</a>.)</p>\n<p><strong>BoxF1</strong>:</p>\n<blockquote>\n<ol>\n<li>Preclinical (animal) testing.<br></li>\n<li>An investigational new drug application (IND) outlines what the sponsor of a new drug proposes for human testing in clinical trials.<br></li>\n<li>Phase 1 studies (typically involve 20 to 80 people).<br></li>\n<li>Phase 2 studies (typically involve a few dozen to about 300 people).<br></li>\n<li>Phase 3 studies (typically involve several hundred to about 3,000 people).<br></li>\n<li>The pre-NDA period, just before a new drug application (NDA) is submitted. A common time for the FDA and drug sponsors to meet.</li>\n<li>Submission of an NDA is the formal step asking the FDA to consider a drug for marketing approval.<br></li>\n<li>After an NDA is received, the FDA has 60 days to decide whether to file it so it can be reviewed.<br></li>\n<li>If the FDA files the NDA, an FDA review team is assigned to evaluate the sponsor's research on the drug's safety and effectiveness.<br></li>\n<li>The FDA reviews information that goes on a drug's professional labeling (information on how to use the drug).<br></li>\n<li>The FDA inspects the facilities where the drug will be manufactured as part of the approval process.<br></li>\n<li>FDA reviewers will approve the application or issue a complete response letter.<br></li>\n</ol>\n</blockquote>\n<p>Now that's a generally satisfactory answer.</p>\n<p>While #1, #2, and ... describe &quot;what action is to be taken&quot;, it is not clear who is to perform these action. However, #1 is likely to be a matter for the drug companies (sponcer) side.　Perhaps the action should be taken by the sponsor, except for the step where the subject of the action is specified as the FDA　(For example #8).</p>\n<p>The #2 above is an explanation of the role of the document being reviewed, not &quot;what action will be taken,&quot; but the reality is probably &quot;the action will be that this document will be submitted at this step.</p>\n<p>Also, although it's not specified in the Box above, I think you probably need to get permission to conduct a separate clinical trial for each　of phase 1 to 3 (see #3 through #5 in the Box above). But, I don't have the rationale for that at the moment.</p>\n<p>The <a href=\"https://www.fda.gov/drugs/investigational-new-drug-ind-application/pre-ind-consultation-program\" rel=\"nofollow noreferrer\">Pre-IND Consultation</a> described in the questions section also appears to be a real process in the US.</p>\n<p>Note that, in addition to the INDs and NDAs mentioned in the Box above, the <a href=\"https://www.fda.gov/drugs/special-features/frequently-asked-questions-about-fda-drug-approval-process\" rel=\"nofollow noreferrer\">following types</a> of drug applications that can be submitted to FDA.</p>\n<ul>\n<li>Abbreviated New Drug Application (ANDA)</li>\n<li>Biologic License Application (BLA)</li>\n</ul>\n<p><a href=\"https://www.fda.gov/patients/learn-about-drug-and-device-approvals/drug-development-process\" rel=\"nofollow noreferrer\">Other FDA's resources</a> have been narrowed down to five from BoxF1's (See Box F2); it omits typical administrative procedures, such as IND, NDA,... . On the other hand, it also contains an explanation of post marketing surveillance, which is not described in Box F1.</p>\n<p><strong>BoxF2</strong> :</p>\n<blockquote>\n<p><strong>STEP1:</strong> Discovery and Development<br>\nResearch for a new drug begins in the laboratory.<br>\n<strong>STEP2:</strong> Preclinical Research<br>\nDrugs undergo laboratory and animal testing to answer basic questions about safety.<br>\n<strong>STEP3:</strong> Clinical Research<br>\nDrugs are tested on people to make sure they are safe and effective.<br>\n<strong>STEP4:</strong> FDA Review<br>\nFDA review teams thoroughly examine all of the submitted data related to the drug or device and make a decision to approve or not to approve it.<br>\n<strong>STEP5:</strong> FDA Post-Market Safety Monitoring<br>\nFDA monitors all drug and device safety once products are available for use by the public.<br></p>\n</blockquote>\n<p>I also found <a href=\"https://www.fda.gov/training-and-continuing-education/cderlearn-training-and-education/drug-approval-case-studies\" rel=\"nofollow noreferrer\">more detailed course</a> designed for non expert .</p>\n<p>The FDA has committees that advise on drugs, medical devices and regenerative medicine products. That is discussed in this <a href=\"https://medicalsciences.stackexchange.com/questions/24980/relationship-between-fda-agencies-and-the-advisory-committee\">Q&amp;A</a>.</p>\n<hr />\n<p><strong>(2)EMA <br></strong>\nFor EMA, the followings are beneficial.</p>\n<ul>\n<li><a href=\"https://www.ema.europa.eu/en/from-lab-to-patient-timeline\" rel=\"nofollow noreferrer\">https://www.ema.europa.eu/en/from-lab-to-patient-timeline</a></li>\n<li><a href=\"https://www.ema.europa.eu/en/news/how-are-new-medicines-approved-ema\" rel=\"nofollow noreferrer\">https://www.ema.europa.eu/en/news/how-are-new-medicines-approved-ema</a></li>\n<li><a href=\"https://www.ema.europa.eu/en/human-regulatory/marketing-authorisation/evaluation-medicines-step-step\" rel=\"nofollow noreferrer\">https://www.ema.europa.eu/en/human-regulatory/marketing-authorisation/evaluation-medicines-step-step</a></li>\n<li><a href=\"https://www.ema.europa.eu/en/documents/other/laboratory-patient-journey-centrally-authorised-medicine_en.pdf\" rel=\"nofollow noreferrer\">https://www.ema.europa.eu/en/documents/other/laboratory-patient-journey-centrally-authorised-medicine_en.pdf</a></li>\n</ul>\n<p>EMA's schema of Drug Review includes the followings (This is a regular approve route. Not a shortcut-way;<br></p>\n<p><strong>BoxE1</strong></p>\n<blockquote>\n<ul>\n<li>Scientific advice <br>・EMA can provide scientific advice to help medicine developers generate robust data on medicines.<br>・Developers ask specific questions about their plans to develop their medicine.<br>・EMA responds to the questions, often consulting additional experts and patients.<br>・EMA provides its advice, which is not binding either on EMA regarding future assessment of the medicine or on the developer, which can decide not to follow it.</li>\n<li>Research &amp; development<br>・Pharmaceutical and biotechnology companies, doctors and academics research new medicines.</li>\n<li>Evaluation <br>・Developers apply for marketing authorization and submit data.<br>・EMA starts its assessment and prepares questions for the medicine developer.<br>・EMA often consults additional experts, healthcare professionals and patients.<br>・EMA recommends whether or not the medicine can be authorized for use in patients.</li>\n<li>Authorization<br>The European Commission takes a final decision on whether the medicine can be marketed in the EU</li>\n<li>Access<br>National and regional authorities decide on pricing and reimbursement.</li>\n<li>Safety monitoring <br> Once the medicine is authorized, EMA and national authorities continuously monitor its safety.</li>\n</ul>\n</blockquote>\n<p>The European Medicines Agency (EMA) has following seven <a href=\"https://www.ema.europa.eu/en/committees/how-committees-work\" rel=\"nofollow noreferrer\">scientific committees</a>.</p>\n<ul>\n<li>Committee for Medicinal Products for Human Use (CHMP)</li>\n<li>Pharmacovigilance Risk Assessment Committee (PRAC)</li>\n<li>Committee for Medicinal Products for Veterinary Use (CVMP)</li>\n<li>Committee for Orphan Medicinal Products (COMP)</li>\n<li>Committee on Herbal Medicinal Products (HMPC)</li>\n<li>Committee for Advanced Therapies (CAT)</li>\n<li>Paediatric Committee (PDCO)</li>\n</ul>\n<p>According to the EMA's <a href=\"https://www.ema.europa.eu/en/committees/how-committees-work\" rel=\"nofollow noreferrer\">site</a>, committees and working parties also contribute to the development of medicines and medicine regulation, by the followings;</p>\n<p><strong>Box E2</strong></p>\n<blockquote>\n<ul>\n<li>providing scientific advice to companies researching and developing new medicines;</li>\n<li>preparing scientific guidelines and regulatory guidance to help pharmaceutical companies prepare marketing authorisation applications;</li>\n<li>contributing to the harmonisation of regulatory requirements n the EU and internationally.</li>\n</ul>\n</blockquote>\n<p>Medical devices in Europe seem to be <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326593/\" rel=\"nofollow noreferrer\">CE-mark based</a>, but now it's in the middle of the confusion. I don't understand this, so I'd like to split the question separately.</p>\n", "score": 2 } ]

[ "clinical-study", "drug-administration", "regulatory-agencies" ]

[ { "answer_id": 25029, "body": "<p>First, I think it's useful to clarify exactly what the surgeon is doing here:</p>\n<blockquote>\n<p><a href=\"http://doi.org/10.1097/PRS.0b013e3182121618\" rel=\"nofollow noreferrer\"><strong>The Five-Step Lower Blepharoplasty: Blending the Eyelid-Cheek Junction.</strong></a>\nRohrich <em>et al.</em> <em>Plastic and Reconstructive Surgery.</em> 2011.</p>\n<blockquote>\n<p>In addition to aesthetic benefits, the functional and supportive role of cheek fat on lower lid shape has been elucidated by numerous surgeons. Whether cheek-lower lid soft tissue is augmented through fat mobilization, direct injection, or by means of implants, the goal remains the same.</p>\n</blockquote>\n</blockquote>\n<p>What we're seeing at the ~12 minute mark is fat processing and mobilization. Why is the surgeon doing this? Because, as the tissue has been severed from its original blood supply, &quot;fat grafts must obtain oxygen via diffusion until neovascularization occurs:&quot;</p>\n<blockquote>\n<p><a href=\"http://doi.org/10.1097/10.1097/GOX.0000000000000183\" rel=\"nofollow noreferrer\"><strong>Diffusion and Perfusion: The Keys to Fat Grafting.</strong></a>\nKhouri <em>et al.</em> <em>PRS Global Open.</em> 2014.</p>\n<blockquote>\n<p>Therefore, it seems that the core principle of fat graft survival is that oxygen concentration at any point in a graft is a function of the oxygen concentration of the surrounding capillaries, the diffusion rate of oxygen to reach that point in the tissue, the distance from the oxygen source, and the metabolic rate. In other words, at every point within a fat graft, there is a race between the rate at which oxygen is needed by the cells and the rate at which oxygen can be delivered by the capillaries and diffused through the adipose tissue.\n<a href=\"https://i.stack.imgur.com/QgAuP.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/QgAuP.png\" alt=\"Figure1\" /></a></p>\n</blockquote>\n</blockquote>\n<p>Although this review largely centers on fat grafting via <em>injection</em>, the relationship between oxygen diffusion limits and tissue thickness (graft radius) holds true regardless of the exact surgical method of fat harvesting, processing, and reinjection. In my comment, I summarized this as &quot;reducing the perfusion requirements of the tissue,&quot; which is technically true, but it should be noted that the grafted fat is initially dependent on <em>diffusion</em> (circumventing &quot;perfusion requirements&quot;) before eventual revascularization.</p>\n", "score": 1 } ]

[ "surgery", "body-fat", "plastic-surgery" ]

[ { "answer_id": 25635, "body": "<p>Supplementation of vitamins and minerals in the context of Inflammatory Bowel Disease (IBD) should be <strong>specific to existing deficiencies</strong> in each patient (<a href=\"https://scholar.google.com/scholar_lookup?title=Nutritional+management+of+inflammatory+bowel+diseases:+a+comprehensive+guide&amp;publication_year=2016&amp;\" rel=\"nofollow noreferrer\">1</a>).</p>\n<p>There is little evidence in this context for blind ingestion of over the counter supplements without a diagnostic correlate for, or at least reasonable clinical suspicion of a particular deficiency.</p>\n<blockquote>\n<p>Do guidelines exist for how people with Inflammatory Bowel Disorder should supplement with multiminerals and not risk a flare?</p>\n</blockquote>\n<p>Guidelines exist for management of IBD including treatment of deficiency (for example: <a href=\"https://academic.oup.com/ecco-jcc/article/13/2/144/5078195#130780346\" rel=\"nofollow noreferrer\">2</a>, <a href=\"https://www.gesa.org.au/public/13/files/Education%20%26%20Resources/Clinical%20Practice%20Resources/IBD/2018_IBD_Clinical_Update_May_update.pdf\" rel=\"nofollow noreferrer\">3</a>). The intended audience is physicians. Informational resources for patients are also available (for instance: <a href=\"http://www.gesa.org.au/public/13/files/Education%20%26%20Resources/Patient%20Resources/Diet%20in%20IBD/Diet_in_IBD_Final_2018.pdf\" rel=\"nofollow noreferrer\">4</a>, <a href=\"https://www.gesa.org.au/public/13/files/Education%20%26%20Resources/Patient%20Resources/IBD/IBD_Crohns_Colitis_Factsheet.pdf\" rel=\"nofollow noreferrer\">5</a>). Patients should consult with their physicians to determine the necessity of taking supplements.</p>\n<blockquote>\n<p>...as their gut is already compromised such conventional supplements are contraindicated.</p>\n</blockquote>\n<p>IBDs are variable in their severity: the function of the gut is not necessarily <em>continuously</em> compromised and different sections of the gut can be affected. As such the choice of supplement and method of administration must be tailored to the individual situation: disease activity, patient tolerance, degree of deficiency and success or failure of a given supplement are relevant factors.</p>\n<blockquote>\n<p>Are there other ways of supplementing?</p>\n</blockquote>\n<p>Application methods depend on the substance. The most common deficiencies in the context of IBD are Iron, Vitamin D, Vitamin B12, Zinc and Calcium (<a href=\"https://academic.oup.com/ibdjournal/article/18/10/1961/4608026\" rel=\"nofollow noreferrer\">6</a>). All of these can be administered per os or intravenously (1, 6). As pointed out elsewhere, Vitamin B12 and Vitamin D can be administered under the skin or in the muscle (<a href=\"https://onlinelibrary.wiley.com/doi/full/10.1111/jgh.13359\" rel=\"nofollow noreferrer\">7</a>).</p>\n", "score": 1 }, { "answer_id": 25623, "body": "<blockquote>\n<p>Are there other ways of supplementing? Are there supplements that are not contraindicated?</p>\n</blockquote>\n<p>Yes. There are ways to deliver vitamins directly to the cell without needing to be passed by the intestinal system.</p>\n<p>E.g. Vitamin B12, one of the most commonly deficient vitamins observed in IBD and crohn's patients as uptake is mainly oral and the main site of oral absorption being in the ileum, can be delivered intramuscularly via injection. [<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5112015/\" rel=\"nofollow noreferrer\">1</a>]</p>\n<p>Oral Vitamin D supplements also tend to be less effective in IBD patients with active inflammation in the small bowel as that is where most absorption takes place. And can be supplemented through natural biosynthesis by the keratinocytes in the epidermis when in the presence of UV light.</p>\n", "score": 0 } ]

[ "supplement", "gastroenterology", "minerals", "crohns", "ulcerative-colitis" ]

[ { "answer_id": 25538, "body": "<p>It's indeed the same &quot;big magnet&quot; machine as for normal MRI, but in WB-MRI (ideally) multiple coils are placed on the patient's body, e.g.:</p>\n<p><a href=\"https://i.stack.imgur.com/4TnED.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/4TnED.png\" alt=\"enter image description here\" /></a></p>\n<p>The process does indeed last 30-60 minutes (as Carey noted) as multiple scans passes are made. (More technical details in the <a href=\"https://cdn0.scrvt.com/39b415fb07de4d9656c7b516d8e2d907/1800000005233721/0ae8b57d0026/mreadings_mr-in-rt_4th-edition_whole-body-mri-at-1-5t_mcguire_1800000005233721.pdf\" rel=\"nofollow noreferrer\">article linked</a>.)</p>\n<p>There's a bit of history and/or variation in WB-MRI techniques\ndiscussed on p. 1110 of <a href=\"https://core.ac.uk/download/pdf/7752049.pdf\" rel=\"nofollow noreferrer\">another paper</a>. There exists\na variant (commercially) called AngioSURF/BodySURF which sacrifices\nspatial resolution by making the patient glide under\nthe body coil itself (which in that setup is a spine coil). A bit of searching found an image of what that looks like, in one of the papers referenced</p>\n<p><a href=\"https://i.stack.imgur.com/NmraQ.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/NmraQ.png\" alt=\"enter image description here\" /></a></p>\n", "score": 2 } ]

[ "mri" ]

[ { "answer_id": 25061, "body": "<p>The 2009 systematic review {1} summarized the likelihood of scarring and/or skin discoloration (e.g., hyper- or hypopigmentation) after the use of topical <a href=\"https://en.wikipedia.org/w/index.php?title=Fluorouracil\" rel=\"nofollow noreferrer\">fluorouracil</a> cream to treat a basal cell carcinoma (BCC):</p>\n<p><a href=\"https://i.stack.imgur.com/0032S.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/0032S.png\" alt=\"enter image description here\" /></a></p>\n<p><a href=\"https://i.stack.imgur.com/8WSRr.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/8WSRr.png\" alt=\"enter image description here\" /></a></p>\n<p>Note that I believe it is very likely the likelihood of skin discoloration (e.g., hyper- or hypopigmentation) depends on the skin type and the size+location of the BCC tumor.</p>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} Love WE, Bernhard JD, Bordeaux JS. Topical imiquimod or\nfluorouracil therapy for basal and squamous cell carcinoma: a\nsystematic review. Arch Dermatol. 2009;145(12):1431–8. <a href=\"https://doi.org/10.1001/archdermatol.2009.291\" rel=\"nofollow noreferrer\">https://doi.org/10.1001/archdermatol.2009.291</a></li>\n</ul>\n", "score": 1 } ]

[ "dermatology", "side-effects", "scar-tissue-scars", "hyperpigmentation", "basal-cell-carcinoma" ]

[ { "answer_id": 24993, "body": "<p>It's common for people to use mean and standard deviation in situations where it doesn't make a lot of sense. Sometimes it's okay, but yes it can lead to weird behavior like you've described. You should not interpret &quot;+/-&quot; here to mean that the values range from 0.47-0.64 to 0.47+0.64, just that the standard deviation is 0.64. Whether it makes sense to think of a standard deviation for these data is another matter.</p>\n<p>This doesn't have anything to do with sample vs population standard deviation. Imagine your data are six 0s and two 2s:</p>\n<p>[0 0 0 0 0 0 2 2]</p>\n<p>The mean is 0.5. The standard deviation is about 0.9. You could report that as 0.5 +/- 0.9 but that doesn't really describe the data very well.</p>\n", "score": 2 } ]

[ "health-informatics" ]

[ { "answer_id": 25025, "body": "<p>The information you've aggregated is accurate. Our blood contains RBCs (red blood cells), platelets and plasma (the fluid that carries these RBCs and other proteins like fibrinogen). Ofcourse, there are many other components in there not pertaining to this answer. The purpose of all these haemostatic(clot forming) factors is to stop us from bleeding to death in case of injuries. This is achieved when fibrinogen in plasma gets activated to fibrin which is a mesh or net like structure which traps platelets and RBCs forming what is called a 'fibrin plug' (see <a href=\"https://i.stack.imgur.com/npmTj.png\" rel=\"nofollow noreferrer\">pic</a> below) (<a href=\"https://www.webmd.com/dvt/blood-clots\" rel=\"nofollow noreferrer\">source</a>). This mechanism happens in all of us and saves us every time there is an injury. However, occasionally, in cases of coexisting comorbidities, this mechanism may lead to complications like DVT, stroke, MI etc..</p>\n<p><a href=\"https://i.stack.imgur.com/npmTj.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/npmTj.png\" alt=\"blood clot\" /></a></p>\n", "score": 0 } ]

[ "blood", "blood-circulation", "hematology" ]

[ { "answer_id": 25051, "body": "<blockquote>\n<p>Is there a minimum percentage that will produce herd immunity?</p>\n</blockquote>\n<p>Answer from the <a href=\"https://www.who.int/news-room/q-a-detail/herd-immunity-lockdowns-and-covid-19#:%7E:text=The%20percentage%20of%20people%20who,a%20population%20to%20be%20vaccinated.\" rel=\"nofollow noreferrer\">WHO</a> (<a href=\"https://web.archive.org/web/20201104034709/https://www.who.int/news-room/q-a-detail/herd-immunity-lockdowns-and-covid-19\" rel=\"nofollow noreferrer\">mirror</a>):</p>\n<blockquote>\n<p>The percentage of people who need to have antibodies in order to achieve herd immunity against a particular disease varies with each disease. For example, herd immunity against measles requires about 95% of a population to be vaccinated. The remaining 5% will be protected by the fact that measles will not spread among those who are vaccinated. For polio, the threshold is about 80%.</p>\n</blockquote>\n<p>The estimation of the threshold for COVID-19 herd immunity is 70% according to the <a href=\"https://www.mayoclinic.org/diseases-conditions/coronavirus/in-depth/herd-immunity-and-coronavirus/art-20486808\" rel=\"nofollow noreferrer\">Mayo Clinic</a> (<a href=\"https://web.archive.org/web/20201104034707/https://www.mayoclinic.org/diseases-conditions/coronavirus/in-depth/herd-immunity-and-coronavirus/art-20486808\" rel=\"nofollow noreferrer\">mirror</a>):</p>\n<blockquote>\n<p>Even if infection with the COVID-19 virus creates long-lasting immunity, a large number of people would have to become infected to reach the herd immunity threshold. <strong>Experts estimate that in the U.S., 70% of the population — more than 200 million people — would have to recover from COVID-19 to halt the epidemic</strong>.</p>\n</blockquote>\n", "score": 2 } ]

[ "covid-19" ]

[ { "answer_id": 25048, "body": "<p>Masks with exhalation valves are meant to be used to protect against particulates like sawdust or smoke. <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/respirator-use-faq.html\" rel=\"nofollow noreferrer\">They must not be used in a pandemic because a large part of the usefulness of masks is <strong>preventing people who are infected and don't know it from spreading the virus</strong>. If you have an exhalation valve on your mask you're exposing everyone around you.</a></p>\n<p>Public health guidelines would suggest you continue to use a surgical mask and do not advise using masks with exhalation valves.</p>\n", "score": 4 } ]

[ "covid-19", "coronavirus", "face-mask-respirator", "protection" ]

[ { "answer_id": 25060, "body": "<p>The transmission onset of an individual is the time when the individual first contaminated someone else, as defined in the <a href=\"https://www.sciencedirect.com/science/article/pii/S1201971220306123\" rel=\"nofollow noreferrer\">paper you mentioned</a>, section Procedures, first paragraph, P_j definition:</p>\n<p><a href=\"https://i.stack.imgur.com/BIW1O.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/BIW1O.png\" alt=\"enter image description here\" /></a></p>\n", "score": 1 } ]

[ "covid-19", "epidemiology", "disease-transmission" ]

[ { "answer_id": 25066, "body": "<blockquote>\n<p>Could the case be made for the flu shot still being necessary if living conditions return to normal for the second half of the season</p>\n</blockquote>\n<p>Yes, one argument would be that even with the current precautions, there are still currently half a million new covid cases daily, so it's preferable to have only one pandemic instead of two.</p>\n", "score": 2 } ]

[ "covid-19", "vaccination", "influenza" ]

[ { "answer_id": 25115, "body": "<blockquote>\n<p>Are there any scientific studies about the effects of them for a healthy person at different ages?</p>\n</blockquote>\n<p>Regarding NMN: study {1} shows it is safe to use on humans, but no study yet on the efficiency in terms of lifespan increase. Studies on NMN have been on other animals. See <a href=\"https://en.wikipedia.org/wiki/Nicotinamide_mononucleotide\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Nicotinamide_mononucleotide</a> for some references.</p>\n<p>Regarding the efficiency of resveratrol in terms of lifespan increase, see <a href=\"https://en.wikipedia.org/w/index.php?title=Resveratrol&amp;oldid=981556075#Lifespan\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/w/index.php?title=Resveratrol&amp;oldid=981556075#Lifespan</a>:</p>\n<blockquote>\n<p>There is insufficient evidence to indicate that consuming resveratrol has an effect on human lifespan.</p>\n</blockquote>\n<p>FYI: <a href=\"https://medicalsciences.stackexchange.com/q/18931/43\">Is there any downside in combining the ingestion of NR and NMN supplements to increase one's level of NAD+?</a></p>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} <a href=\"https://www.jstage.jst.go.jp/article/endocrj/advpub/0/advpub_EJ19-0313/_pdf/-char/en\" rel=\"nofollow noreferrer\">&quot;Effect of oral administration of nicotinamide mononucleotide on clinical parameters and nicotinamide metabolite levels in healthy Japanese men&quot;</a>. <em>Endocrine Journal</em>. November 2019.</li>\n</ul>\n", "score": 0 } ]

[ "supplement" ]

[ { "answer_id": 25182, "body": "<p>You're looking at a non-peer-reviewed study with some sloppy conventions. There is not enough information contained in the paper to answer your questions about it.</p>\n<p>You can assume what you want for many of your questions, but they are better directed at the authors, who have not indicated when they present means or medians, standard deviations or IQR, etc.</p>\n<p>It's really quite sloppy, but these mistakes happen. Ordinarily they get caught by careful peer reviewers before final publication (or journal staff, or, preferably, their own coauthors before they post a preprint).</p>\n", "score": 2 } ]

[ "covid-19", "lasting-effects-duration", "covid-19-datasets" ]

[ { "answer_id": 25218, "body": "<p>There is a historical and obsolete term in English called <a href=\"https://en.wikipedia.org/wiki/Benign_hypertension\" rel=\"nofollow noreferrer\">Benign hypertension</a>. According to the <a href=\"https://en.wikipedia.org/wiki/History_of_hypertension\" rel=\"nofollow noreferrer\">History of hypertension</a> article in Wikipedia:</p>\n<blockquote>\n<p>... hypertension was often classified into &quot;malignant&quot; and &quot;benign&quot; ... Charles Friedberg's 1949 classic textbook &quot;Diseases of the Heart&quot;,[17] stated that &quot;people with 'mild benign' hypertension ... [defined as blood pressures up to levels of 210/100 mm Hg] ... need not be treated&quot;.[15] However, the tide of medical opinion was turning: it was increasingly recognised in the 1950s that <strong>&quot;benign&quot; hypertension was not harmless</strong>.[18] Over the next decade increasing evidence accumulated from actuarial reports[2][19] and longitudinal studies, such as the Framingham Heart Study,[20] that &quot;benign&quot; hypertension increased death and cardiovascular disease.</p>\n</blockquote>\n", "score": 4 }, { "answer_id": 25219, "body": "<p>I also found this expression: <strong>habitual blood pressure</strong>. I don't know how common it is.</p>\n<p>An excerpt from <em><a href=\"https://www.cambridge.org/core/journals/amg-acta-geneticae-medicae-et-gemellologiae-twin-research/article/constitutional-disorders-of-homeostasis-the-genetic-aspect-of-diabetes-mellitus-essential-hypertension-and-obesity/F191D93B196EB0E00B234A0AC851DEB7\" rel=\"nofollow noreferrer\">Constitutional disorders of homeostasis. The genetic aspect of diabetes mellitus, essential hypertension and obesity</a></em> by Julius Bauer:</p>\n<p><a href=\"https://i.stack.imgur.com/gYHVB.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/gYHVB.png\" alt=\"enter image description here\" /></a></p>\n", "score": 0 } ]

[ "terminology", "blood-pressure" ]

[ { "answer_id": 25248, "body": "<p>The correct interpretion of R is on a population-based, statistical level. In your example, if two infected people have contact with one person who becomes infected, we do not say they each have an &quot;individual R&quot; of 1, we say the population has an R of 0.5: 2 infected people result in 1 infected person.</p>\n<p>Because you are basing R on population level statistics, you would never count an infected person multiple times based on multiple contacts, they are just one infection.</p>\n<p>Sometimes R might be estimated from contact tracing, and in this case the situation you describe may be a problem, if you assume everyone in contact with a patient who goes on to get infected was infected by that person. Breban et al addresses this concern and is strongly relevant to your question (there might be better resources, too, this was just the first I found). The contact tracing method is more accurate if you have very few infected people such that it is unlikely that someone would be exposed to more than one possible source.</p>\n<p>Breban, R., Vardavas, R., &amp; Blower, S. (2007). Theory versus data: how to calculate R 0?. PLoS One, 2(3), e282.</p>\n", "score": 3 } ]

[ "covid-19", "pandemic" ]

[ { "answer_id": 25336, "body": "<p>The mechanism of action of L-Theanine is not quite well understood and at some degree recent studies find themselves in contradictory with the results, nevertheless I think the essencial is this</p>\n<p><strong>Glutamate</strong> is a powerful excitatory neurotransmitter. It plays an important role in cognitive functions such as learning and memory due to its role in synaptic plasticity.</p>\n<p>Now, <a href=\"https://www.sciencedirect.com/science/article/pii/S2221169117308420\" rel=\"nofollow noreferrer\">L-Theanine</a></p>\n<blockquote>\n<p>blocks the reuptake of glutamine and glutamate</p>\n</blockquote>\n<p>and thus it will increase the concentration of glutamate in the synaptic cleft,\nprolonging the effect</p>\n<p>The mechanism of action of caffeine at the Central Nervous System can be summed up to one thing</p>\n<p><a href=\"https://en.wikipedia.org/wiki/Adenosine\" rel=\"nofollow noreferrer\"><strong>Adenosine</strong></a></p>\n<blockquote>\n<p>In general, adenosine has an inhibitory effect in the central nervous system (CNS)</p>\n</blockquote>\n<p><a href=\"https://go.drugbank.com/drugs/DB00201\" rel=\"nofollow noreferrer\">Regarding Caffeine</a></p>\n<blockquote>\n<p>Caffeine demonstrates antagonism of all 4 adenosine receptor subtypes (A1, A2a, A2b, A3) in the central nervous system</p>\n</blockquote>\n<p>which means that caffeine will have an excitatory effect on the central nervous system.</p>\n<p>They are both stimulants of the CNS, however when combining the two we have an interesting conclusion by the authors in this <a href=\"https://www.sciencedirect.com/science/article/pii/S2221169117308420\" rel=\"nofollow noreferrer\">article</a> so that</p>\n<blockquote>\n<p>l-theanine can counteract the stimulatory effect of caffeine. In rats, after caffeine administration intravenously with theanine at the same dose, the stimulant effect of caffeine was blunted. Whereas given by normal dose of caffeine with a smaller dose of theanine administration resulted in excitatory effects of caffeine, which suggested a dose specific dual activity of theanine</p>\n</blockquote>\n<p>In summary it depends on the dose.</p>\n", "score": 2 } ]

[ "medications", "caffeine", "drug-metabolism", "drug-interactions", "half-life" ]

[ { "answer_id": 25341, "body": "<p>As with anything, it depends. As a surgeon who often covers trauma call, I will accompany my sick and traumatically injured patients to the CT scanner from the emergency room. Often times, in the setting of trauma, the injuries I am looking for are obvious immediately (such as a subdural hematoma or a large liver laceration). As soon as I see these images on the tech's monitor, I can begin the process of moving to the operating room or arranging ICU admission.</p>\n<p>As an additional &quot;rule&quot; (really a variant of Murphy's law), if a sick patient is going to code, it will probably happen in the CT scanner. So I like to be there for my sick patients so I can intervene immediately if necessary.</p>\n<p>For non-emergent or elective imaging - no, typically I will not be there.</p>\n", "score": 1 } ]

[ "practice-of-medicine", "medical-imaging" ]

[ { "answer_id": 25332, "body": "<p>Nope -- unipennate refers to the way in which the muscle fibers spread out from the head(s), while unicipital refers to the number of heads (aka origns).</p>\n<p>All the best with your studies!</p>\n", "score": 0 } ]

[ "hand" ]

[ { "answer_id": 25344, "body": "<p>The higher transmissibility of this VUI-202012/01 strain (if it is confirmed) is almost certainly due to mutations in the spike gene of the virus; see <a href=\"https://www.cogconsortium.uk/wp-content/uploads/2020/12/Report-1_COG-UK_19-December-2020_SARS-CoV-2-Mutations.pdf\" rel=\"nofollow noreferrer\">preliminary report from COG UK</a>; another <a href=\"https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations\" rel=\"nofollow noreferrer\">version</a> of that with slightly more analysis confirms that one of the (17) mutations involved had been previously confirmed as causing higher transmissibility in a mouse model</p>\n<blockquote>\n<p>N501Y has been associated with increased infectivity and virulence in a mouse model (Gu et al. 2020).</p>\n</blockquote>\n<p>I think even the epidemiological implications haven't been quite dissected yet; I've seen the newspaper <a href=\"https://www.reuters.com/article/us-health-coronavirus-britain-variant-de/factbox-uk-says-new-coronavirus-variant-up-to-70-more-transmissible-idINKBN28T0V8\" rel=\"nofollow noreferrer\">reports</a> of (up to) 70% more contagiousness and R increase by 0.4 and that it's responsible for more infections in some areas, but I haven't seen any more scientific publications on the epidemiology of that strain (unlike for its genetics).</p>\n<p>It's also premature to conclude anything about masks with respect to transmission of this strain.</p>\n<p>N.B., the ECDC has a <a href=\"https://www.ecdc.europa.eu/sites/default/files/documents/SARS-CoV-2-variant-multiple-spike-protein-mutations-United-Kingdom.pdf\" rel=\"nofollow noreferrer\">lengthier report</a> on it now, although it doesn't add much in the way of facts (other than the strains was seen in a few cases in continental Europe too.)</p>\n<p><em>Science</em> has a more insightful <a href=\"https://www.sciencemag.org/news/2020/12/mutant-coronavirus-united-kingdom-sets-alarms-its-importance-remains-unclear\" rel=\"nofollow noreferrer\">coverage</a>, in that some experts have questioned the epidemiological conclusions as possibly rushed, but also there being a real concern because N501Y has apparently been seen in a different strain in South Africa that apparently also spreads faster, although data on this is still/also unpublished:</p>\n<blockquote>\n<p>A fortunate coincidence helped show that B.1.1.7 (also called VUI-202012/01, for the first “variant under investigation” in December 2020), appears to be spreading faster than other variants in the United Kingdom. One of the PCR tests used widely in the country, called TaqPath, normally detects pieces of three genes. But viruses with 69-70del lead to a negative signal for the gene encoding the spike gene; instead only two genes show up. That means PCR tests, which the U.K. conducts by the hundreds of thousands daily and which are far quicker and cheaper than sequencing the entire virus, can help keep track of B.1.1.7.</p>\n<p>In a press conference on Saturday, chief science advisor Patrick Vallance said that B.1.1.7, which first appeared in a virus isolated on 20 September, accounted for about 26% of cases in mid-November. “By the week commencing the 9th of December, these figures were much higher,” he said. “So, in London, over 60% of all the cases were the new variant.” Boris Johnson added that the slew of mutations may have increased the virus’s transmissibility by 70%.</p>\n<p>Christian Drosten, a virologist at Charité University Hospital in Berlin, says that was premature. “There are too many unknowns to say something like that,” he says. For one thing, the rapid spread of B.1.1.7 might be down to chance. Scientists previously worried that a variant that spread rapidly from Spain to the rest of Europe—confusingly called B.1.177—might be more transmissible, but today they think it is not; it just happened to be carried all over Europe by travelers who spent their holidays in Spain. Something similar might be happening with B.1.1.7, says Angela Rasmussen, a virologist at Georgetown University. Drosten notes that the new mutant also carries a deletion in another viral gene, ORF8, that previous studies suggest might reduce the virus’s ability to spread.</p>\n<p>But further reason for concern comes from South Africa, where scientists have sequenced genomes in three provinces where cases are soaring: Eastern Cape, Western Cape, and KwaZulu Natal. They identified a lineage separate from the U.K. variant that also has the N501Y mutation in the spike gene. “We found that this lineage seems to be spreading much faster,” says Tulio De Oliveira, a virologist at the University of KwaZulu Natal whose work first alerted U.K. scientists to the importance of N501Y. (A preprint of their results on the strain, which they are calling 501Y.V2, will be released on Monday, De Oliveira says.)</p>\n<p>[...] In the case of N501Y, more young people may be getting sick because many more are getting infected; Oliveira says some recent post-exam celebrations in South Africa have turned into superspreading events. Studies in cell culture and animal experiments will have to show how a virus with several or all of the mutations carried by the new variant compares with previous variants, says Drosten.</p>\n<p>[...] In the lab, Gupta’s group found that virus carrying the two mutations [ 69-70del and D796H] was less susceptible to convalescent plasma from several donors than the wildtype virus. That suggests it can evade antibodies targeting the wildtype virus, Gupta wrote in a preprint published this month. He also engineered a lentivirus to express mutated versions of the spike protein and found that the deletion alone made that virus twice as infectious. He is now conducting similar experiments with viruses that carry both the deletion and the N501Y mutation. The first results should appear just after Christmas, Gupta says.</p>\n</blockquote>\n", "score": 3 } ]

[ "covid-19", "disease-transmission", "infectious-diseases", "face-mask-respirator", "airborne-transmission" ]

[ { "answer_id": 25506, "body": "<p><a href=\"https://www.health.harvard.edu/a_to_z/double-vision-diplopia-a-to-z#:%7E:text=The%20double%20vision%20continues%20even,front%20surface%20of%20the%20cornea.\" rel=\"nofollow noreferrer\">Diplopia is not one of the more common symptoms of astigmatism, however it is certainly one of the possible manifestations.</a> In general diplopia (double vision) is categorized as either binocular (you only have double vision when both eyes are open) or monocular (you have double vision even if only the affected eye is open). Binocular diplopia is typically caused by misalignment of the eyes (most commonly a problem with the muscles that control the eyes), while monocular diplopia is typically caused by a problem within an eye itself.</p>\n<p><a href=\"https://www.aoa.org/healthy-eyes/eye-and-vision-conditions/astigmatism?sso=y\" rel=\"nofollow noreferrer\">Astigmatism most commonly presents as blurry vision due to irregularities in the cornea</a>. However if the irregularity causes the lens to refract the same image to two different areas of the retina, one would see two copies of that object and thus would have monocular diplopia.</p>\n", "score": 2 } ]

[ "eye", "symptoms" ]

[ { "answer_id": 25540, "body": "<p>My career choice (primarily Emergency Medicine) guaranteed that it would be necessary to postpone micturition on a regular basis. A nights-only colleague in our very busy ED would succinctly sum up how busy the night was: a) &quot;Not a wink&quot; (too busy to grab any sleep), b) &quot;Not a bite&quot; (too busy to stop to eat), or c) &quot;Not a pee&quot; (so busy there was no time for a bathroom break.) Since I mostly worked days, which are busier than nights, I often had 12 hour &quot;type c&quot; shifts.</p>\n<p>Does one's bladder accommodate? Yes, it does.</p>\n<blockquote>\n<p><a href=\"https://www.sciencedirect.com/topics/medicine-and-dentistry/bladder-filling\" rel=\"nofollow noreferrer\">The normal adult bladder response to filling at a <strong>physiologic rate</strong></a> is an almost imperceptible change in intravesical pressure. During at least the initial stages of bladder filling, after unfolding of the bladder wall from its collapsed state, this very high compliance (Δ volume/Δ pressure) of the bladder primarily results from its elastic and viscoelastic properties. Elasticity allows the constituents of the bladder wall to stretch to a certain degree without any increase in tension. Viscoelasticity allows stretch to induce a rise in tension, followed by a decay (i.e., stress relaxation) when the filling (i.e., stretch stimulus) slows or stops. ...<em>The urothelium also expands but must preserve its barrier function while doing so.</em> ...In the usual clinical setting, <strong>filling cystometry</strong> seems to show a slight increase in intravesical pressure, but Klevmark elegantly showed that this pressure rise is a function of the fact that cystometric filling is carried out at a greater than physiologic rate and, at physiologic filling rates, there is essentially no rise in bladder pressure until bladder capacity is reached.</p>\n</blockquote>\n<p>&quot;Physiological&quot; means, basically, normal human activity, including heavy fluid consumption. &quot;Filling cystometry&quot; is not &quot;normal/physiological&quot;: it's a bladder with a catheter that is filled by forcing fluid into the bladder trough the catheter at a much faster rate than the kidney can produce urine. (It's unpleasant.)</p>\n<p>In plain English, the empty bladder is wrinkled and folded upon itself <em>somewhat</em> like a raisin. Think of raisin -&gt; grape. There is basically no change in pressure (which would result in backing up into the ureters/kidney) from fully empty to fully full. At that point, you couldn't hold it in anymore; you'd <em>&quot;leak&quot;</em>.</p>\n<blockquote>\n<p>Suppose a person, drank 400ml-800ml of water, and he pees after 6 hours, when he wakes after sleep in the night. ...could (this) cause kidneys to damage (or fail!)</p>\n</blockquote>\n<p>No. If your bladder is small (some people do have smaller bladders than others), you will awaken with an urge to go long before urine backs up into the ureters to the kidney (urine backing up is <em>not</em> normal. It indicates pathology of some kind.) 400 cc is only 13 oz, or a bit more than 1.5 cups. During sleep, the pituitary gland secretes Antidiuretic Hormone (ADH) which decreases the production of urine, one of the adaptions that lets us get a full night's sleep. You probably wouldn't wake up for that. 800 cc, on the other hand, is a (relative) lot of water. You might wake up during the night with the urge to go. I probably would not.</p>\n<p>_{Have you ever noticed that even if you urinate on getting up, you still need to urinate a relatively short time (1-2 hrs) later? That's partly because ADH secretion is turned off.)}</p>\n<p>_{<em>Some</em> of what that article stated is true, but not much, and not for the correct reasons. Beware of believing what &quot;sounds true enough&quot; on the internet. Reliable sources will have citations to reputable literature. While this article does have citations (click on <em>5 Sources</em>), the author has misinterpreted and cherry-picked bits. That's why people with advanced Biology degrees <strong>must</strong> learn how to evaluate the literature. MDs are even tested on their ability to best interpret papers. PhDs learn by doing it day in and day out. Ask me how I know.}</p>\n<p>_{If holding urine back caused kidney damage, I'd be on dialysis and the kidney transplant list right now!}</p>\n", "score": 3 } ]

[ "kidney", "kidney-disease", "urinary-system", "urination", "urinary-tract-infect-uti" ]

[ { "answer_id": 25583, "body": "<p>Found this that appears to answer the question of the differences between two types of syringes.\nApparently the mean loss difference is 0.082 ml. Over the course of 5 inoculations (using a new syringe each time) a total of 0.41 ml would be conserved using the low dead-space syringe. Since the dosage per patient is 0.3, ml, theoretically 1 more inoculation can be obtained when using low dead space syringes. (20% increase). This is in agreement with what Ron Klain was saying.</p>\n<p>Going beyond that however it also appears that 7 doses per vial is feasible (which would represent a 40% increase in the number of innoculations per vial.</p>\n<p>The Pfizer vaccine vial is prefilled with 0.45 ml, and to that the clinician is to add 1.80 ml, so that the total volume per vial is 2.250 ml.</p>\n<p>If using a &quot;high&quot; dead space syringe, drawn to .3 ml, the total withdrawn from the vial is 0.382 ml per dose. With the vial volume at 2.250 ml, only 5 complete doses can be withdrawn</p>\n<p>OTOH, if using the &quot;low&quot; dead space syringe, drawn to 0.3 ml, the total withdrawn from the vial is 0.302 ml per dose. With the vial volume at 2.250 ml, 7 complete doses can be withdrawn.</p>\n<p>7 doses per vial versus 5 is a 40% increase.</p>\n<p>What I was hoping to see was that the WH COVID19 scientists were making and publishing similar calculations.</p>\n<p><a href=\"https://i.stack.imgur.com/5WagG.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/5WagG.jpg\" alt=\"Wikipedia image comparing syringes\" /></a></p>\n", "score": 1 } ]

[ "covid-19", "vaccination", "coronavirus" ]

[ { "answer_id": 25544, "body": "<p>The latter paper (Crouse, et al.) discusses this:</p>\n<blockquote>\n<p>Interestingly, metformin has previously been shown to also have anti-inflammatory (16, 17) and anti-thrombotic effects (18, 19) and excessive inflammatory responses, e.g., cytokine storm as well as disseminated thromboembolic events have been recognized as deadly complications of COVID-19 infection (20–22). It is therefore tempting to speculate that by exerting some of its anti-fibrinolytic activities (18) and inhibiting inflammatory cytokines such as tumor necrosis factor alpha or interleukin-6 (16, 17), suspected to play a role in the immune response to COVID-19 (12), metformin might improve outcome.</p>\n</blockquote>\n<p>It wouldn't be surprising given that dexamethasone is <a href=\"https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bcp.14540\" rel=\"nofollow noreferrer\">basically</a> used for that anti-thrombotic effect in treating Covid-19. I'm not sure how much of an anti-thrombotic effect metformin has in comparison; you may wan to check the refs cited in Crouse, et al.</p>\n", "score": 1 }, { "answer_id": 25549, "body": "<p>The following information obtained by searching PUBMED is NOT a systematic review.</p>\n<p>The search yields interesting information in support of the speculation by the previous answer (and by Crouse) that an effect of metformin in reducing the risk of mortality in patients with COVID-19 might be explained by an anti-thrombotic effect of metformin. One of the three identified studies (Xin) involving rats is cited by Crouse et al. The two epidemiologic studies provide direct evidence of a possible anti-thrombotic effect of metformin in humans.</p>\n<p>THREE PERTINENT STUDIES</p>\n<p><em>Metformin in Experimental Study in Diabetic and Non-Diabetic Rats</em></p>\n<p>In a study that involved rats with and without diabetes published in 2016, metformin treatment:</p>\n<blockquote>\n<p>“significantly decreased the incidence of pulmonary embolism (Fig.\n4G), reduced the weight and length of arterial and venous thrombus\n(Fig. 4A–F), prolonged the average time to occlusive thrombosis in\nFeCl3-induced inferior vena cava and carotid arteries injury\n(Supplementary Fig. 3C,D), and improved blood viscosity (Supplementary\nTable 1).”</p>\n</blockquote>\n<p>Xin G, Wei Z, Ji C, et al. Metformin Uniquely Prevents Thrombosis by Inhibiting Platelet Activation and mtDNA Release. Sci Rep. 2016;6:36222. Published 2016 Nov 2. doi:10.1038/srep36222</p>\n<p><a href=\"https://pubmed.ncbi.nlm.nih.gov/27805009/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/27805009/</a></p>\n<p><em>Epidemiologic Studies in Humans</em></p>\n<p>In a record linkage study based on data about 14,945 people with Type 2 diabetes published in 2014, the adjusted hazard ratio for deep vein thrombosis comparing 7,167 people who had a prescription for metformin with 7,778 people who had no prescription for metformin (matched by age, sex, and co-morbidity) was 0.43 (95% confidence interval 0.24-0.76).</p>\n<p>Lu DY, Huang CC, Huang PH, et al. Metformin use in patients with type 2 diabetes mellitus is associated with reduced risk of deep vein thrombosis: a non-randomized, pair-matched cohort study. BMC Cardiovasc Disord. 2014;14:187. Published 2014 Dec 15. doi:10.1186/1471-2261-14-187</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274716/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274716/</a></p>\n<p>In an epidemiologic cohort study based on data from 277 patients age 65+ years with a venous thromboembolism that was published in 2020, the adjusted hazard ratio for recurrent venous thromboembolism was 0.16 (95% confidence interval 0.08-0.33) in patients who took metformin.</p>\n<p>Aleidan FAS. The Cumulative Incidence and Risk Factors of Recurrent Venous Thromboembolism in the Elderly. Vasc Health Risk Manag. 2020;16:437-443. Published 2020 Oct 19. doi:10.2147/VHRM.S264814</p>\n<p><a href=\"https://pubmed.ncbi.nlm.nih.gov/33116554/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/33116554/</a></p>\n", "score": 1 } ]

[ "covid-19", "diabetes", "type-2-diabetes", "metformin" ]

[ { "answer_id": 25586, "body": "<p>You have observed a relationship in <em>phase/frequency</em> of these two signals, which indicates that you can use both to get the same rate information. In this case, that information is the <em>heart rate</em>.</p>\n<p>You cannot infer from this that there is sufficient information in one signal to predict the amplitude of the other. For a given recording, you may be able to use regression to attempt this, but you will likely find the accuracy is not good, and certainly not good enough to extrapolate and predict blood pressure in other patients with only PLETH.</p>\n<p>When measuring blood pressure, we are not typically concerned as much with the shape of the waveform as with the mean, maximum, and minimum pressures observed. External blood pressure monitoring is not particularly invasive. When invasive blood pressure monitoring is used it is for the improved accuracy and rapid information; you won't obtain these features with a surrogate.</p>\n", "score": 0 } ]

[ "blood-pressure", "blood-circulation", "pulse-oximeter" ]

[ { "answer_id": 25693, "body": "<p>The CDC published <a href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7007e1.htm\" rel=\"nofollow noreferrer\">a study</a> on this recently, but it's not doubling the same mask.</p>\n<blockquote>\n<p><a href=\"https://i.stack.imgur.com/JDho5.gif\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/JDho5.gif\" alt=\"enter image description here\" /></a></p>\n<p><strong>Double mask refers to a three-ply medical procedure mask covered by a three-ply cloth cotton mask.</strong> A knotted and tucked medical procedure mask is created by bringing together the corners and ear loops on each side, knotting the ears loops together where they attach to the mask, and then tucking in and flattening the resulting extra mask material to minimize the side gaps.</p>\n<p><a href=\"https://i.stack.imgur.com/06ydq.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/06ydq.jpg\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>Basically, the whole study was more geared to improving mask <em>fit</em>. Wearing a different type mask on top is basically one way to achieve that.</p>\n<blockquote>\n<p>During January 2021, CDC conducted experimental simulations using pliable elastomeric source and receiver headforms to assess the extent to which two modifications to medical procedure masks, 1) wearing a cloth mask over a medical procedure mask (double masking) and 2) knotting the ear loops of a medical procedure mask where they attach to the mask’s edges and then tucking in and flattening the extra material close to the face (knotted and tucked masks), could improve the fit of these masks and reduce the receiver’s exposure to an aerosol of simulated respiratory droplet particles of the size considered most important for transmitting SARS-CoV-2. The receiver’s exposure was maximally reduced (&gt;95%) when the source and receiver were fitted with modified medical procedure masks. <strong>These laboratory-based experiments highlight the importance of good fit to optimize mask performance.</strong> Until vaccine-induced population immunity is achieved, universal masking is a highly effective means to slow the spread of SARS-CoV-2** when combined with other protective measures, such as physical distancing, avoiding crowds and poorly ventilated indoor spaces, and good hand hygiene. Innovative efforts to improve the fit of cloth and medical procedure masks to enhance their performance merit attention.</p>\n<p>At least two recent studies examined use of mask fitters to improve the fit of cloth and medical procedure masks. Fitters can be solid (2) or elastic (3) and are worn over the mask, secured with head ties or ear loops. The results indicated that <strong>when fitters are secured over a medical procedure mask, they can potentially increase the wearer’s protection by ≥90% for aerosols in the size range considered to be the most important for transmitting SARS-CoV-2 (generally &lt;10 μm)</strong>. Other studies found that knotting and tucking a medical procedure mask or placing a sleeve made of sheer nylon hosiery material around the neck and pulling it up over either a cloth or medical procedure mask (3,4) also significantly improved the wearer’s protection by fitting the mask more tightly to the wearer’s face and reducing edge gaps. A recent expert commentary (5) proposed double masking as another means to improve the fit of medical procedure masks and maximize the filtration properties of the materials from which they are typically constructed, such as spun-bond and melt-blown polypropylene. Based on experiments that measured the filtration efficiencies of various cloth masks and a medical procedure mask (6), it was estimated that the better fit achieved by combining these two mask types, specifically a cloth mask over a medical procedure mask, could reduce a wearer’s exposure by &gt;90%.</p>\n<p>[...]</p>\n<p>Results from the first experiment demonstrated that the unknotted medical procedure mask alone blocked 42.0% of the particles from a simulated cough (standard deviation [SD] = 6.70), and the cloth mask alone blocked 44.3% (SD = 14.0). The combination of the cloth mask covering the medical procedure mask (double mask) blocked 92.5% of the cough particles (SD = 1.9).</p>\n<p>In the second experiment, adding a cloth mask over the source headform’s medical procedure mask or knotting and tucking the medical procedure mask reduced the cumulative exposure of the unmasked receiver by 82.2% (SD = 0.16) and 62.9% (SD = 0.08), respectively. When the source was unmasked and the receiver was fitted with the double mask or the knotted and tucked medical procedure mask, the receiver’s cumulative exposure was reduced by 83.0% (SD = 0.15) and 64.5% (SD = 0.03), respectively. When the source and receiver were both fitted with double masks or knotted and tucked masks, the cumulative exposure of the receiver was reduced 96.4% (SD = 0.02) and 95.9% (SD = 0.02), respectively.</p>\n<p>[...] these experiments did not include any other combinations of masks, such as cloth over cloth, medical procedure mask over medical procedure mask, or medical procedure mask over cloth.</p>\n</blockquote>\n<p>Don't ask me why they haven't tested the other combos.</p>\n<p>Most of the media headlines reporting on this study are already (perhaps by necessity) already glossing over the details and reporting that double masking gives &gt;90% protection or something like that. :/</p>\n<p>If you're curious, <a href=\"https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2774266\" rel=\"nofollow noreferrer\">one</a> of those previous studies cited has these more elaborate details on improving mask efficiency, but not [really] by double masking (unless you want to consider the nylon hosiery on top as such):</p>\n<blockquote>\n<p>As expected based on data from our previous work, a National Institute for Occupational Safety and Health–approved 3M 9210 N95 respirator used as a reference control provided very high mean FFE (98.4% [0.5%]; n = 1) (Table). The medical procedure masks with elastic ear loops tested in this study had a mean (SD) FFE of 38.5% (11.2%), which was lower than that of medical surgical masks with tie strings (71.5% [5.5%]; n = 4). Tying the ear loops and tucking in the corners of the procedure mask to minimize gaps in the sides of the mask increased the mean (SD) FFE to 60.3% (11.1%). The “fix-the-mask” 3–rubber band modification and the nylon hosiery sleeve modifications, which were also intended to reduce gaps between the mask and the wearer’s face, improved mean (SD) FFE to 78.2% (3.3%) and 80.2% (3.1%), respectively.</p>\n</blockquote>\n<p>I've cropped part of the table to the most relevant mods (which are illustrated in the subsequent figure):</p>\n<blockquote>\n<p><a href=\"https://i.stack.imgur.com/dWIAj.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/dWIAj.png\" alt=\"enter image description here\" /></a></p>\n<p><a href=\"https://i.stack.imgur.com/p9vpP.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/p9vpP.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>I'm not sure how much one can learn from this bit alone, but that study\nalso contrasted/tested a commercial mask with (and without) inserts:</p>\n<blockquote>\n<p>For example, the 2-layer nylon mask with ear\nloops was tested under various conditions, including with and\nwithout an aluminum nose bridge, with and without a commercially\navailable insert, and after 1 wash cycle in a standard\nhousehold washing machine (air-dried on a drying rack). <strong>The\nunwashed nylon mask without a nose bridge or insert had an\nFFE of 44.7%. The addition of a nose bridge reduced visible\ngaps around the nose and increased FFE to 56.3%. Adding a\nfilter insert to the mask with the nose bridge in place resulted\nin a further increase in FFE to 74.4%. Interestingly,\nthe FFE of the nylon mask (with the nose bridge but without\nthe filter insert) improved slightly to 79.0% after washing.\nIt is unclear why washing alone improved the FFE from\n56.3%to 79.0%. It may be that the washing/drying process unraveled\nsome of the fibers to increase the overall filtration surface,\nand thus filtration efficiency, of the medium, or perhaps\nit modified the mask shape or size in away that improved fit\nor both.</strong> The washing/drying test was not repeated with additional\nnylon masks. Further investigation to assess the association\nof single and multiple washing with mask integrity and\nmaterial disposition would be necessary to validate any improvement\nin FFE.</p>\n<p><a href=\"https://i.stack.imgur.com/2TbbK.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/2TbbK.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>The mask discussed in that last para looks like this, i.e. has fairly good side fit:</p>\n<blockquote>\n<p><a href=\"https://i.stack.imgur.com/5TC7o.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/5TC7o.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>although that image doesn't really show all the [inner] details (nose bridge, inserts).</p>\n<p>As the paper noted, the odd bit is that while inserts surely helped in the new state, washing it achieved the same effect (without inserts)...</p>\n", "score": 2 } ]

[ "covid-19", "face-mask-respirator" ]

[ { "answer_id": 25595, "body": "<p>After posting this, I did a lot more research and I was finally able to find some publications with controlled experiments on Na+ neonatal/infant intake, mostly in animals of course, with a few human experiments when they were ethical to do so (e.g. testing two Na+ supplementation regime in Na+ deficient neonates).</p>\n<p>[1]. <a href=\"https://link.springer.com/article/10.1007/BF01213376\" rel=\"nofollow noreferrer\">Haycock, The influence of sodium on growth in infancy.</a></p>\n<p>This review article quotes a number of experiments on rats and other animals, and to my untrained eye, the methodology looks to be gold standard. In one experiment, some populations of rats are apparently in completely indistinguishable environments, except that the concentration of Na+ is varied across these groups (Cl- is constant across all groups). Na+ deprivation seems to lead to growth delay, progressively larger dose of Na+ mitigate this delay up to a certain threshold where normal development is achieved. This article describes many more related experiments studying related aspects, e.g. showing that Na+ deprivation followed by adequate Na+ intake does not produce &quot;catch-up&quot; growth (the growth gap is permanent).</p>\n<p>This paper also describes two experiments on human neonates. The first such experiment had substantial Na+ losses in the ileostomy fluid. There does not seem to be any controls, and no mention of blinding the clinicians. These infants failed to grow, which was remedied when the infants were provided with Na+ supplementation.</p>\n<p>A second clinical experiment on humans is described. Premature neonates (&lt;34 weeks) were provided either 4-5mmol/kg/day (treatment group) or 1-1.5/mmol/kg/day (&quot;control&quot; group) of Na+. The &quot;control group&quot; seems to have delayed growth compared to the treatment group. Further observations are described, comparing &quot;mature&quot; maternal milk against maternal milk of mothers whose infants are premature, and whey-based formula with high mineral contents. It wasn't clear to me how many of these experiments were double-blind controlled, but also the three treatments don't prove much about Na+ because so many other atoms and molecules vary between the three treatments.</p>\n<p>Elsewhere in the literature, I've seen many mentions that &lt;34 week preemies should receive Na+ supplementation, but &gt;34 week preemies should not. Although it is scientifically correct in the abstract, not to give unproven treatments to patients, it may be that the question of Na+ sufficiency in mature neonates is an open problem. I was not able to find scientific evidence to support confident assertions that mature neonates and infants have sufficient Na+ intake from maternal milk. For example:</p>\n<p>[2]. <a href=\"https://www.sciencedirect.com/science/article/pii/S093947531200097X?casa_token=_4q-VgUMfywAAAAA:j7uuo9FZRJY6sTw8pl28icirHS-T4KDBZGG8c2aWurb59kV7WPknH3Rmw07pfUYXRokQ3Z7Paw\" rel=\"nofollow noreferrer\">Strazzullo, Campanozzi, Avallone. Does salt intake in the first two years of life affect the development of cardiovascular disorders in adulthood?</a></p>\n<p>[2] is a highly cited paper that sets out excellent protocols for the clinical setting. However, I am using [2] as an example because I feel that the wording they use is sometimes stronger than the scientific evidence that they have. This is par for the course in medicine, but as a mathematician, and for the context of my question, I am looking for unambiguous, objective, gold-standard science.</p>\n<p>In [2], the authors write &quot;The amount of sodium to be retained by an infant for proper physiological growth is largely covered by breast feeding (or low sodium formula milk) in the first six months...&quot; However, according to my reading, they do not have gold-standard double blind controlled experiments on humans to prove this. One piece of their argument is to cite a rat experiments co-authored by Hancock (the author of [1]) and extrapolate to humans. Their argument is that rats need 0.3mmol/day, and they somehow conclude that therefore humans would need 0.9mmol/day. If that were the case, there is a good likelihood that maternal milk would indeed be sufficient, but this begs the question: why does maternal milk contain 60+mmol/L of Na+? Also, I am suspicious of this extrapolation, tripling from newborn rats to newborn humans.</p>\n<p>Apart from the rat evidence, these authors attempt to link &quot;salt preference&quot; with later bad outcomes, but this is not the sort of science I am looking for. It suffers from the usual flaws. Observational studies can, at best, show correlations. You can never tell the direction of the causality, and you can never uncover confounding factor. My favorite way of teaching confounding factors and causation is the story of Bob, who always gets a headache after sleeping with his shoes on. Because of the time difference, people assume that Bob's shoes are magical headache-causing footwear but the reality is that Bob only sleeps in his shoes after partying at the pub.</p>\n<p>I realize that if [2] had used confusing language like &quot;we recommend no Na+ supplementation for mature neonates, although the question of Na+ sufficiency for such patients remains an open problem&quot;, that would be confusing for clinicians and it's a lot easier to publish papers that have a clear message.</p>\n<p>My personal, unscientific opinion is that it is likely that mature neonates and young infants have sufficient salt, but it is also possible that they do not. Salt sufficiency is presumed because it is assumed that maternal milk is &quot;perfect food&quot; for neonates. But this is in tension with the consensus elsewhere that breastfed children are iron deficient. Would prehistoric infant mammals somehow get iron intake from their environments? Would they also get sodium intake from their environments? I don't think these questions have been answered, from what I can tell.</p>\n", "score": 1 } ]

[ "diet", "research", "pediatrics", "salt", "scientific-method" ]

[ { "answer_id": 25590, "body": "<p>According to one <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994165/\" rel=\"noreferrer\">2010 paper</a>, which actually tried to identify the correlates of the behavior, albeit in a small sample (n=13, 3 males, 10 females) that was referred to a clinic:</p>\n<blockquote>\n<p>The median age at the first incident was 19.5 months (range, 4-36 months); the median masturbation frequency, 4 times/day; and the median duration of each event, 3.9 min. The subjects masturbated in both prone (n=10) and supine positions (n=3); two subjects used the knee-chest position. All subjects showed facial flushing; 6, friction between the thighs; 5, sweating; 9, sleeping after the event; and 12, disturbance on interruption. EEG was abnormal in one of eight subjects tested, and neuroimages were normal in all of nine subjects examined. The case and control groups had comparable levels of all sex hormones, except estradiol, which showed significantly lower levels in the case group (P=.02).</p>\n<p>CONCLUSION:\nMasturbation in children seems to be associated with reduced estradiol levels, but not with other sex hormones. Further studies are needed to confirm our findings.</p>\n</blockquote>\n<p>So, there was nothing too obviously wrong with these children otherwise...</p>\n<p>The sample is from a clinic in Jordan but I didn't sense any obvious cultural bias, except for the higher presumed referral rate... and lack of follow-up:</p>\n<blockquote>\n<p>Since Jordan is a sexually conservative country with no formal sex education, childhood masturbation may create more parental concern than in Western societies, and the referral rate may differ. Ten (77%) of our children did not attend any follow-up visits after their parents were informed about the diagnosis of childhood masturbation, possibly due to the concern of stigmatization.</p>\n</blockquote>\n<p>By the way, there is a term for this masturbation-like behavior in children (as mentioned in the paper) namely <a href=\"https://en.wikipedia.org/wiki/Gratification_disorder\" rel=\"noreferrer\">gratification disorder</a>. Alas the Wikipedia article cites only a handful of even older articles, to say that not much research was done.</p>\n<p>Some similar studies conducted <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1719833/pdf/v089p00225.pdf\" rel=\"noreferrer\">in the UK</a> and <a href=\"https://pubmed.ncbi.nlm.nih.gov/10834518/\" rel=\"noreferrer\">in Turkey</a> actually had somewhat larger samples, but otherwise there's not a lot to say about this. The UK study had a broader age range... and there's the odd bit about the car seat:</p>\n<blockquote>\n<p>Thirty one patients were diagnosed (11 males and 20 females). [...] The median age at first symptoms was 10.5 months (range 3 months to 5 years 5 months). The median age at diagnosis was 24.5 months (range 5 months to 8 years). [...] Events occurred in any situation in 10 children, and in a car seat in 11.</p>\n</blockquote>\n<p>The discussion section also notes something about stigma:</p>\n<blockquote>\n<p>Masturbation in children is commonly recognised to be a\nvariant of normal behaviour. Once the diagnosis is made and\nthere are no suspicions of child sexual abuse requiring\nfurther investigation and management, reassurance seems to\nbe the most effective management. Parents prefer the term\ngratification (or even benign idiopathic infantile dyskinesia)\nto infantile masturbation as there is less social stigma\nattached to these terms.</p>\n</blockquote>\n<hr />\n<p>Classification-wise, one 2008 <a href=\"https://link.springer.com/article/10.1007/s00431-008-0766-2\" rel=\"noreferrer\">review</a> says that</p>\n<blockquote>\n<p>CM is defined as self-stimulation of the genitalia in a\nprepubescent child. It is not included in the DSM-IV,\nthe Diagnostic and Statistical Manual of Mental Disorders\n(4th edition) of the American Psychiatric Association,\nwhich means that it is not classified as a (specific)\npsychiatric disorder. The WHO places (excessive) CM\nunder the title “Other specified behavioural and emotional\ndisorders with onset usually occurring in childhood and\nadolescence” (F98.8) in the ICD-10, the International\nStatistical Classification System of Diseases and Related\nHealth Problems.</p>\n</blockquote>\n<p>And to help answer your title question, this review actually does cite (and even include a table from) a study on prevalence, although this was assessed indirectly (parental reporting):</p>\n<blockquote>\n<p>In a study of Friedrich, the frequencies of a lot of\ndifferent sexual behaviours in 1,114 2- to 12-year-old\nchildren were rated by their mothers (by means of the\nCSBI and the CBCL). Friedrich excluded children with a\nhistory or suspicion of sexual abuse in order to compose a\nnormative sample. His results were consistent with earlier\nresearch and showed that a broad spectrum of sexual\nbehaviours appears in children with varying frequencies.\nSelf-stimulation is one of the most frequently seen sexual\nbehaviours (Table 1).</p>\n</blockquote>\n<p><a href=\"https://i.stack.imgur.com/pkrOW.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/pkrOW.png\" alt=\"enter image description here\" /></a></p>\n<p>That <a href=\"https://pubmed.ncbi.nlm.nih.gov/9521975/\" rel=\"noreferrer\">study</a> actually used a combined sample from Los Angeles and Minnesota, with the stated reason for doing so to average over possible cultural bias of the respondents.</p>\n<p>There's yet another <a href=\"https://macpeds.com/documents/TheEvaluationofSexualBehaviorsinChildren.pdf\" rel=\"noreferrer\">2009 review</a> which is open-access, but on the broader topic sexual-like behaviors in childhood including such interactions with other children, exhibitionism etc. This review notes that &quot;more than 50% of children will engage in some type of sexual behavior before their 13th birthday&quot; but this is across the aforementioned broader range of behaviors. For childhood masturbation proper, they don't cite any other study besides Friedrich's already discussed above. But (I guess mainly from that) they summarize in a table of &quot;Examples of Sexual Behaviors in Children 2 to 6 Years of Age&quot; that &quot;Normal, Common Behaviors&quot; include &quot;Touching/masturbating genitals\nin public/private&quot;.</p>\n<p>Actually Friedrich is a co-author to another <a href=\"https://pubmed.ncbi.nlm.nih.gov/10506230/\" rel=\"noreferrer\">study</a> that (using a translated questionnaire) had roughly similar findings in a Dutch sample, but a bit lower e.g. only 9.2% for &quot;masturbates with hand&quot; in the 2-5 y.o. I've cropped the most relevant part of their questionnaire report:</p>\n<p><a href=\"https://i.stack.imgur.com/3KIsh.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/3KIsh.png\" alt=\"enter image description here\" /></a></p>\n<p>They also note some parental correlates of higher reporting, which not surprisingly include a more liberal attitude towards nudity, homosexuality etc.\nA more <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0145213419303539\" rel=\"noreferrer\">recent study</a> mentions that results turned out not to be so easily generalizable because what parents report seems to vary across cultures...</p>\n<blockquote>\n<p>Comparison of the available research based on US, European, and Asian samples, reveals that European parents score highest on the CSBI total (de Graaf &amp; Rademakers, 2007), whereas Asian children hardly show any sexual behavior according to the CSBI total score (<a href=\"https://www.psychiatryinvestigation.org/journal/view.php?doi=10.4306/pi.2013.10.4.336\" rel=\"noreferrer\">Jin, Chung, Jeong, &amp; Lee, 2013</a>).</p>\n</blockquote>\n<p>One good news (perhaps) is that within the same culture, mothers and fathers make consistent reports on their children. The latter paper does note, culture-wise:</p>\n<blockquote>\n<p>we must take into consideration the conservative Korean culture based on Confucian strictures including sexual taboos even among the adults, which likely affected the parents' ability to observe and report their children's sexual behavior.</p>\n</blockquote>\n", "score": 6 } ]

[ "pediatrics", "sexuality", "children-kids", "developmental-milestones" ]

[ { "answer_id": 25630, "body": "<p>The closest thing I have found to this is a tool called the <a href=\"https://docs.google.com/spreadsheets/d/16K1OQkLD4BjgBdO8ePj6ytf-RpPMlJ6aXFg3PrIQBbQ/edit#gid=519189277\" rel=\"nofollow noreferrer\">COVID-19 Airborne Transmission Estimator</a>. It is basically a spreadsheet on which you can tweak various parameters and get an estimate of the number of people infected at a given gathering. It was developed last summer by a professor at the University of Colorado; he is not a doctor but is a chemist who studies aerosols. Here is <a href=\"http://cires1.colorado.edu/jimenez/\" rel=\"nofollow noreferrer\">a page about his research group</a> and here is <a href=\"https://cires.colorado.edu/news/covid-19-airborne-transmission-tool-available\" rel=\"nofollow noreferrer\">a brief press release about the tool</a>. As far as I can tell there has been no peer review of this model and it seems to be still quite provisional.</p>\n<p>The Spanish newspaper El Pais wrote <a href=\"https://english.elpais.com/society/2020-10-28/a-room-a-bar-and-a-class-how-the-coronavirus-is-spread-through-the-air.html\" rel=\"nofollow noreferrer\">an article</a> which describes some examples of risk based on the model. National Geographic also did <a href=\"https://www.nationalgeographic.com/science/2020/08/how-to-measure-risk-airborne-coronavirus-your-office-classroom-bus-ride-cvd/\" rel=\"nofollow noreferrer\">an article</a> showing some graphs of risk in various situations based on the model.</p>\n<p>Those articles are useful because the spreadsheet itself can be somewhat overwhelming to use. The model requires values for certain parameters that the average person has no real knowledge about, such as the volume of air breathed in by a person in an hour and the rate at which the air in the space is replaced with fresh air from an external source; as well as parameters that are not definitively known or may be quite variable, such as the number of infectious doses of the virus exhaled per hour.</p>\n<p>Thus the model comes with a major &quot;garbage in, garbage out&quot; caveat. Also, of course, it is not so much an analysis of experimental data as a mathematical model, and it relies on many simplifying assumptions. For instance, it does not consider the details of airflow within the space, although there is evidence that that can be important. Nonetheless, it is the only model I've seen that attempts to push the numbers all the way through to direct estimates of infection. The author is quoted in the National Geographic article as saying, &quot;We do not have a ton of information, but we cannot afford to wait for a ton of information.&quot;</p>\n", "score": 3 }, { "answer_id": 28884, "body": "<p>I'll note that a more recent &quot;room simulation&quot; paper was published <a href=\"https://science.sciencemag.org/content/372/6549/1439\" rel=\"nofollow noreferrer\">in <em>Science</em></a> (a top journal). This paper was basically based on a Fangcang Hospital simulation (200 people in a 500m² x 10m high hall--see supplementary material) and lots of data on infectious dose estimates, mask filtration efficiency etc., but neither the authors of the paper nor the <em>Science</em> editors could conclude from it something &quot;in layperson's terms&quot; about some other setting like a restaurant, a bus etc. The editors' best attempt at summarizing the results were something like:</p>\n<blockquote>\n<p>In indoor settings, it is impossible to avoid breathing in air that someone else has exhaled, and in hospital situations where the virus concentration is the highest, even the best-performing masks used without other protective gear such as hazmat suits will not provide adequate protection.</p>\n</blockquote>\n<p>Meh. A slightly more daring simulation study (in terms of conclusions) was <a href=\"https://www.pnas.org/content/118/17/e2018995118/tab-figures-data\" rel=\"nofollow noreferrer\">published in PNAS</a>. They offered this summary graph for a classroom and respectively a nursing home:</p>\n<p><a href=\"https://i.stack.imgur.com/Bp7fw.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Bp7fw.png\" alt=\"enter image description here\" /></a></p>\n<p>Basically such models are informed (by real-world parameter estimates) but not really calibrated, since you can't easily check their predictions conform to some experimental results.</p>\n<p>I'm personally pretty skeptical of the predictions in this latter (PNAS) study. It almost looks engineered to predict that a classroom is safe <em>without</em> masks at normal occupancy (6ft distance) and natural ventilation, for the duration of a fairly normal school day (6-7 hrs)... and with (cloth) masks, basically indefinitely. The paper's statement:</p>\n<blockquote>\n<p>For normal occupancy and without masks, the safe time after an infected individual enters the classroom is 1.2 h for natural ventilation and 7.2 h with mechanical ventilation, according to the transient bound, SI Appendix, Eq. S8. Even with cloth mask use (pm=0.3), these bounds are increased dramatically, to 8 and 80 h, respectively. Assuming 6 h of indoor time per day, a school group wearing masks with adequate ventilation would thus be safe for longer than the recovery time for COVID-19 (7 d to 14 d), and school transmissions would be rare. We stress, however, that our predictions are based on the assumption of a “quiet classroom”, where resting respiration (Cq=30) is the norm. Extended periods of physical activity, collective speech, or singing would lower the time limit by an order of magnitude (Fig. 2).</p>\n</blockquote>\n<p>But a recent <a href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7035e2.htm\" rel=\"nofollow noreferrer\">CDC case study</a> found that a teacher who at least occasionally didn't wear a mask when lecturing very likely was the source of an outbreak, infecting (in two days) all the children in the front row, and some/fewer in the back, in a nearly similar setup, i.e. 6ft distance [supposedly] maintained, even though the children supposedly were wearing masks, and the windows were open; this is with the delta variant though.</p>\n", "score": 1 } ]

[ "covid-19", "disease-transmission" ]

[ { "answer_id": 25651, "body": "<p>I agree the presentation is confusing. There are 4 categories, two are the same category except separated by age. The other two categories are not separated by age. There are two gray colors; the darker one is &quot;NHAP patients, not bedridden&quot; (nursing home acquired pneumonia), and is the one you refer to.</p>\n<p>You'll note that only 3 categories are present at any age range except 60-69, because that decade includes both above/below 65.</p>\n", "score": 4 } ]

[ "clinical-study" ]

[ { "answer_id": 25678, "body": "<p>As pointed out in <a href=\"https://www.mytutor.co.uk/answers/14609/GCSE/Biology/How-do-glucose-and-oxygen-get-into-the-blood-to-be-used-for-respiration/\" rel=\"nofollow noreferrer\">mytutor.co.uk</a> in the basic biology section</p>\n<blockquote>\n<p>When we breathe we inhale oxygen from the air into our lungs. The alveoli are tiny air sacs in the lung where oxygen diffuses into the blood via small blood vessels, known as capillaries. The blood in these capillaries has a low concentration of oxygen which allows oxygen in the alveoli to diffuse down the concentration gradient and into the blood. When we eat food, it is broken down by enzymes, such as amylase, in the digestive system. Glucose is formed by the breakdown of carbohydrates in the small intestine. Glucose is then absorbed into the blood from the small intestine via the villi by active transport. Glucose and oxygen travel in the bloodstream and are taken up into cells. Respiration takes place in the mitochondria, producing energy.</p>\n</blockquote>\n<p>Glucose transporters are a wide group of membrane proteins that facilitate the transport of glucose across the plasma membrane, a process known as facilitated diffusion (<a href=\"https://en.wikipedia.org/wiki/Glucose_transporter\" rel=\"nofollow noreferrer\">Wikipedia</a>).</p>\n<blockquote>\n<p>Role of Diffusion: Glucose and other small molecules (but not macromolecules) diffuse in and out of capillaries through the liquid filled spaces between the cells, not by diffusing across the cell membrane. Most proteins are too big to enter or leave capillaries by diffusion (<a href=\"http://www.columbia.edu/cu/biology/courses/c2006/lectures11/lect6.11.html\" rel=\"nofollow noreferrer\">Colombia University</a>).</p>\n</blockquote>\n<p>The blood glucose levels are expressed as millimoles per litre (mmol/l) and stay stable amongst people <strong>without</strong> diabetes at around 4-8mmol/L.</p>\n<p>When the body processes sugar, glucose in the bloodstream naturally attaches to haemoglobin, a protein within red blood cells that carries oxygen throughout your body.</p>\n<p>The amount of glucose that combines with this protein is directly proportional to the total amount of sugar that is in your system at that time.</p>\n<blockquote>\n<p>Because red blood cells in the human body survive for 8-12 weeks before renewal, measuring glycated haemoglobin (or HbA1c) can be used to reflect average blood glucose levels over that duration, providing a useful longer-term gauge of blood glucose control. (<a href=\"https://www.diabetes.co.uk/what-is-hba1c.html\" rel=\"nofollow noreferrer\">Diabetes UK</a>)</p>\n</blockquote>\n<p>Normal (non-diabetic) HbA1c levels will give a measurement of below 42 mmol/mol (below 6%).</p>\n", "score": 1 } ]

[ "blood", "blood-tests", "blood-circulation", "glucose", "blood-sugar" ]

[ { "answer_id": 25699, "body": "<blockquote>\n<p>Are there <em>in vitro</em> studies that find ivermectin directly effective against the SARS-CoV-2 spike or its other proteins?</p>\n</blockquote>\n<p>There are <em>in vitro</em> studies: <a href=\"https://www.sciencedirect.com/science/article/pii/S0166354220302011\" rel=\"nofollow noreferrer\">The FDA-approved drug ivermectin inhibits the replication of SARS-CoV-2 in vitro</a>, but the exact mechanism appears to be uncertain:</p>\n<blockquote>\n<p>Taken together these results demonstrate that ivermectin has antiviral\naction against the SARS-CoV-2 clinical isolate in vitro, with a single\ndose able to control viral replication within 24–48 h in our system.\n<strong>We hypothesise that this is likely through inhibiting IMPα/β1-mediated\nnuclear import of viral proteins (Fig. 1G), as shown for other RNA\nviruses</strong> (Tay et al., 2013; Wagstaff et al., 2012; Yang et al., 2020);\nconfirmation of this mechanism in the case of SARS-CoV-2, and\nidentification of the specific SARS-CoV-2 and/or host component(s)\nimpacted (see (Yang et al., 2020)) is an important focus <strong>future work</strong>\nin this laboratory. Ultimately, development of an effective anti-viral\nfor SARS-CoV-2, if given to patients early in infection, could help to\nlimit the viral load, prevent severe disease progression and limit\nperson-person transmission. Benchmarking testing of ivermectin against\nother potential antivirals for SARS-CoV-2 with alternative mechanisms\nof action (Dong et al., 2020; Elfiky, 2020; Gordon et al., 2020; Li\nand De Clercq, 2020; Wang et al., 2020) would thus be important as\nsoon as practicable. This Brief Report raises the possibility that\nivermectin could be a useful antiviral to limit SARS-CoV-2, in similar\nfashion to those already reported (Dong et al., 2020; Elfiky, 2020;\nGordon et al., 2020; Li and De Clercq, 2020; Wang et al., 2020); until\none of these is proven to be beneficial in a clinical setting, all\nshould be pursued as rapidly as possible.</p>\n</blockquote>\n", "score": 2 } ]

[ "sars-cov-2", "antivirals" ]

[ { "answer_id": 25742, "body": "<p>The drug development process has several stages and before proceeding to human trials, parameters such as relative safety and probable therapeutic action are evaluated in order to assure safety and effectiveness on the treatment.</p>\n<blockquote>\n<p>Some information about the pharmacokinetics of a compound is also required before clinical evaluation is begun. - Katzung and Trevor's Pharmacology</p>\n</blockquote>\n<p><a href=\"https://i.stack.imgur.com/nVmku.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/nVmku.jpg\" alt=\"image1\" /></a></p>\n<p>In Katzung and Trevor's Pharmacology, pharmacological profile is defined as</p>\n<p><a href=\"https://i.stack.imgur.com/JRfaD.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/JRfaD.jpg\" alt=\"pharmacological profile\" /></a></p>\n<p>Regarding your question, <em>favorable pharmacological profile</em> means that, in general, the pharmacological effect studied in the drug [YTX-7739] (cardiovascular, gastrointestinal, renal, CNS, etc.) had a beneficial behavior and ensured the therapeutic safety for the people being tested.</p>\n", "score": 1 } ]

[ "terminology" ]

[ { "answer_id": 25789, "body": "<p>Although <em>Candida Albicans</em> can be transmitted sexually, generally it is developed without sexual contact. WebMD gives <a href=\"https://www.medicalnewstoday.com/articles/322722#types-of-infections\" rel=\"nofollow noreferrer\">the following details</a></p>\n<blockquote>\n<p>Normally, a type of bacteria called <em>Lactobacillus</em> keeps the amount of Candida in the genital area under control. However, when <em>Lactobacillus</em> levels are disrupted in some way, <em>Candida</em> can overgrow and cause an infection.</p>\n<p>You can also develop a Candida genital infection after participating in certain sexual activities, particularly those that involve oral-genital contact.</p>\n<p>Although otherwise healthy individuals can get genital Candida infections, the following groups are at an increased risk:</p>\n<ul>\n<li>people that have taken antibiotics recently</li>\n<li>people with uncontrolled diabetes</li>\n<li>immunosuppressed individuals</li>\n<li>pregnant women</li>\n<li>people that are taking oral contraceptives or who are on hormone therapy</li>\n</ul>\n</blockquote>\n", "score": 1 } ]

[ "sti", "fungal-infection" ]

[ { "answer_id": 25793, "body": "<p>By &quot;natural protein intake&quot; they are referring to normal dietary protein intake, in contrast to amino acid supplements given as protein substitutes for people with disorders related to protein/amino acid metabolism. See for example from <a href=\"https://en.wikipedia.org/wiki/Phenylketonuria#Treatment\" rel=\"nofollow noreferrer\">Wikipedia</a>:</p>\n<blockquote>\n<p>Supplementary &quot;protein substitute&quot; formulas are typically prescribed for people PKU (starting in infancy) to provide the amino acids and other necessary nutrients that would otherwise be lacking in a low-phenylalanine diet.</p>\n</blockquote>\n<p>Some other sources where this phrasing is used:</p>\n<p>Evans, M., Truby, H., &amp; Boneh, A. (2017). The relationship between dietary intake, growth and body composition in Phenylketonuria. Molecular genetics and metabolism, 122(1-2), 36-42.</p>\n<p>Hoeksma, M., Van Rijn, M., Verkerk, P. H., Bosch, A. M., Mulder, M. F., de Klerk, J. B., ... &amp; van Spronsen, F. J. (2005). The intake of total protein, natural protein and protein substitute and growth of height and head circumference in Dutch infants with phenylketonuria. Journal of Inherited Metabolic Disease: Official Journal of the Society for the Study of Inborn Errors of Metabolism, 28(6), 845-854.</p>\n<p>Huemer, M., Huemer, C., Möslinger, D., Huter, D., &amp; Stöckler-Ipsiroglu, S. (2007). Growth and body composition in children with classical phenylketonuria: results in 34 patients and review of the literature. Journal of inherited metabolic disease, 30(5), 694-699.</p>\n", "score": 1 } ]

[ "nutrition", "terminology", "metabolism" ]

[ { "answer_id": 25820, "body": "<p>Short answer: there are many different EHR systems, and they don’t like to talk to each other.</p>\n<p>Long answer: There are a lot of different pieces of software out there for EHR systems. Soarian, Epic, Powerchart are a few of the ones I have worked with. Usually, an EHR system will be throughout a Health System. All the hospitals in that system will be able to share data and medical records. To send medical records to a physician or hospital not in that system, they, in my experience, are printed and faxed over.</p>\n<p>Even if two systems use the same EHR program, those programs are usually customized to that system, and won’t necessarily transfer data between them.</p>\n<p>I highly recommend requesting and keeping your own copies of your medical records for this very reason.</p>\n", "score": 4 } ]

[ "health-informatics", "medical-records" ]

[ { "answer_id": 25890, "body": "<p>After being educated on the issue by a virologist (Georges Natsoulis), I understand the question needs answers at two completely different levels. First, our very own human genome has been in good part developed in conjunction with the input of left over viruses. Thus, without the input from viruses we would not be who we are. Second, viruses within our bodies do have their own virome (counterpart to the bacteria microbiome). And, the virome does influence our health and survival in a multitude of ways.</p>\n<p>Back to the first answer that viruses make up a good part of our human genome, among the more frequent gene in our genome is reverse transcriptase, the key gene in retroviruses (e. g. HIV and relatives). Some scientists estimate that we have about 20,000 functional genes and up to 10,000 copies of reverse transcriptase. So, the latter (virus derived genes) would represent around half of the former (our own genes).</p>\n<p>Many of our genes are in fact coopted versions of viral genes. Thus, viruses are an essential ingredient of our very own genome. And, these virus-related genes are very stable, passed on from one generation to the next just like any other genes. They do change slowly over time due to natural selection factors in a similar way as other genes.</p>\n<p>Now, back to the second answer about the virome, the study reference disclosed by Chris Rogers (<a href=\"https://www.sciencedaily.com/releases/2015/04/150430170750.htm\" rel=\"nofollow noreferrer\">American Society for Microbiology, 2015</a>) within the comment section under my question indicates that some viruses are explicitly beneficial. For instance some types of herpes viruses protect against various cancers. The virome, just like the microbiome are pretty lively and dynamic and can change quite a bit over the life of an individual depending on lifestyle, recent infections, etc.</p>\n<p>Just like bacteria, nature is probably in a chronic state of fragile disequilibrium/equilibrium. A bacteria located within a certain organ can be very &quot;good.&quot; While the very same bacteria located elsewhere in the body may be very &quot;bad.&quot; Viruses may follow a fairly similar pattern.</p>\n<p>When we suffer from a viral disease, we are only aware of the negative effect of a given virus without always fully understanding its implications (including good ones).</p>\n<h2>References</h2>\n<p>American Society for Microbiology. (2015). Viruses: You've heard the bad; here's the good. <em>ScienceDaily</em>. <a href=\"https://www.sciencedaily.com/releases/2015/04/150430170750.htm\" rel=\"nofollow noreferrer\">https://www.sciencedaily.com/releases/2015/04/150430170750.htm</a></p>\n", "score": 1 } ]

[ "virus", "immune-system", "disease-transmission", "bacteria", "influenza" ]

[ { "answer_id": 25929, "body": "<p><a href=\"https://www.quora.com/profile/Liam-Goldstein-5\" rel=\"nofollow noreferrer\">Liam Goldstein</a> <a href=\"https://qr.ae/pGXARc\" rel=\"nofollow noreferrer\">pointed</a> me to the <a href=\"https://vaers.hhs.gov/\" rel=\"nofollow noreferrer\">Vaccine Adverse Event Reporting System (VAERS)</a> in the United States.</p>\n<p><a href=\"https://vaers.hhs.gov/faq.html#collapse17\" rel=\"nofollow noreferrer\">https://vaers.hhs.gov/faq.html#collapse17</a>:</p>\n<blockquote>\n<p>Healthcare providers [in the United States] are required to report to VAERS the following adverse events after COVID-19 vaccination [under Emergency Use Authorization (EUA)], and other adverse events if later revised by CDC:</p>\n</blockquote>\n<p>The VAERS makes their data available for download at <a href=\"https://vaers.hhs.gov/data.html\" rel=\"nofollow noreferrer\">https://vaers.hhs.gov/data.html</a>.</p>\n<p><a href=\"https://www.cdc.gov/coronavirus/2019-ncov/vaccines/safety/adverse-events.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/coronavirus/2019-ncov/vaccines/safety/adverse-events.html</a>:</p>\n<blockquote>\n<p>Over <strong>109 million doses of COVID-19 vaccines were administered in the United States</strong> from December 14, 2020, through March 15, 2021. During this time, <strong>VAERS received 1,913 reports of death (0.0018%) among people who received a COVID-19 vaccine</strong>. CDC and FDA physicians review each case report of death as soon as notified and CDC requests medical records to further assess reports. A review of available clinical information including death certificates, autopsy, and medical records revealed <strong>no evidence that vaccination contributed to patient deaths</strong>. CDC and FDA will continue to investigate reports of adverse events, including deaths, reported to VAERS.</p>\n</blockquote>\n<p>Note, from <a href=\"https://www.dw.com/en/fact-check-no-links-found-between-vaccination-and-deaths/a-56458746\" rel=\"nofollow noreferrer\">https://www.dw.com/en/fact-check-no-links-found-between-vaccination-and-deaths/a-56458746</a></p>\n<blockquote>\n<p>As far back as 2015, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599698/\" rel=\"nofollow noreferrer\">a study</a> assessing claims of deaths from vaccinations highlights that data from the VAERS system is skewed, as it is a system which &quot;accepts any submitted report of an adverse event without judging its clinical significance or whether it was caused by a vaccination.&quot; The <a href=\"https://www.cdc.gov/vaccines/acip/meetings/downloads/slides-2021-01/06-COVID-Shimabukuro.pdf\" rel=\"nofollow noreferrer\">Centers for Disease Control and Prevention</a> also warns against reporting bias and inconsistent data quality in the VAERS system.</p>\n</blockquote>\n", "score": 1 } ]

[ "covid-19", "statistics", "covid-19-datasets" ]

[ { "answer_id": 25961, "body": "<p><a href=\"https://en.wikipedia.org/wiki/San_Marino\" rel=\"nofollow noreferrer\">San Marino</a> is, from an epidemiology perspective, effectively a city in Italy. It's also quite small (just over 30,000 people), and the total number of deaths there from your source is 80. This is a tiny sample compared to the other countries on that list.</p>\n<p>Italy is also quite high on that list. ~175 deaths vs ~237 deaths per 100,000 is certainly in the same ballpark. From the statistics posted by the <a href=\"https://www.nytimes.com/interactive/2020/world/europe/italy-coronavirus-cases.html#states\" rel=\"nofollow noreferrer\">NY Times</a>, there are several regions in Italy that have higher death rates than San Marino, for example:</p>\n<p>Valle d'Aosta, 333</p>\n<p>Lombardy, 299</p>\n<p>Friuli Venezia Giulia, 262</p>\n<p>Emilia-Romagna, 259</p>\n<p>Emilia-Romagna is particularly relevant, because this is the region of Italy that most surrounds San Marino (Marche is the other, with 166 deaths per 100,000). So really, there is nothing unusual about San Marino relative to the region of Italy it is located in; it falls right between the rates for the broader regions that surround it.</p>\n<hr />\n<p>You can expect CFRs to be strongly influenced by three factors: demographic susceptibility (for example, an older population), testing (CFR goes down if you test extensively and find more asymptomatic/mild cases), and actual medical care.</p>\n<p>Let's start with testing, because in many ways this is the &quot;least interesting&quot; factor: it reflects something with the data rather than anything &quot;real&quot; about the CFR.</p>\n<p>From <a href=\"https://www.worldometers.info/coronavirus/\" rel=\"nofollow noreferrer\">worldometer</a>, San Marino has done 1.5 million tests per 1 million residents, with 132k cases/mil, 29 tests per case. Bosnia and Herzegovina have 234k tests per 1 million residents, with 49k cases/mil, less than 5 tests per case. Of course expressing these in #s/million is a bit funny for San Marino, which is far from having 1000000 residents, but at least these numbers can be compared with other places.</p>\n<p>Using Italy again for comparison, Italy had 791k tests per million and 57k cases per million, about 14 tests per case, with a CFR of 3.1%, falling between the other two countries on both measures.</p>\n<p>These numbers suggest that there was less overall less testing in Bosnia and Herzegovina vs San Marino, which you'd expect to show up as a higher CFR (fewer mild cases in the denominator).</p>\n<hr />\n<blockquote>\n<p>Does this mean that in B&amp;H way more people who get the disease end up dying from it, but somehow San Marino ended up on the first place in relative death cases despite the much lower CFR?</p>\n</blockquote>\n<p>A more thorough statistical analysis would be required to discover smaller measurable differences between countries, but the basic anomalies you point out do not seem unusual when these influential factors are considered. The simplest explanation is that San Marino is a small enclave in a severely impacted region of Italy. The deaths per population there are not unusual for local region. The differences in CFR are most easily explained by differences in testing that influence the number of mild cases included in the CFR calculations.</p>\n<p>The other big factor in how many deaths per population is in how many <em>actual</em> cases per population there are. We can't know this number exactly, only estimate from assumptions about how many cases are tested positive, but the numbers suggest that probably more people in San Marino (along with the adjacent regions of Italy) were infected, so more people there died. An older population could have also contributed slightly.</p>\n", "score": 3 } ]

[ "covid-19", "statistics" ]

[ { "answer_id": 25965, "body": "<p>They're called that because they look like they have little granules in them. Anatomists and histologists often start out with describing what they see, and they often see things well before any function is understood; often the names stick.</p>\n<p>Wikipedia has a page on granulocytes: <a href=\"https://en.m.wikipedia.org/wiki/Granulocyte\" rel=\"nofollow noreferrer\">https://en.m.wikipedia.org/wiki/Granulocyte</a></p>\n<p>It seems you've already gathered that they are white blood cells.</p>\n", "score": 2 } ]

[ "white-blood-count" ]

[ { "answer_id": 26014, "body": "<p>According to the <a href=\"https://www.beckershospitalreview.com/public-health/when-will-smell-taste-come-back-5-covid-19-questions-answered.html\" rel=\"nofollow noreferrer\">summary</a> of one study:</p>\n<blockquote>\n<p>Of 2,581 COVID-19 patients studied, 95 percent of patients regained their sense of smell within six months, according to the study in the Journal of Internal Medicine.</p>\n</blockquote>\n<p>The study appears to be <a href=\"https://pubmed.ncbi.nlm.nih.gov/33403772/\" rel=\"nofollow noreferrer\">this one</a> (on patients from continental Europe) and it has more details even its abstract:</p>\n<blockquote>\n<p>A total of 328 patients (24.1%) did not subjectively recover olfaction 60 days after the onset of the dysfunction. The mean duration of self-reported OD [olfactory dysfunction] was 21.6 ± 17.9 days. [...] At 60 days and 6 months, 15.3% and 4.7% of anosmic/hyposmic patients did not objectively recover olfaction, respectively.</p>\n</blockquote>\n<p>I'm not sure if there's any study that has tracked those &lt;5% who had not recovered at 6 months for a longer period.</p>\n<p>In general, there are more studies on short[er] term recovery, e.g. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7341046/\" rel=\"nofollow noreferrer\">one in the US</a> which also has a summary of\nother studies:</p>\n<blockquote>\n<p>Initial publications from Europe and Asia report higher rates of recovery. A French study of PCR-tested patients showed 98% experiencing a complete subjective recovery within 28 days, with mean duration of anosmia near 9 days. Workers in the United Kingdom repeated surveys 1 week after initial survey, revealing that 80% had experienced some recovery, while only 17% remained anosmic. They also noted a “plateau” in recovery after approximately 3 weeks, with a 70% recovery rate for those with anosmia of 3 or more weeks duration. Similarly, a study from Korea using daily phone surveys of almost 500 newly diagnosed COVID-19 patients showed median duration of anosmia or ageusia of 7 days, and almost all recovering within 3 weeks. [...]</p>\n<p>This study presents 1-month follow-up of patients with chemosensory changes participating in a large national longitudinal survey during the COVID-19 pandemic. Despite the severity of smell and taste loss experienced by most patients, nearly three-quarters will recover to normal or near-normal chemosensation within 2 months. The continued improvement noted between 14-day and 1-month surveys suggests that ongoing recovery is still in progress. Long term recovery and treatment effects will be a topic of further investigation.</p>\n</blockquote>\n", "score": 1 } ]

[ "covid-19", "smell", "taste" ]

[ { "answer_id": 26039, "body": "<p>Paronychia could be seen as an umbrella term for any inflammation around the nails of fingers or toes. Cellulitis being one kind.</p>\n<p>The umbrella term is referring to the anatomical region as it is</p>\n<blockquote>\n<p>Latin, from Greek [παρωνυχία] paronykhia &quot;whitlow,&quot; from <a href=\"https://www.etymonline.com/word/paronychia\" rel=\"nofollow noreferrer\">para- &quot;beside&quot; (see para- (1)) + onyx &quot;nail&quot; (see nail (n.)) + abstract noun ending -ia.</a></p>\n</blockquote>\n<p>See <a href=\"https://en.m.wikipedia.org/wiki/Paronychia#Differential\" rel=\"nofollow noreferrer\">this Wikipedia section</a> for differential (more specific) diagnoses of paronychia.</p>\n<p>You said:</p>\n<blockquote>\n<p>I am not aware of any other anatomical location where skin infections get such a specific name.</p>\n</blockquote>\n<p>Many names for inflammatory conditions come from the place on the body <a href=\"https://globalrph.com/medical-terms-introduction/\" rel=\"nofollow noreferrer\">and have the suffix <em>-itis</em> meaning inflammation</a>. You already mentioned cellulitis. There are also, for example:</p>\n<ul>\n<li>Conjunctivitis (also known as pink eye) is inflammation of the conjunctiva (<a href=\"https://www.ncbi.nlm.nih.gov/books/NBK519502/\" rel=\"nofollow noreferrer\">outer layer of the white of the eye</a>). It also affects the inner surface of eyelids? That's an inflammation.</li>\n<li>Gingivitis which is inflammation of the gingiva (<a href=\"https://www.sciencedirect.com/topics/medicine-and-dentistry/gingiva\" rel=\"nofollow noreferrer\">the gums</a>)</li>\n</ul>\n", "score": 1 } ]

[ "infection", "terminology", "fingers" ]

[ { "answer_id": 26109, "body": "<p>As you correctly mentioned, Korotkoff sounds are caused by a turbulent flow wave, going through the artery - which, by definition, occurs when the heart muscle contracts. So yes, what you hear is the same as what you would feel when taking a pulse.</p>\n<p>*<em>Additional note: in some cases peripheral pulse might not represent the exact heart beat (see <a href=\"https://study.com/academy/lesson/pulse-deficit-definition-causes.html\" rel=\"nofollow noreferrer\">pulse deficit</a>)</em></p>\n", "score": 1 } ]

[ "blood", "blood-pressure" ]

[ { "answer_id": 26080, "body": "<p>When plants photosynthesize, the net reactions are to turn water and carbon dioxide into sugars and oxygen, using energy from the sun.</p>\n<p>When animals and other aerobic organisms obtain usable energy from sugars and other compounds, the net outcome is the inverse: turning sugars and oxygen into water and carbon dioxide.</p>\n<p>Therefore, humans are net <em>producers</em> of water through digestion. See <a href=\"https://biology.stackexchange.com/questions/74561\">this Biology.SE Q&amp;A</a> and <a href=\"https://en.wikipedia.org/wiki/Metabolic_water\" rel=\"nofollow noreferrer\">Wikipedia: metabolic water</a>.</p>\n<p>Of course water is also used and lost by animals in many ways: it's used in anabolic reactions (just like in plants), used to cool through sweat, excrete waste through urine, etc, and a lot is lost in respiration. There's also a lot of water used in the digestive process, it's just that it is ordinarily reabsorbed in the digestive tract (failure to reabsorb this water causes <a href=\"https://en.wikipedia.org/wiki/Diarrhea\" rel=\"nofollow noreferrer\">diarrhea</a>). Therefore, over a span of days it is necessary to intake some additional water beyond that which is obtained through metabolism to replace what is lost.</p>\n", "score": 2 } ]

[ "nutrition", "digestion", "water", "fasting" ]

[ { "answer_id": 26084, "body": "<p>Yes, it is absolutely possible. There are several poisons, most notably cyanide, which interfere with the body's ability to take up or use oxygen from the blood, despite it being present in ample amounts to otherwise support life. This is known as <a href=\"https://en.wikipedia.org/wiki/Histotoxic_hypoxia\" rel=\"nofollow noreferrer\">histotoxic hypoxia</a>.</p>\n<p>As an example, a telltale sign of cyanide poisoning is a flushing of the skin, turning deep red over time. This is caused by veins, which typically carry oxygen-deficient blood, carrying oxygen-rich blood as the cells are unable to use the oxygen before arteries become veins at the capillaries. Cyanide interferes with one of the enzymes, <a href=\"https://en.wikipedia.org/wiki/Cytochrome_c_oxidase\" rel=\"nofollow noreferrer\">cytochrome c oxidase</a>, involved in the <a href=\"https://en.wikipedia.org/wiki/Electron_transport_chain\" rel=\"nofollow noreferrer\">electron transport chain</a> and ultimately responsible for producing <a href=\"https://en.wikipedia.org/wiki/Adenosine_triphosphate\" rel=\"nofollow noreferrer\">ATP</a>. Without this step in the electron transport chain, ATP production slows to a halt, and so does the consumption of oxygen, so many victims of cyanide poisoning have close to 100% blood oxygen saturation at their time of death.</p>\n", "score": 2 } ]

[ "breathing", "death" ]

[ { "answer_id": 26100, "body": "<p>Yep, in fact there is a '<a href=\"https://www.moillusions.com/reverse-color-blindness-test/\" rel=\"noreferrer\">Reverse Color Blind Test</a>' that is difficult for normal sighted people to pass but is relatively easy for colorblind people to pass. Here's an example:</p>\n<p><a href=\"https://i.stack.imgur.com/YaoEG.gif\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/YaoEG.gif\" alt=\"enter image description here\" /></a></p>\n<p>BTW, the word is &quot;NO&quot;</p>\n", "score": 5 } ]

[ "eye", "vision" ]

[ { "answer_id": 26107, "body": "<p>Look at the graph carefully. In the second week of March less than half of 50M have been vaccinated. It is April's third week and if you look carefully almost as many people who had to take a second jab seem to have taken it. Majority of first shots have been taken in the end of March so we need to check the data at the end of April i.e after a month because that is the recommended gap between the two shots. Moreover the vaccine is said to have been made free of cost at government hospitals. Dr.Reddy's a reputed pharma company reported that SputnikV shall be arriving very soon into India. The graph should go up soon.</p>\n<p>There were some issues though:</p>\n<ol>\n<li><p>The only two vaccines that had been granted emergency use authorization by the <a href=\"https://www.google.com/url?sa=t&amp;source=web&amp;rct=j&amp;url=https://www.mohfw.gov.in/pdf/FAQsforHCWs%26FLWs.pdf&amp;ved=2ahUKEwiM6L6BnpHwAhWg7XMBHW2iBMcQFjAOegQIGBAC&amp;usg=AOvVaw0-IfYugOSN6waixYUF7C3O&amp;cshid=1619073334574\" rel=\"nofollow noreferrer\">Central Drugs Standard Control Organization</a> (CDSCO) in India are Covishield® (AstraZeneca's vaccine manufactured by Serum Institute of India) and Covaxin® (manufactured by Bharat Biotech Limited). <a href=\"https://en.m.wikipedia.org/wiki/COVID-19_vaccination_in_India\" rel=\"nofollow noreferrer\">Here</a> you can read about the latest developments.</p>\n</li>\n<li><p>Both these vaccines were not trusted by the public. Blood clotting side effect of Astra-Zeneca and <a href=\"https://www.latimes.com/world-nation/story/2021-01-14/india-begins-covid-19-vaccinations-amid-doubts-over-drug?_amp=true\" rel=\"nofollow noreferrer\">because Covaxin wasn't put through the final trial phase before allowing it's use</a>. One of the very esteemed <a href=\"https://www.google.com/amp/s/www.thehindu.com/sci-tech/health/i-would-not-take-the-vaccine-without-efficacy-data-gagandeep-kang/article33527186.ece/amp/\" rel=\"nofollow noreferrer\">scientists</a> also denied taking the Covaxin because of the lack of efficacy data.\nBharat Biotech recently provided efficacy data and the public might've started trusting it since then and hence the recent surge in first vaccine shots.</p>\n</li>\n<li><p>It was recently <a href=\"https://www.google.com/amp/s/www.ndtv.com/india-news/coronavirus-huge-vaccine-wastage-by-states-till-april-11-most-in-tamil-nadu-rti-shows-2417643%3famp=1&amp;akamai-rum=off\" rel=\"nofollow noreferrer\">reported</a> that a huge number of COVID vaccines were wasted. Some news articles like <a href=\"https://www.google.com/amp/s/www.livemint.com/news/india/why-6-5-of-coronavirus-vaccine-doses-in-india-are-going-to-waste/amp-11615993563664.html\" rel=\"nofollow noreferrer\">this</a> explain why this is happening.</p>\n</li>\n</ol>\n", "score": 4 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 26168, "body": "<p>Here’s one way, assuming your suggestion is relevant to the UK.</p>\n<p><a href=\"https://www.nihr.ac.uk/patients-carers-and-the-public/i-want-to-help-with-research/suggest-a-research-topic.htm\" rel=\"nofollow noreferrer\">https://www.nihr.ac.uk/patients-carers-and-the-public/i-want-to-help-with-research/suggest-a-research-topic.htm</a></p>\n<p>Though generally most lay people are not well placed to come up with tractable research questions. Most clinicians can’t do it either.</p>\n", "score": 2 } ]

[ "medications", "treatment", "guidelines" ]

[ { "answer_id": 26176, "body": "<p>Tritium decays by emission of low-energy (&lt;19 keV) electrons (and anti-neutrinos that are irrelevant here) [1]. Such particles have a very short range in matter, of the order of a few cm in air, and less than a micrometer in water [1]. These electrons are most likely stopped by whatever material houses the tritium. For instance in a watch, the light comes from the interactions of the electrons with a phosphor mixed with tritium in a paint used on the watch dial [2], so there is little risk if the watch is intact. Inhaling or ingesting tritium is, however, a health risk, as is diffusion of tritium through the skin after contact [1].</p>\n<p>[1] Myers and Johnson 1991, Toxicity and Dosimetry of Tritium: A Review <a href=\"https://inis.iaea.org/collection/NCLCollectionStore/_Public/23/082/23082972.pdf?r=1\" rel=\"nofollow noreferrer\">https://inis.iaea.org/collection/NCLCollectionStore/_Public/23/082/23082972.pdf?r=1</a>.</p>\n<p>[2] Frame, Radioluminescent Paint <a href=\"https://www.orau.org/ptp/collection/radioluminescent/radioluminescentinfo.htm\" rel=\"nofollow noreferrer\">https://www.orau.org/ptp/collection/radioluminescent/radioluminescentinfo.htm</a></p>\n", "score": 1 } ]

[ "radiation" ]

[ { "answer_id": 26179, "body": "<p>The Skin Cancer Foundation covers this:</p>\n<blockquote>\n<p>[A]fter the sunburn fades, lasting damage remains.</p>\n<p>Sunburn accelerates skin aging and is a leading cause in the majority of cases of <a href=\"https://skincancer.org/skin-cancer-information/basal-cell-carcinoma/\" rel=\"nofollow noreferrer\">basal cell carcinoma</a>, <a href=\"https://skincancer.org/skin-cancer-information/squamous-cell-carcinoma/\" rel=\"nofollow noreferrer\">squamous cell carcinoma</a> and <a href=\"https://skincancer.org/skin-cancer-information/melanoma/\" rel=\"nofollow noreferrer\">melanoma</a>, the deadliest form of <a href=\"https://skincancer.org/skin-cancer-information/\" rel=\"nofollow noreferrer\">skin cancer</a>.</p>\n</blockquote>\n<p>The later went on to say:</p>\n<blockquote>\n<ul>\n<li><strong>Skin damage builds up over time</strong> starting with your very first sunburn. The more you burn, the greater your risk of skin cancer. Subsequent UV damage can occur even when there is no obvious burn.</li>\n<li><strong>Five or more sunburns</strong> more than doubles your risk of developing potentially deadly melanoma</li>\n</ul>\n</blockquote>\n<p>Cancer Research UK <a href=\"https://www.cancerresearchuk.org/about-cancer/causes-of-cancer/sun-uv-and-cancer/how-does-the-sun-and-uv-cause-cancer\" rel=\"nofollow noreferrer\">says similar</a>.</p>\n<p>The Centers for Disease Control and Prevention (CDC) <a href=\"https://www.cdc.gov/cancer/skin/basic_info/risk_factors.htm\" rel=\"nofollow noreferrer\">points out</a>:</p>\n<blockquote>\n<p>Any change in skin color after UV exposure (whether it is a tan or a burn) is a sign of injury, not health. Over time, too much exposure to UV rays can cause skin cancers including melanoma (the deadliest type of skin cancer), basal cell carcinoma, and squamous cell carcinoma. UV exposure can also cause cataracts and cancers of the eye (ocular melanoma). <strong>Every time you tan, you increase your risk of getting skin cancer.</strong></p>\n</blockquote>\n<p>More can be read in <a href=\"https://wwwnc.cdc.gov/travel/yellowbook/2020/noninfectious-health-risks/sun-exposure\" rel=\"nofollow noreferrer\">Chapter 3 of the CDC Traveller's Health Yellow Book 2020</a> <strong>(Free access via the CDC)</strong> which lists the following references:</p>\n<h2>References</h2>\n<p>American Cancer Society (n.d.). <em>Skin cancer</em>. <a href=\"https://www.cancer.org/cancer/skin-cancer.html\" rel=\"nofollow noreferrer\">https://www.cancer.org/cancer/skin-cancer.html</a></p>\n<p>Diaz, J. H., &amp; Nesbitt Jr, L. T. (2013). Sun exposure behavior and protection: recommendations for travelers. <em>Journal of travel medicine, 20</em>(2), 108-118. <a href=\"https://doi.org/10.1111/j.1708-8305.2012.00667.x\" rel=\"nofollow noreferrer\">https://doi.org/10.1111/j.1708-8305.2012.00667.x</a></p>\n<p>Monteiro, A. F., Rato, M., &amp; Martins, C. (2016). Drug-induced photosensitivity: Photoallergic and phototoxic reactions. <em>Clinics in dermatology, 34</em>(5), 571-581. <a href=\"https://doi.org/10.1016/j.clindermatol.2016.05.006\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/j.clindermatol.2016.05.006</a></p>\n<p>Skin Cancer Foundations (n.d.). Sun protection. <a href=\"https://www.skincancer.org/skin-cancer-prevention/sun-protection/\" rel=\"nofollow noreferrer\">https://www.skincancer.org/skin-cancer-prevention/sun-protection/</a></p>\n<p>Young, A. R., Claveau, J., &amp; Rossi, A. B. (2017). Ultraviolet radiation and the skin: Photobiology and sunscreen photoprotection. <em>Journal of the American Academy of Dermatology, 76</em>(3), S100-S109. <a href=\"https://doi.org/10.1016/j.jaad.2016.09.038\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/j.jaad.2016.09.038</a></p>\n", "score": 2 } ]

[ "cancer", "radiation", "sun-exposure" ]

[ { "answer_id": 26227, "body": "<p>A device to constantly measure &quot;vitals&quot; such as pulse and blood oxygen would be expensive, possibly invasive (a pulse oximeter on your finger while you lie in a hospital bed is no big deal, but will really get in the way while you're cooking or gardening) and subject to many false positives, such as when the device slips or the person removes it. Further, daily reporting would be of no value, you would need to detect dangerous patterns and send immediate help: this raises the cost, the complexity, and so on.</p>\n<p>Many older or medically fragile people do have &quot;alert buttons&quot; that they can push if they experience dramatic pain, weakness, neurological symptoms and so on. Often these are set up with two-way voice and if the person doesn't reply when the call centre responds to the button push, the call centre sends an ambulance.</p>\n<p>You may worry that something would strike you without warning. In that case you would most likely collapse. Some of these &quot;alert buttons&quot; have fall detectors for this reason. They won't help if the medical emergency happens when the person is in bed, but covers all the rest of the possible problems. If you fall down and when the call centre responds, you don't talk -- we don't need to know your pulse, blood sugar, blood pressure, or anything else, an ambulance is on the way.</p>\n<p>Finally some of these buttons are connected to the home's landline, others to the person's cell phone, while others have a SIM card of their own so that they work if the person has gone for a walk or is out doing errands.</p>\n", "score": 2 } ]

[ "home-medical-equipment", "elderly-seniors-aged-old" ]

[ { "answer_id": 26244, "body": "<p>Astrazeneca uses a modified chimpanzee adenovirus vector. Sputnik uses a modified hybrid human adenovirus vector. Since many (most?) humans have been previously exposed to human adenoviruses (but not chimp adenoviruses), some will have previously-existing antibodies and cellular immunity that may be enough to block a human-adenovirus-based vaccine from fully working. This is also a likely problem with at least one of the Chinese adenovirus-based vaccines.</p>\n<p>None of the vaccines &quot;require&quot; one dose or two doses (or even three :) -- it's just a choice made by the manufacturer, trading off convenience vs. level of protection. Since clinical trials are complex and time-consuming, each had to choose an initial dosing regime. The more doses, the better the expected level of protection, but the more complicated the administration (records of when billions of people got their first shots and are due for second ones!), and the more doses needed.</p>\n<p>The difference in efficacy is likely mostly because they are different vaccines, but is also affected by the number of doses and the amount of viral vector used for one dose. Astrazeneca made some dosing mistakes in their trial and surprisingly found that the smaller of the two amounts of vector they were testing worked better!</p>\n<p>Refs:\n&quot;COVID-19: How do viral vector vaccines work?&quot;\n<a href=\"https://www.medicalnewstoday.com/articles/covid-19-how-do-viral-vector-vaccines-work\" rel=\"noreferrer\">https://www.medicalnewstoday.com/articles/covid-19-how-do-viral-vector-vaccines-work</a>\n&quot;A Novel Chimpanzee Adenovirus Vector with Low Human Seroprevalence: Improved Systems for Vector Derivation and Comparative Immunogenicity&quot;\n<a href=\"https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0040385\" rel=\"noreferrer\">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0040385</a>\n&quot;Sputnik V COVID-19 vaccine candidate appears safe and effective&quot;\n<a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)00191-4/fulltext\" rel=\"noreferrer\">https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)00191-4/fulltext</a></p>\n", "score": 4 } ]

[ "covid-19", "vaccination", "covid", "immunology" ]

[ { "answer_id": 26257, "body": "<p>In the US, medical devices including those used in dentistry both for diagnostic equipment and for things like cement, amalgams, etc are <a href=\"https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=872&amp;showFR=1\" rel=\"nofollow noreferrer\">regulated by the FDA</a>. Presumably in other countries the equivalent regulatory agencies are involved. FDA device regulation is similar to that of drugs, and in some ways can be even more stringent due to the difficulty in removing medical devices (vs stopping medication) should problems arise. The specific support required for approval will depend on what exactly the device is.</p>\n<p>The <a href=\"https://ec.europa.eu/health/scientific_committees/emerging/docs/scenihr_o_040.pdf\" rel=\"nofollow noreferrer\">EU guidance</a> seems to be that exposure to BPA from medical devices (including dental devices) is low and not of much concern. Most BPA release from dental products is within the first hour after implant and at levels below that which causes harm.</p>\n", "score": 3 } ]

[ "dentistry", "toxicity" ]

[ { "answer_id": 26309, "body": "<p>Apparently, you are asking whether CFR (i.e. chance of dying given a confirmed infection) is lower in the vaccinated group. Note that chance of getting a [symptomatic] infection in vaccinated groups is much lower, so your question isn't capturing the whole effect of vaccines.</p>\n<p>But nonetheless, Public Health England has published some such <a href=\"https://www.cebm.net/covid-19/recent-falls-in-age-specific-estimates-of-the-case-fatality-ratio-in-england/\" rel=\"nofollow noreferrer\">data in Feb 2021</a> relative to the previous month.</p>\n<blockquote>\n<p>[CFR] estimates exhibit large falls in recent weeks, particularly in the 80+ population that was first prioritised for vaccination.</p>\n<p><a href=\"https://i.stack.imgur.com/6fzES.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/6fzES.png\" alt=\"enter image description here\" /></a></p>\n<p><a href=\"https://i.stack.imgur.com/QP7d1.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/QP7d1.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>As I noted in my comments, it's also pointed out in this study that one needs to be careful with interpreting such observational studies. This one was possible because at the time there were different rates of vaccination among different age groups, the over 80 were vaccinated in [much] greater numbers, and [in the graphs above] the CFR reduction was noted among them:</p>\n<blockquote>\n<p>While the 80+ population was prioritised for vaccination and was vaccinated in much greater proportion as a result, substantial numbers of the under 80 population have also been vaccinated. While this would tend to dampen down our ability to detect any impact, the much greater extent of vaccination among the 80+ population should still allow the detection of such an effect: as of 7 January, just over one month ago, official Public Health England figures show around 28% of the 80+ population to have been vaccinated compared to only 3% of the 75-79 population. Furthermore, smaller numbers of deaths in younger age groups may make more difficult the accurate estimation of the CFR for younger such groups.</p>\n</blockquote>\n<p>Nonetheless, there was also other unexplained variation in CFR among other age groups [in those graphs] so one cannot be totally certain of the causality.</p>\n<p>If, on the other hand, you want to consider the combined effect of not getting a symptomatic case plus death, vaccines (even the Chinese ones) do much better, as e.g. shown in this <a href=\"https://jakartaglobe.id/news/indonesia-says-sinovacs-vaccine-98-effective-to-prevent-deaths-from-covid19\" rel=\"nofollow noreferrer\">study/data in Indonesia</a>:</p>\n<p>(table not formatted as block quote as that seems to mess up the table.)</p>\n<blockquote>\n<p>The number of Covid-19 deaths among health workers in the study</p>\n</blockquote>\n<div class=\"s-table-container\">\n<table class=\"s-table\">\n<thead>\n<tr>\n<th>Groups</th>\n<th>Deaths</th>\n<th>Total</th>\n<th>%</th>\n</tr>\n</thead>\n<tbody>\n<tr>\n<td>Not vaccinated</td>\n<td>17</td>\n<td>28,055</td>\n<td>0.66</td>\n</tr>\n<tr>\n<td>Vaccinated with the first dose</td>\n<td>3</td>\n<td>8,458</td>\n<td>0.03</td>\n</tr>\n<tr>\n<td>Vaccinated with the second dose</td>\n<td>1</td>\n<td>91,777</td>\n<td>0.001</td>\n</tr>\n</tbody>\n</table>\n</div>\n<blockquote>\n<p>Source: Health Ministry</p>\n</blockquote>\n<p>As for the number of cases:</p>\n<blockquote>\n<p>The number of Covid-19 infection among health workers in the study</p>\n</blockquote>\n<div class=\"s-table-container\">\n<table class=\"s-table\">\n<thead>\n<tr>\n<th>Groups</th>\n<th>Infected</th>\n<th>Total</th>\n<th>%</th>\n</tr>\n</thead>\n<tbody>\n<tr>\n<td>Not vaccinated</td>\n<td>2,431</td>\n<td>28,055</td>\n<td>8.66</td>\n</tr>\n<tr>\n<td>Vaccinated with the first dose</td>\n<td>657</td>\n<td>8,458</td>\n<td>7.76</td>\n</tr>\n<tr>\n<td>Vaccinated with the second dose</td>\n<td>521</td>\n<td>91,777</td>\n<td>0.56</td>\n</tr>\n</tbody>\n</table>\n</div>\n<blockquote>\n<p>Source: Health Ministry</p>\n</blockquote>\n<p>If you want to do a quick CFR estimate here: for those vaccinated with both doses 1/521 = 0.19% vs no vaccine 17/2,431 = 0.7% doesn't seem that much of an improvement (although there is some), but deaths relative to the treatment/control group size (0.001% vs 0.66%) certainly is a much more noticeable improvement for the vaccine group.</p>\n", "score": 2 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 28810, "body": "<p>A potential way the &quot;carcinogenic substances in prostate sections&quot; hypothesis took off is when <a href=\"https://www.cancervic.org.au/research/researchers/graham-giles.html\" rel=\"nofollow noreferrer\">Graham Giles</a> began doing interviews with the lay press<a href=\"https://www.newscientist.com/article/dn3942-masturbating-may-protect-against-prostate-cancer/\" rel=\"nofollow noreferrer\">¹</a>ʼ<a href=\"https://web.archive.org/web/20160413005939/https://www.newscientist.com/article/mg17924041-400-can-masturbating-each-day-keep-the-doctor-away/\" rel=\"nofollow noreferrer\">²</a>.</p>\n<blockquote>\n<p>Generating the fluid involves concentrating these components from the bloodstream up to 600-fold – and this could be where the trouble starts. Studies in dogs show that carcinogens such as 3-methylcholanthrene, found in cigarette smoke, are also concentrated in prostate fluid. “It’s a prostatic stagnation hypothesis,” says Giles. “The more you flush the ducts out, the less there is to hang around and damage the cells that line them.”</p>\n</blockquote>\n<p>There are many examples in human physiology where epithelial cells can concentrate ions or other substances including in the salivary glands and kidney<a href=\"https://accessmedicine.mhmedical.com/content.aspx?bookid=3047&amp;sectionid=255088845\" rel=\"nofollow noreferrer\">³</a>. And Junqueira notes:</p>\n<blockquote>\n<p>The tubuloacinar glands of the prostate are lined by simple or pseudostratified columnar epithelium and produce a fluid that contains a complex mixture of exosomes, various glycoproteins, enzymes, and small molecules, such as prostaglandins, and is stored until ejaculation.</p>\n</blockquote>\n<p>The dog studies in question seem to have been conducted decades ago. In one study, conducted in 1977<a href=\"https://pubmed.ncbi.nlm.nih.gov/875049/\" rel=\"nofollow noreferrer\">⁴</a>, the authors found that after exposure the concentration of a particular carcinogen (3-methylcholanthrene) was sometimes higher in the prostatic fluid than the plasma.</p>\n<p>Here is one of their graphs:</p>\n<p><a href=\"https://i.stack.imgur.com/zKveV.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/zKveV.png\" alt=\"enter image description here\" /></a></p>\n<p>I personally don't feel this is very good evidence for particular strong concentration of carcinogens in prostate fluid (and certainly not 600-fold as intimated in the New Scientist article), but I'm not a prostate biologist.</p>\n<p>Overall, it seems that this aspect of the stagnation hypothesis is based on concentration of exogenous carcinogens into prostate fluid rather than constituents of physiologic prostate secretions. The experimental evidence for this hypothesis seems mostly based on decades old animal experiments which have not been reproduced in humans.</p>\n", "score": 2 } ]

[ "cancer", "prostate", "prostatitis", "carcinogens", "enlarged-prostate-bph" ]

[ { "answer_id": 26363, "body": "<p>Two facts you need: first, clinical trials have very strict rules for who can be in them. Second, some trials are &quot;drug A vs placebo&quot; while others are &quot;Drug A vs Drug B&quot; or &quot;Drug A vs Drugs A and B together&quot; not to mention variations in dose etc. It's not all a matter of &quot;we won't treat half the participants.&quot;</p>\n<p>I was in a trial for &quot;dose X1 of drug A and dose Y1 of drug B&quot; vs &quot;dose X2 of drug A and dose Y2 of drug B&quot;. Previous studies had shown that both of these had the same efficacy, and this study was to compare side effects. There were entrance rules like &quot;no brain metastases&quot; and on each day of treatment, rules about how ill you were allowed to be. I personally came very close to being too ill for the study so I learned quite a lot about that. Your hypothetical patient in very poor condition is more likely to be removed from the study, at which point they can only get the current treatment, not the intervention being studied. (In some cases their doctor can arrange for them to get the study drug outside the study; this depends on how medications are regulated where they live.)</p>\n<p>Clinical trials in the US are listed on clinicaltrials.gov. Here is the <a href=\"https://clinicaltrials.gov/ct2/show/NCT04482621\" rel=\"nofollow noreferrer\">record for one study</a> I chose at random, studying a possible Covid treatment. You can see that it makes clear what is being compared (this one is drug vs placebo, but explore the site and you'll find drug vs drug, dose vs dose and more), how many are in the study (12 at first, later a total of 40) and the eligibility criteria (quite a way down the page) ruling large sets of people out for being too ill. It doesn't say there that patients will be removed if they develop an exclusion criteria, but that is the practice.</p>\n<p>The matter of it being unethical to give someone a placebo is far more complicated than you think, and cannot be solved by giving the sickest people the drug on compassionate grounds. (For example, those people might die at a higher rate than others, making the drug look bad and causing less people to get the drug over the coming years.) Generally, people go into studies knowing they may not be saved by the study and have made peace with that. I can tell you that I did.</p>\n<p>As a third fact, in the majority of modern day trials nobody (not the patient, not the people administering the treatment, not the people assessing the subsequent health of the patient -- recovery and side effects) have any idea who is getting what. In my study, there was ONE PERSON I never met who actually put the drug in an IV bag with coded number stickers on it and delivered it to the chemo nurses who administered it. Everything was done the same no matter what arm of the study the patients happen to be in. In placebo studies this includes carefully infusing saline, giving people all the same process as if they were actually getting IV meds. THis would make it impossible for a doctor to do as you suggest even if it was a good idea (which it isn't.)</p>\n<p>Studies are sometimes stopped early when those assessing outcomes can see a strong partition into two groups. They ask for permission to &quot;unblind&quot; and if there is a strong and clear difference between drug and placebo, will stop early so as to be able to give the drug to everyone. Here is <a href=\"https://news.yahoo.com/gilead-leukemia-drug-trial-unblinded-early-due-success-165310387--finance.html\" rel=\"nofollow noreferrer\">one example from 2015</a> for a leukemia study. That article says:</p>\n<blockquote>\n<p>Independent safety monitors oversee blinded trials so that they can be halted or unblinded early in case it is determined that the drug is causing harm or if the benefit becomes clear so that the medicine can be offered to placebo patients. A trial can also be stopped for futility if monitors determine the study is doomed to fail.</p>\n</blockquote>\n<p>This is a rare thing and is not based on some participants being really ill.</p>\n", "score": 4 }, { "answer_id": 26385, "body": "<p>Two things:</p>\n<ul>\n<li>Clinical trials are generally double-blinded, meaning that neither the subjects nor the researchers know what the subject is receiving, and</li>\n<li>Potential ethical issues are considered ahead of time by both the researchers as well as Human Subject Review Committees who have to approve the research protocol.</li>\n</ul>\n", "score": 2 } ]

[ "clinical-study", "placebo" ]

[ { "answer_id": 27462, "body": "<p>Your analysis looks similar to:</p>\n<blockquote>\n<p><a href=\"https://en.wikipedia.org/wiki/Incremental_cost-effectiveness_ratio\" rel=\"nofollow noreferrer\">Incremental Cost-Effectiveness Ratio</a> (ICER)</p>\n</blockquote>\n<p>which:</p>\n<blockquote>\n<p>ICER ... is used in cost-effectiveness analysis to summarise the cost-effectiveness of a health care intervention. It is defined by the difference in cost between two possible interventions, divided by the difference in their effect.</p>\n</blockquote>\n<p>In your case, because of your normalization, ε is effectively a measure of relative cost, and so the denominator is ignored.</p>\n", "score": 2 } ]

[ "statistics", "effectiveness", "reference-request", "public-health" ]

[ { "answer_id": 27428, "body": "<p>Canada decided to delay second doses of the three main vaccines in use here: Pfizer, Moderna, and AstraZeneca. The motivation was to get more first doses into people. The math there was</p>\n<blockquote>\n<p>100 people get first doses, about 70% protection -- 70 protected people</p>\n</blockquote>\n<blockquote>\n<p>50 people get both doses, about 95% protection -- 48 protected people.</p>\n</blockquote>\n<p>Since 70 is more than 48, that was the public health choice made.</p>\n<p>Now what you're asking is, when it comes time for second dose, will some people now get 90% instead of 95% because it was delayed?</p>\n<p>The early studies on second doses did them really quickly. 4 weeks, even 3. But there were other studies with longer gaps and there was real world data with longer gaps where for various reasons people waited 12 weeks or 16 weeks. While many expected waiting would make it worse, that's not what happened. Waiting improved protection. People were more protected 12 weeks after their first shot (without a second) than 3 or 4 weeks after it. Then yes, it goes up even further when they get that second shot. (Quotes later in this answer.) They seem to show that 12 weeks is the &quot;sweet spot&quot; for a second dose, but the truth is from a public health point of view, it's not about maximizing one individual's protection to 96 or 97 rather than 95, but about the overall population protection.</p>\n<p>Here in Canada we were originally scheduled for second doses 16 weeks after firsts, but it is now changing to 12. This is not so much because you get better protection at 12 than at 16 as it is that Delta does much better on singly-vaccinated people than the other variants do, so it's important to get a lot of people onto second shots before Delta takes hold here as it has in the UK.</p>\n<p>This <a href=\"https://www.cbc.ca/news/health/canada-covid-19-vaccine-second-dose-delay-variants-1.6045226\" rel=\"nofollow noreferrer\">CBC news article</a> quotes some experts:</p>\n<blockquote>\n<p>&quot;There is no question that for the whole of Canada, from the perspective of lives saved, that giving single doses to people and asking them to defer their second dose was the best idea,&quot; said Dr. Allison McGeer, a medical microbiologist and infectious diseases specialist at Toronto's Mount Sinai Hospital.</p>\n</blockquote>\n<blockquote>\n<p><a href=\"https://www.medrxiv.org/content/10.1101/2021.05.24.21257744v1\" rel=\"nofollow noreferrer\">A new Canadian preprint study, which has not yet been peer reviewed</a>, found the Pfizer-BioNTech and Moderna vaccines' effectiveness grew from 48 per cent 14 to 21 days after the first dose to 71 per cent after 35 to 41 days.</p>\n</blockquote>\n<p>So, I have no numbers about Sputnik's effectiveness after 12 weeks vs after 16. I am just showing you that the decision isn't based on that. It's based on vaccine supply, and the effectiveness of a single shot against the variants that are currently circulating. If you think that you should get a second shot now rather than someone else getting their first, taking two shares from a limited supply, let me give you quote from Dr. McGeer from that article:</p>\n<blockquote>\n<p>&quot;Of course I want my two doses of vaccine. But if the price of that is somebody else maybe dying because of it — that's just not OK. I think we can all see that.&quot;</p>\n</blockquote>\n", "score": 4 } ]

[ "covid-19" ]

[ { "answer_id": 27446, "body": "<p>The hypothesis is that the free hormone is the fraction which is available for uptake into the cells and interaction with nuclear receptors. The bound hormone represents actually a circulating storage that is not immediately available for such an uptake.\nSince some drugs and illnesses can alter concentrations of binding proteins or the binding capacity, the free and total hormone concentrations may not be concordant. Therefore, you may find an elevated T4 when there is an excess in thyroxine-binding globuline (TBG), for example estrogene-induced TBG excess, where the free T4 is normal.</p>\n<p>References:</p>\n<p>Best Pract Res Clin Endocrinol Metab. 2013 Oct;27(5):689-700.\ndoi: 10.1016/j.beem.2013.05.012. Epub 2013 Jun 25.</p>\n<p>Clin Chem. 1992;38(7):1289 (found this reference somewhere, but the full text is not available)</p>\n", "score": 1 } ]

[ "endocrinology", "thyroid", "hyperthyroid", "hypothyroid" ]

[ { "answer_id": 27442, "body": "<p>You're right, evidence shows its viruses and bacteria that cause cold.</p>\n<p>The question is, does cold temperatures contribute to increasing your chances of contracting a virus? The simple answer is yes, this is why the myth persists. Of course the devil is in the details.</p>\n<p>The evidence suggests that its in fact the lack of vitamin D especially in the winter months which contributes to suppressing your immune response and therefore you are more prone to becoming ill.</p>\n<p>The average person sees this and makes a link with cold weather and using fault logic, applies this to car aircon or your hair being wet etc.</p>\n<p><a href=\"https://www.medicalnewstoday.com/articles/323431#:%7E:text=Many%20researchers%20believe%20that%20exposure,due%20to%20reduced%20sun%20exposure\" rel=\"nofollow noreferrer\">https://www.medicalnewstoday.com/articles/323431#:~:text=Many%20researchers%20believe%20that%20exposure,due%20to%20reduced%20sun%20exposure</a>.</p>\n", "score": 1 } ]

[ "common-cold", "medical-myths" ]

[ { "answer_id": 27467, "body": "<p>As you have refereed these medications <em>are very similar</em> in the sense that both antidepressants present a similar mechanism of action, consisting of inhibition of serotonin and norepinephrine reuptake. Altough</p>\n<blockquote>\n<p>binding affinity for serotonin and norepinephrine reuptake pumps is higher for desvenlafaxine than venlafaxine, which <strong>theoretically</strong> could translate to greater efficacy <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK507128/\" rel=\"noreferrer\">reference</a></p>\n</blockquote>\n<p>However the major difference that one can find, at a glance, is the fact that venlafaxine undergoes primarily through a phase I metabolization by the CYP 2D6-mediated oxidative reactions to be converted into O-desmethylvenlafaxine. While desvenlafaxine, on the other hand,</p>\n<blockquote>\n<p>is mainly eliminated unchanged by renal excretion, and to a lesser\nextent metabolized by phase II enzymes to form desvenlafaxine-Oglucuronide <a href=\"https://www.longdom.org/open-access/metabolism-studies-of-desvenlafaxine-jbb.1000076.pdf\" rel=\"noreferrer\">reference</a></p>\n</blockquote>\n<p>Which lead us to conclude that its biodegradation isn't influenced by the enzymatic system of cytochromes P450 (CYP 2D6).</p>\n<p>This has at least two main implications</p>\n<ol>\n<li>more suitable for liver diseases and in geriatric patients</li>\n</ol>\n<p>since it doesn't require an extensive metabolization by the liver to be ready for excretion</p>\n<ol start=\"2\">\n<li>more advantageous in patients with genetic polymorphisms of CYP2D6</li>\n</ol>\n", "score": 4 } ]

[ "drug-metabolism" ]

[ { "answer_id": 27475, "body": "<p>&quot;Moderate&quot; and &quot;modest&quot; are just descriptive adjectives. They don't have any quantitative meaning, and I'm not aware of any effort to standardize their meaning for these sorts of measures (blood pressure, heart rate, temperature), nor do the authors reference any such effort in using those terms. I think it would be fair to characterize these adjectives as referring to effects that are measurable but not of immediate clinical concern according to the authors. However, experts could of course vary on what sizes of effects they consider clinically concerning. One might compare to other types of &quot;normal&quot; baselines besides rest, like parameters one would observe during moderate exercise, but these authors haven't done that directly.</p>\n<p>&quot;Significant&quot; is refering to <a href=\"https://en.wikipedia.org/wiki/Statistical_hypothesis_testing\" rel=\"nofollow noreferrer\">statistical hypothesis testing</a>, where &quot;significant&quot; refers to an effect that passes some predetermined threshold for deciding an effect is unlikely to have resulted purely by chance. Statistical significance says very little to nothing about the size of an effect, besides saying that it is probably different from zero. If you had a sufficiently sensitive scale (and/or a large enough sample size), you could weigh people before and after eating a cough drop and state that cough drops cause significant weight gain. After all, someone's weight after eating a ~3 gram cough drop will be approximately equal to their prior weight plus the 3 gram weight of a cough drop. There is a push in medical statistics these days to emphasize measures of <a href=\"https://en.wikipedia.org/wiki/Effect_size\" rel=\"nofollow noreferrer\">effect size</a> instead of or in addition to measures of statistical significance to avoid overstating the importance of effects that are statistically, but not clinically, significant.</p>\n", "score": 2 } ]

[ "physiology", "body-temperature", "hypertension", "toxicology", "cardiac-physiology" ]

[ { "answer_id": 27499, "body": "<p>Resting heart rate is measured sitting down after having rested for at least 10 minutes and for accuracy, not under the influence of any stimulants (like caffeine).</p>\n<p>The normal range in general is between 60-100bpm however, there appears to be some differentiation of ranges between men and women.</p>\n<p>Source: <a href=\"https://doi.org/10.1016/0002-9149(92)90947-w\" rel=\"nofollow noreferrer\">Operational definition of normal sinus heart rate</a></p>\n", "score": 1 } ]

[ "exercise", "cardiology", "blood-circulation", "heart", "heart-rate" ]

[ { "answer_id": 27521, "body": "<p>The value of dilation of the pupil far outweighs the inconvenience.In fact, I'd offer that if an exam is done without it, you potentially lose the following:</p>\n<p>--full access to all the structure of the retina, macula, and associated blood vessels. Dilation opens up the aperture of the pupil enough for the examiner to see all there is to see. I could fill up two pages on what's &quot;discoverable&quot; on an eye exam.</p>\n<p>--depending on age, dilation also paralyzes the ciliary muscle of the lens which is responsible for near-vision (sic: accommodation). The older you are, and the more you stare at a computer, the more that muscle stays tonically-contracted. When a distance vision exam is done on a tonically-contracted (accomodated) eye, the refraction may show a near-sighted condition that really doesn't exist.</p>\n<p>Keep this in-mind: distance vision is a function of the cornea-macula distance. The lens is at its most flat state, adding next to nothing to visual acuity. When you get inside 20-inches, the lens changes configuration to increase the refractive index to keep object in focus. As people age, the ciliary muscle weakens and the lens becomes stiffer, which results in a gradual and progressive loss of ability to see up-close. Hence, the need for reading glasses. The two processes--near-sightedness and the inability to see up close as you age (Presbyopia) are two different processes.</p>\n<p>To get back to &quot;dilating&quot; the eye, you can certainly bully and optometrist into not dilating your eyes, but you lose value and increase risk when you try to side-step that part of the exam. R.S. Carnes, M.D.</p>\n<p>References: For physiology of the eye, the standard first-year medical school text is good enough: Hall and Guyton, “Medical Physiology.” For use of cycloplegics and fundascopic exams of the retina, almost any clinical practice manual, but “Harrisons Principals of Internal Medicine” details the range of diseases and conditions discoverable on fundascopic exam.</p>\n", "score": 2 } ]

[ "eye", "ophthalmology", "optometry", "eye-exam" ]

[ { "answer_id": 27535, "body": "<p>I’m a retired anesthesiologist, and my first thought when reading this post is that there needs to be more context, by the author, to make sense of what she is reporting.</p>\n<p>So, I have to make some conjectures and add in some skepticism.</p>\n<p>An epidural catheter was placed to either supplement general anesthesia or provide pain management, Post-op, or both. Epidural catheters are placed in a potential space outside the dural membrane that encloses the spinal cord which is bathed in spinal fluid. It works by diffusing drugs to the spinal roots that emerge at each segment of the spinal. The two classes of “chemicals” commonly used are narcotics and local anesthetics. While not neutral pH neither are likely to cause “burns” if left on the skin.</p>\n<p>However, if a the patient was placed on a warming blanket, there is always the potential for a combination of liquid (increased thermal conduction) and pressure to cause a superficial burn, rarely severe unless the case goes on for a long time (&gt;4hrs) and that’s malpractice if it happens.</p>\n<p>Harvesting a kidney: the patient is usually placed on their side, not back. Any leaking fluid would not likely have much effect either with, or without, a heating blanket.</p>\n<p>Finally, “dislodging an epidural” is next to impossible, under normal operating conditions. First, it doesn’t just slip out even if left unsecured. Second anesthesiologists secure it pretty compulsively.</p>\n<p>So, I can only conjecture either profound incompetence by an anesthesiologist (not career sustaining) or the story has lost some fidelity.</p>\n<p>How a 1st or 2d degree burn would effect the frequency of migraines is outside my field, but I can’t think of any rational scientific connection.</p>\n<p>The quoted segment doesn’t describe the “aggressive treatment plan”, so that’s pure hyperbole—an unsupported assertion.</p>\n<p>So, the anesthesia/epidural study is far-fetched. One tip-off about the writer: most physicians don’t describe FDA-approved drugs as “chemicals.” That is either dumbing down for the reader or a person impersonating a physician.</p>\n<p>Finally, to make sure I answer the question: No. Epidural drugs (narcotics, anesthetics) don’t cause burns on the skin or elsewhere. I can’t imagine FDA approving a drug for epidural use that would.</p>\n", "score": 4 } ]

[ "epidural" ]

[ { "answer_id": 27554, "body": "<p>This is a reasonably recent review of old and new treatments for polycystic ovary syndrome (PCOS).</p>\n<p>Bednarska S, Siejka A. The pathogenesis and treatment of polycystic ovary syndrome: What's new? Adv Clin Exp Med. 2017 Mar-Apr;26(2):359-367. doi: 10.17219/acem/59380. PMID: 28791858.</p>\n<p><a href=\"https://pubmed.ncbi.nlm.nih.gov/28791858/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/28791858/</a></p>\n<p>As indicated in this review, combined estrogen/progestin oral contraceptives that have anti-androgenic effects are the “first line” recommendation for women with PCOS not seeking to become pregnant because they:</p>\n<blockquote>\n<p>“restore regular periods, reduce symptoms of hyperandrogenism\n(hirsutism, acne, alopecia) and reduce risk of endometrial\nhyperplasia”</p>\n</blockquote>\n<p>The review identifies the following non-OC anti-androgenic medications that are used to treat women with PCOS:</p>\n<p>GnRH (gonatrophen releasing hormone) analogs, ketoconazole, steroids, spironolactone, and flutamide. (an androgen receptor antagonist). Finasteride (a 5-alpha reductase inhibitor) is mentioned as a medication that can be used specifically to manage alopecia in women with PCOS.</p>\n<p>All of these non-OC antiandrogenic treatments used to treat PCOS are also associated with side effects, described in Table 2 of the review.</p>\n<p>A second reasonably recent review of PCOS recommends against flutamide in women with PCOS because of it is hepatotoxic and expensive.</p>\n<p>McCartney CR, Marshall JC. CLINICAL PRACTICE. Polycystic Ovary Syndrome. N Engl J Med. 2016 Jul 7;375(1):54-64. doi: 10.1056/NEJMcp1514916. PMID: 27406348; PMCID: PMC5301909.</p>\n<p><a href=\"https://pubmed.ncbi.nlm.nih.gov/27406348/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/27406348/</a></p>\n<p>This review mentions that:</p>\n<blockquote>\n<p>“Antiandrogens may disrupt androgen-dependent processes (e.g.,\nformation of external genitalia) in a male fetus; this mandates\nconcomitant use of reliable contraception.”</p>\n</blockquote>\n<p>Thus, while there are non-OC anti-androgens that can be used to manage hirsutism and acne (and alopecia) in women with PCOS, these medications are not without side effects that might be worse than OCs and a woman taking these non-OC anti-androgens would still need to use contraception if fertile.</p>\n", "score": 2 } ]

[ "side-effects", "endocrinology", "female", "pcos", "hormonal-imbalance" ]

[ { "answer_id": 27538, "body": "<p>In professional terms, you're asking about <a href=\"https://en.wikipedia.org/wiki/Pharmacokinetics\" rel=\"nofollow noreferrer\">pharmacokinetics</a> - what fate does a drug have once administered and how fast does it get there.</p>\n<p>Yes, for some drugs, the goal is to keep a roughly steady concentration of the drug. For example, if you were taking a medication to regulate high blood pressure, you'd want it acting fairly constantly all the time, otherwise you'd have spikes in blood pressure when the drug wears off.</p>\n<p>For an antibiotic, that's not necessarily the case. You're trying to kill bacteria, and it may not matter much if you reduce the bacterial population by the same amount after 24 hours whether that's because all the activity happened in the first hour or if it happened gradually. You also don't necessarily need the drug to be in the blood: for example, if you are treating a urinary tract infection, you might only care about the drug concentration in the urinary tract. However, there are other limits like side effects that you want to limit that might be worse if the serum concentration is too high, and you might get diminishing returns if the drug is administered all at once versus over a long time.</p>\n<p>For amoxicillin itself, I found this paper:</p>\n<p><em>Arancibia, A., Guttmann, J., Gonzalez, G., &amp; Gonzalez, C. (1980). Absorption and disposition kinetics of amoxicillin in normal human subjects. Antimicrobial agents and chemotherapy, 17(2), 199-202.</em></p>\n<p>among several others. For this paper, they gave 500 mg amoxicillin to 9 healthy humans.</p>\n<p>Intravenous amoxicillin has bi-exponential kinetics - that is, the concentration is well-described by the sum of two exponential decay functions. You can measure the parameters for this equation by sampling the serum concentration of the drug over time and then look at variance in the population.</p>\n<p>Since it's a bi-exponential, there are two different &quot;half-lifes&quot;, alpha and beta. Arancibia measured the beta half life as mean = 3.40 hours, standard deviation = 1.88; alpha half life as mean = 0.27 hours, standard deviation = 0.15 hours. So yes, there's quite a bit of variability among subjects.</p>\n<p>Another measurement is the AUC, &quot;area under the curve&quot;. If you imagine the drug concentration plotted as a function of time, this is literally the area under that curve, which provides a nice summary of how much drug is available and for how long. The mean AUC was 37.0, standard deviation 9.7 (units are in mg/liter/hour). So there's a ballpark of ~25% variability in how much drug is &quot;around and available&quot; among the population.</p>\n", "score": 3 } ]

[ "statistics", "concentration" ]

[ { "answer_id": 27591, "body": "<p>We can't really measure vaccine efficacy outside of trials the same way it is measured in trials. In trials, you give some people the vaccine and others not, and then compare the two groups. When you start vaccinating the public, you don't have a randomized control group anymore, you have differences in the groups including A) Higher vaccination rates among vulnerable groups, and B) self-selection for vaccination once the vaccine is broadly available.</p>\n<p>It's also difficult to measure because maybe some of the people who would not get vaccinated are the same people who would not get tested to confirm that their symptoms are indeed being caused by COVID-19, or perhaps the same people who would engage in riskier behaviors like traveling without masks and meeting in large groups while transmission rates are high.</p>\n<p>However, the <a href=\"https://apnews.com/article/coronavirus-pandemic-health-941fcf43d9731c76c16e7354f5d5e187\" rel=\"nofollow noreferrer\">Associated Press</a> looked specifically at 18,000 people who <em>died</em> in the US in the month of May 2021. They found that only 150, less than 1%, of those who died were fully vaccinated, despite about half of people in the US being vaccinated. It's not possible to directly convert this into an efficacy for preventing death due to the caveats I mentioned above, but it is at least highly suggestive evidence that vaccination is highly effective.</p>\n", "score": 2 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 27599, "body": "<p>From the <a href=\"https://www.cdc.gov/nchs/nvss/vsrr/mortality-technical-notes.htm\" rel=\"nofollow noreferrer\">CDC</a> (bold added by me):</p>\n<blockquote>\n<p>Provisional estimates by causes of death are subject to some nonrandom sampling error. This is because the delay in receiving the report of a death depends on the cause of death. The quarterly provisional estimates are based on data that is more incomplete for the most recent months. Causes of death with more delayed reporting tend to be underrepresented in the sample, so the weighting scheme tends to underestimate their rates in the most recent months.</p>\n</blockquote>\n<blockquote>\n<p>Furthermore, <strong>for some deaths, the final cause may not be available</strong> at the time the provisional estimates are computed. <strong>In those cases, the causes of death may be reported as unknown or pending investigation and coded to the category Other ill-defined and unspecified causes of mortality (ICD–10 code R99)</strong>, a subcategory of symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified (ICD–10 codes R00–R99). <strong>In the final data, some of the deaths of unknown cause will be reassigned to specific causes</strong> if further, more specific cause-of-death information is provided.</p>\n</blockquote>\n<p>I think what you are seeing isn't that R00-R99 deaths are actually <em>increasing</em>, but that in these provisional data, more recent weeks have more deaths that are <strong>temporarily</strong> listed as R00-R99 because a specific cause has not yet been assigned.</p>\n<p>You would expect the chart to look like this (more R00-R99 deaths in recent weeks) <strong>any time you view it</strong>, not just now. For example if you pulled the data on 2020-12-05, you'd see much higher counts with this code for weeks in Sept-Dec 2020 than you see in these data.</p>\n<p>These are <em>provisional</em> data that are <em>changing</em>, not set in stone. If you wait several weeks/months, you'd expect the numbers to decrease and likely eventually reach the steady baseline you see. You can't conclude that there is any increase until those deaths are reclassified.</p>\n", "score": 4 } ]

[ "statistics", "death", "mortality-rate" ]

[ { "answer_id": 27654, "body": "<p>The neurobiology of crying in infants and adults is complex and poorly understood. As you might expect, direct physiologic studies of infants are lacking; however, some experiments have been performed in adults. Multiple investigators<a href=\"https://pubmed.ncbi.nlm.nih.gov/29687400\" rel=\"nofollow noreferrer\">¹</a> have concluded that emotive crying is associated with increased sympathetic nervous system activity. ​</p>\n<p>Experiments conducted many decades ago reveal that mediators of the sympathetic nervous system directly increase body temperature in mammals<a href=\"https://pubmed.ncbi.nlm.nih.gov/7296400/\" rel=\"nofollow noreferrer\">²</a>.</p>\n<p>Moreover, the act of vocalizing the sounds of crying requires activation of the muscles of respiration. Muscle contraction intrinsically generates heat<a href=\"https://pubmed.ncbi.nlm.nih.gov/10766936/\" rel=\"nofollow noreferrer\">³</a>.</p>\n<p>Taken together, we can expect that the increase in sympathetic nervous system activity and heat generated by the muscles of respiration may physically increase the body temperature of a crying infant. This increase in body temperature can potentially make the infant &quot;feel hot&quot;. In my opinion, the same physiologic mechanisms would (and do) apply to older children and adults.</p>\n<p>One might argue that, depending on the age of the infant, cognition might not have sufficiently developed to the point where the infant can perceive the concept of hot, but that is probably a subject for another question.</p>\n", "score": 4 } ]

[ "infant", "heat", "heat-exhaustion", "heatstroke" ]

[ { "answer_id": 29160, "body": "<p>Isovolumetric contraction of heart is a type of isometric contraction of muscles because something is resisting applying the equal and opposite force, in case of heart it is the blood which is applying opposite pressure thus increasing the pressure inside heart and volume remaining constant because the valves are closed as the same way you can push a wall but it won’t move but the muscles will be in tension as the wall is applying an equal and opposite force.</p>\n<p>You can imagine it like this suppose myosin is pulling actin fibres towards the center of sarcomere but the equal and opposite force is resisting it</p>\n", "score": 1 } ]

[ "physiology", "cardiac-physiology" ]

[ { "answer_id": 28702, "body": "<p>With regard to underlying biological mechanisms, most research has been devoted to BP-raising effects of caffeine. However, there are many other substances in coffee, such as polyphenols, soluble fibre and potassium, which could exert a beneficial effect in the cardiovascular system. Although the precise nature of the relation between coffee and BP is still unclear, <code>most evidence suggests that regular intake of caffeinated coffee does not increase the risk of hypertension</code>.</p>\n<p>for more education go to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605331/\" rel=\"nofollow noreferrer\">this</a></p>\n", "score": 1 } ]

[ "tendinopathy", "caffeine", "blood-circulation", "ligament" ]

[ { "answer_id": 28696, "body": "<p>We have no real scientific data released yet, but here are some things to think about.</p>\n<ol>\n<li>Being infected, feeling sick and being contagious are three different things.</li>\n<li>Certainly, many fewer of the vaccinated are getting infected, even with the delta variant.</li>\n<li>Many fewer of the vaccinated are feeling sick even if they get infected, even with the delta variant.</li>\n<li>The CDC director apparently said they have some info that some subgroup of vaccinated people who get infected with the delta variant may be significantly contagious. Apparently at least some have significant levels of virus in their nose and throat.</li>\n</ol>\n<p>(4) above does not apply to all vaccinated people. We don't know which subgroup it applies to - perhaps only a small subset of vaccinated people who get infected and feel sick.</p>\n<p>Re: (4); The nose and throat are important regions for spreading the virus, because that's where your breath picks up virus particles to exhale and infect others. They are not significant regions for making you seriously ill (lungs and perhaps other internal organs are important there). Thus, this fits with the delta variant being easier to spread, but doesn't indicate much about how sick you will get.</p>\n", "score": 2 }, { "answer_id": 28724, "body": "<p>The White House reports (<a href=\"https://www.whitehouse.gov/briefing-room/press-briefings/2021/08/02/press-briefing-by-white-house-covid-19-response-team-and-public-health-officials-47/\" rel=\"nofollow noreferrer\">1</a>) that several studies show that those with breakthrough infections of Delta had viral loads that were similar to people who were infected and unvaccinated, and that in this way, the Delta variant is different from prior strains.</p>\n<p>^{(I surmise SFist is just trying to communicate that SARS-CoV-2 is <em>much more</em> infectious in breakthrough infections of Delta vs breakthrough infections of other strains, not that the latter aren't at all infectious.)}</p>\n", "score": 2 }, { "answer_id": 28728, "body": "<p>Note that I am no virologist but am explaining to the best of my knowledge\nand for practical use from a variety of reports and my own understanding from my background in Nursing and Health Informatics. I think it is worth answering because the reasoning comes up a lot with skeptical friends and family who might question if it's even &quot;worth&quot; getting the vaccine, or &quot;worth&quot; maintaining measures to prevent infection spread.</p>\n<p>To answer your questions in a nutshell--the increased viral load of all variants can be infectious in both vaccinated and unvaccinated people (that is to say, it's not that 1 is infectious and 1 is not--any can be potentially infectious).</p>\n<p>My main takeaway from the <a href=\"https://sfist.com/2021/07/27/cdc-confirms-that-viral-loads-in-vaccinated-people-with-delta-are-indistinguishable-from-unvaccinated/\" rel=\"nofollow noreferrer\">article</a> you shared is that flip-flopping on policies regarding masks may contribute to further spread, since vaccinated folks can still contract/spread the Delta variant. While vaccinated folks are more likely to experience the more mild or asymptomatic symptoms of Delta COVID-19, the inconsistency of mask-enforcement makes infection spread pernicious.</p>\n<p>To further go into my answer for your questions--it is possible that what makes Delta a variant of concern is that it has mutated to replicate much <em>faster</em> than previous variants we've observed. A faster replication rate of SARS-CoV-2 in our cells contributes to a <strong>higher</strong> viral load in a <strong>shorter</strong> amount of time, giving the virus an exponentially greater opportunity to be shed.</p>\n<p>Per <a href=\"https://www.healthline.com/health-news/cdc-says-delta-variant-as-infectious-as-chickenpox-what-to-know-now#What-makes-Delta-so-contagious?\" rel=\"nofollow noreferrer\">Healthline</a>:</p>\n<blockquote>\n<p>With higher viral loads, it’s believed that people who contract SARS-CoV-2 shed more virus, making it easier to transmit the virus to those around them. “<strong>The individuals with Delta have higher viral loads, so the virus is not only more transmissible, but there is more of it in each cough or sneeze</strong> to try and get into your cells,” Nachman explained.</p>\n</blockquote>\n<p>From <a href=\"https://virological.org/t/viral-infection-and-transmission-in-a-large-well-traced-outbreak-caused-by-the-delta-sars-cov-2-variant/724\" rel=\"nofollow noreferrer\">this study</a>, it is suggested that Delta replicates faster based on the observation that the viral load from Delta was ~1000x higher than that of other strains by the time an infected subject tested positive:</p>\n<blockquote>\n<p>Compared to the 19A/19 B strains, the relative viral loads in the Delta variant infections (62 cases, Ct value 24.00 (IQR 19.00~29.00) for ORF1ab gene) were <strong>1260 times higher</strong> than the 19A/19B strains infections (63 cases, Ct value 34.31 (IQR 31.00~36.00) for ORF1ab gene) on the day when viruses were first detected. Considering the daily testing performed for the central isolated subjects since the beginning of quarantine, <strong>the higher within host growth rate of the Delta variant was proposed, which led to the higher viral loads on the time points when viral nucleotides excess the PCR detection threshold.</strong> [...] For the Delta variant infections, 80.65% samples contained &gt;6x105 copies/mL in oropharyngeal swabs when viruses were firstly detected compared to the 19.05% samples in 19A/19B infections. <strong>These data highlight that the Delta variant could be more infectious during the early stage of the infection.</strong></p>\n</blockquote>\n<p>There might be multiple factors as to what else makes Delta spread faster, and spread among both the vaccinated and unvaccinated--and while we have some idea why, we don't have all the pieces just yet.</p>\n<p>From an actual <a href=\"https://hub.jhu.edu/2021/07/19/andrew-pekosz-delta-variants/\" rel=\"nofollow noreferrer\">virologist</a>:</p>\n<blockquote>\n<p>We know that if we look at the spike protein, which is the protein the virus uses to attach to cells and start the infection process, we see that there are mutations that make that protein better at entering human cells. We can also look at the spike protein and see mutations that should reduce the ability of some of the antibodies generated by the vaccine to bind to the virus. So we think it's also finding ways to get around the immunity that we're generating in the population through vaccination.</p>\n</blockquote>\n<p>That said, it's important to emphasize that while some vaccinated folks can still spread infection, today's vaccines are still <a href=\"https://www.nejm.org/doi/full/10.1056/NEJMoa2108891\" rel=\"nofollow noreferrer\">substantially effective</a> in preventing more serious symptoms against both variants. While we're still gathering more numbers, we're <a href=\"https://www.cidrap.umn.edu/news-perspective/2021/07/study-2-covid-vaccine-doses-much-more-effective-1-against-delta\" rel=\"nofollow noreferrer\">seeing</a> vaccines offer a greater likelihood in effectiveness against variants such as Alpha, more than Delta, and an even greater likelihood in reducing serious symptoms leading to hospitalization, ongoing symptoms, or death related to COVID-19 in general.</p>\n<p>Per the same virologist above (<a href=\"https://hub.jhu.edu/2021/07/19/andrew-pekosz-delta-variants/\" rel=\"nofollow noreferrer\">Andrew Pekosz at Johns Hopkins U</a>):</p>\n<blockquote>\n<p>Say, for example, it's a one in a million chance that a mutation will\nbe advantageous to the virus. If you let the virus replicate itself\n900,000 times, odds are that the advantageous mutation will occur. But\nif you limit the overall replication of the virus to 1,000 times, then\nit's much less likely that the random advantageous mutation is going\nto occur. And that's where public health interventions really help us\na lot during this pandemic—by reducing the total amount of virus\nreplication and therefore reducing the chances that the virus can\nimprove or adapt.</p>\n</blockquote>\n<p>TLDR: More people getting vaccinated sooner rather than later substantially helps us in the race against further spread and mutation of SARS-CoV-2.</p>\n", "score": 1 } ]

[ "covid-19", "disease-transmission", "vaccine" ]

[ { "answer_id": 28717, "body": "<h2>BACKGROUND</h2>\n<p>There are a very large number of studies of tea consumption and breast cancer. All of these studies are observational epidemiologic studies. The epidemiologic studies assess black tea and green tea. Concern about the possible carcinogenicity of caffeine is long-standing. It was first evaluated as a possible carcinogen by the International Agency for Research on Cancer (IARC) in 1991.</p>\n<p><a href=\"http://www.inchem.org/documents/iarc/vol51/04-caffeine.html\" rel=\"nofollow noreferrer\">http://www.inchem.org/documents/iarc/vol51/04-caffeine.html</a></p>\n<p>As a beverage containing caffeine, black tea has became an exposure of interest.</p>\n<p>There has been a particular interest in green tea and a possible decrease in the risk of cancer, not limited to breast cancer.</p>\n<p>The reasons for the hypothesis that green tea might decrease the risk of breast cancer are explained in a 2014 review:</p>\n<p>Wu AH, Butler LM. Green tea and breast cancer. Mol Nutr Food Res. 2011;55(6):921-930. doi:10.1002/mnfr.201100006</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196858/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196858/</a></p>\n<p>Thus, these authors explain that:</p>\n<blockquote>\n<p>“Green tea is rich in tea catechins, namely epigallocatechin gallate\n(EGCG), epigallocatechin (EGC), epicatechin (EC), and epicatechin\ngallate (ECG), which have many cancer chemo preventive attributes\nincluding anti-oxidation, anti-inflammatory, anti-proliferative, and\nanti-angiogenic [5]. In addition, EGCG has been found to exhibit\nsteroid hormone activities [6–8] and may influence breast cancer risk\nvia hormonal mediated pathways.”</p>\n</blockquote>\n<h2>UMBRELLA REVIEW OF TEA AND CANCER</h2>\n<p>As explained in the WIKIPEDIA, an umbrella review is:</p>\n<blockquote>\n<p>“a review of systematic reviews or meta-analyses.”</p>\n</blockquote>\n<p><a href=\"https://en.wikipedia.org/wiki/Umbrella_review\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Umbrella_review</a></p>\n<p>An umbrella review published in 2020 looked at tea consumption and the risk of cancer. The review assessed meta-analyses of studies not just of breast cancer but all cancer. In this umbrella review, published meta-analyses of studies of green tea and black tea were identified. The umbrella review was based on a search of the PUBMED and EMBASE databases and was limited to meta-analyses published in English up to April 30, 2019.</p>\n<p>Kim TL, Jeong GH, Yang JW, et al. Tea Consumption and Risk of Cancer: An Umbrella Review and Meta-Analysis of Observational Studies. Adv Nutr. 2020;11(6):1437-1452. doi: <a href=\"https://doi.org/10.1093/advances/nmaa077\" rel=\"nofollow noreferrer\">10.1093/advances/nmaa077</a></p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7666907/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7666907/</a></p>\n<p>Table 4 of the published paper presents the findings of the review in a format that is most easily understood. This Table shows summary (meta-analyzed) estimates of the relative risk of breast cancer for high versus low black tea consumption and high versus low green tea consumption for all studies and separately for cohort and case-control studies. The following are these estimates extracted from Table 4.</p>\n<h3>Breast Cancer Estimated Summary Relative Risk (95% Confidence Interval) High Versus Low Tea Consumption</h3>\n<h4>Black Tea</h4>\n<div class=\"s-table-container\">\n<table class=\"s-table\">\n<thead>\n<tr>\n<th style=\"text-align: left;\">No. of studies</th>\n<th style=\"text-align: left;\">RR (95% CI)</th>\n<th style=\"text-align: left;\">Level of Evidence</th>\n</tr>\n</thead>\n<tbody>\n<tr>\n<td style=\"text-align: left;\">All 28</td>\n<td style=\"text-align: left;\">RR 0.98 (95% CI 0.92, 1.06)</td>\n<td style=\"text-align: left;\">Nonsignificant</td>\n</tr>\n<tr>\n<td style=\"text-align: left;\">15 cohort studies</td>\n<td style=\"text-align: left;\">RR 1.04 (95% CI 0.97, 1.12)</td>\n<td style=\"text-align: left;\">Nonsignificant</td>\n</tr>\n<tr>\n<td style=\"text-align: left;\">13 case-control studies</td>\n<td style=\"text-align: left;\">RR 0.91 (95% CI 0.80, 1.03)</td>\n<td style=\"text-align: left;\">Nonsignificant</td>\n</tr>\n</tbody>\n</table>\n</div><h4>Green Tea</h4>\n<div class=\"s-table-container\">\n<table class=\"s-table\">\n<thead>\n<tr>\n<th style=\"text-align: left;\">No. of studies</th>\n<th style=\"text-align: left;\">RR (95% CI)</th>\n<th style=\"text-align: left;\">Level of Evidence</th>\n</tr>\n</thead>\n<tbody>\n<tr>\n<td style=\"text-align: left;\">All 16</td>\n<td style=\"text-align: left;\">RR 0.82 (95% CI 0.71, 0.96)</td>\n<td style=\"text-align: left;\">Weak</td>\n</tr>\n<tr>\n<td style=\"text-align: left;\">5 cohort studies</td>\n<td style=\"text-align: left;\">RR 0.99 (95% CI 0.83, 1.77)</td>\n<td style=\"text-align: left;\">Nonsignificant</td>\n</tr>\n<tr>\n<td style=\"text-align: left;\">11 case-control studies</td>\n<td style=\"text-align: left;\">RR 0.75 (95% CI 0.61, 0.92)</td>\n<td style=\"text-align: left;\">Suggestive</td>\n</tr>\n</tbody>\n</table>\n</div><h2>UMBRELLA REVIEW: AUTHOR CONCLUSIONS ABOUT BLACK TEA AND GREEN TEA</h2>\n<p>The authors did not state a specific conclusion about the association of black tea with the risk of breast cancer. Based on a comparison of high and low green tea consumption, the authors concluded that the data about green tea and lower breast cancer was “suggestive&quot; but called for more research.</p>\n", "score": 2 } ]

[ "cancer", "tea" ]

[ { "answer_id": 28711, "body": "<p>I would not call it <em>hemophilia</em>, but <a href=\"https://www.cdc.gov/vhf/diseases.html\" rel=\"nofollow noreferrer\">viral hemorrhagic fevers</a> involve coagulopathy (quote from <a href=\"https://en.wikipedia.org/wiki/Viral_hemorrhagic_fever\" rel=\"nofollow noreferrer\">Wikipedia</a>):</p>\n<blockquote>\n<p>small blood clots form in blood vessels throughout the body, removing platelets necessary for clotting from the bloodstream and reducing clotting ability. DIC is thought to cause bleeding in Rift Valley, Marburg, and Ebola fevers.</p>\n</blockquote>\n<p>Ebola would be the disease probably most commonly known to the popular consciousness, but you'll see from that Wikipedia page that there are quite a few virus families that cause similar symptoms, and the severity of those symptoms varies widely.</p>\n<p>For more on the mechanism of the coagulation aspect of ebola, see:</p>\n<p><a href=\"https://doi.org/10.1086/379724\" rel=\"nofollow noreferrer\">Geisbert, T. W., Young, H. A., Jahrling, P. B., Davis, K. J., Kagan, E., &amp; Hensley, L. E. (2003). Mechanisms underlying coagulation abnormalities in ebola hemorrhagic fever: overexpression of tissue factor in primate monocytes/macrophages is a key event. The Journal of infectious diseases, 188(11), 1618-1629.</a></p>\n", "score": 4 } ]

[ "blood", "infectious-diseases" ]

[ { "answer_id": 28762, "body": "<p>Without any knowledge about your personal medical condition, nor any intention to address your personal case (your indigestion, gastric/intestinal pH etc., simply because we cannot and should not, as specified in the right-hand yellow disclaimer and the <a href=\"https://medicalsciences.stackexchange.com/tour\">tour</a>), I would like to address the issue of enteric coating in general:</p>\n<p>Since oral solid dosage forms (tablets, capsules) pass through the stomach on their way to the small intestine to be absorbed into the blood, if they contain an active ingredient that is acid-labile (i.e., may break down in an acidic environment such as the one in the stomach - pH level of 1-3), it is important to help it remain intact until it reaches the duodenum, where the pH is more basic (but not necessarily alkaline, i.e. larger than 7 - this is time- and place-dependent across the duodenum-small intestine axis).</p>\n<p>Manufacturers protect acid-labile active ingredients in oral solid dosage forms through a variety of methods, most commonly enteric coating, which is a coating around the tablet or capsule that resists breakdown in the stomach but breaks down and releases the solid dosage form to disintegrate and liberate the active ingredient in the duodenum or further down the gastrointestinal system.</p>\n<p>For reference, any basic pharmacy book should explain this concept. The Wikipedia entry on <a href=\"https://en.wikipedia.org/wiki/Enteric_coating\" rel=\"nofollow noreferrer\">enteric coating</a> can also be of assistance (which perhaps you should have read before posting your question).</p>\n", "score": 1 } ]

[ "gastroenterology", "acidic", "intestine", "alkaline" ]

[ { "answer_id": 28765, "body": "<p>USP is a third-party verification certification: <a href=\"https://www.usp.org/verification-services/verified-mark\" rel=\"nofollow noreferrer\">https://www.usp.org/verification-services/verified-mark</a></p>\n<p>It's private rather than governmental. On the consumer side, it is intended to achieve the following:</p>\n<blockquote>\n<p>Seeing the USP Verified Mark on a dietary supplement label indicates\nthat the product:</p>\n<ul>\n<li>Contains the ingredients listed on the label, in the declared potency and amounts. Tests have shown that contents of some\nsupplements don't match the label and some contain significantly\nless or more than the claimed amount of key ingredients. USP\nDietary Supplement Verification helps assure customers that they\nare getting the value they expect from a product they are\npurchasing.</li>\n<li>Does not contain harmful levels of specified contaminants. Some supplements have been shown to contain harmful levels of certain<br />\nheavy metals (e.g., lead and mercury), microbes, pesticides, or other\ncontaminants. At specific levels these contaminants can pose serious<br />\nrisks to one's health.</li>\n<li>Will break down and release into the body within a specified amount of time. If a supplement does not break down properly to allow its\ningredients to be available for absorption in the body, the<br />\nconsumer will not get the full benefit of its contents. USP Dietary<br />\nSupplement Verification tests products against performance standards.</li>\n<li>Has been made according to FDA current Good Manufacturing Practices using sanitary and well-controlled procedures. Assurance of safe,\nsanitary, well-controlled, and well-documented manufacturing and\nmonitoring processes indicates that a supplement manufacturer is<br />\nquality-conscious, and that the supplement will be manufactured with<br />\nconsistent quality from batch to batch.</li>\n</ul>\n</blockquote>\n<p>In part, getting the certification on a per-product basis involves:</p>\n<blockquote>\n<p>To obtain the USP Verification Mark, manufacturers must undergo:</p>\n<ul>\n<li>Manufacturing facility audit for compliance with USP General Chapter &lt;2750&gt;: Manufacturing Practices for Dietary Supplements and\nFDA current Good Manufacturing Practices (21 CFR Part 111)</li>\n<li>Review of manufacturing and quality control product documentation;</li>\n<li>Laboratory testing of samples of dietary supplements for conformance to standards of quality found in the USP–NF, or to\nappropriate pharmacopeial or manufacturer specifications and</li>\n<li>Off-the-shelf testing of USP Verified dietary supplements to confirm that the product continues to meet science-based quality\nstandards.</li>\n</ul>\n</blockquote>\n", "score": 1 } ]

[ "supplement" ]

[ { "answer_id": 28778, "body": "<p>The Astra Zeneca vaccine which is similar to Johnson &amp; Johnson's, was studied in combination with Pfizer's; they found using Pfizer as the second dose after a first dose of AZ gave better results than two doses of AZ:\n<a href=\"https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3874014\" rel=\"nofollow noreferrer\">https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3874014</a>\n&quot;Safety and Immunogenicity Report from the Com-COV Study – a Single-Blind Randomised Non-Inferiority Trial Comparing Heterologous And Homologous Prime-Boost Schedules with An Adenoviral Vectored and mRNA COVID-19 Vaccine&quot;</p>\n", "score": 3 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 28803, "body": "<p>Placing bacteria filters on the tubing would be my go-to practice (I am a retired RT) but that seems ineffective since Viral load is much smaller than the sub-micro bacterial load the filters are designed for.</p>\n<p>It’s a wet sloppy job ~ I had 35 years experience and I won’t gloss it over.</p>\n<p>Sorry, I have no practical advice for front-line workers beyond good PPE, FULL VACCINATION/Booster and the other measures we employ, other than removing herself from her high-risk work environment. There are other related occupations, like Classroom Teaching in this field, being a Rep for Mech vent companies/Drug Rep, developing On-Line CE courses, Home Health, a lateral move to Management in another non-direct patient interfacing position come to mind.</p>\n<p>My Best Wishes to your Heroic Wife. Cherish that.</p>\n", "score": 1 } ]

[ "covid-19", "mechanical-ventilation" ]

[ { "answer_id": 28797, "body": "<p>&quot;Person vaccinated-days&quot; is just expressing units of people*days; if one person was vaccinated 7 days ago and another 3 days ago that would be a total of &quot;10 person vaccinated-days&quot;.</p>\n", "score": 5 } ]

[ "vaccination", "thrombosis", "adverse-events" ]

[ { "answer_id": 31962, "body": "<p>It would seem that the evidence is that (injected) corticosteroids don't help much unless the disease is severe (septic shock) and/or has a high inflammatory response, in which case there is some evidence to suggest that they do help, but otherwise no benefit.</p>\n<p>As to why they don't use inhaled - I don't know. Perhaps because we already have very effective drugs (e.g. salbutamol) for this, which don't have the longer term dependence/weaning problems that corticosteroids do.</p>\n<p>Literature:</p>\n<p>Ceccato, A., Russo, A., Barbeta, E. et al. Real-world corticosteroid use in severe pneumonia: a propensity-score-matched study. Crit Care 25, 432 (2021). <a href=\"https://doi.org/10.1186/s13054-021-03840-x\" rel=\"nofollow noreferrer\">https://doi.org/10.1186/s13054-021-03840-x</a></p>\n<p>Stern A, Skalsky K, Avni T, Carrara E, Leibovici L, Paul M. Corticosteroids for pneumonia. Cochrane Database Syst Rev. 2017 Dec 13;12(12):CD007720. doi: <a href=\"https://10.1002/14651858.CD007720.pub3.\" rel=\"nofollow noreferrer\">10.1002/14651858.CD007720.pub3</a>. PMID: 29236286; PMCID: PMC6486210.</p>\n", "score": 2 } ]

[ "lungs", "inflammation", "pneumonia", "anti-inflammatory", "corticosteroids" ]

[ { "answer_id": 28992, "body": "<p>Well, I haven't found that one, but it's probably covering the same data as the <a href=\"https://www.medrxiv.org/content/10.1101/2021.08.27.21262679v1\" rel=\"nofollow noreferrer\">preprint</a> that <a href=\"https://www.medpagetoday.com/infectiousdisease/covid19vaccine/94344\" rel=\"nofollow noreferrer\">impressed</a> Fauci.</p>\n<blockquote>\n<p>Twelve days or more after the booster dose we found an 11.4-fold (95% CI: [10.0, 12.9]) decrease in the relative risk of confirmed infection, and a &gt;10-fold decrease in the relative risk of severe illness. Under a conservative sensitivity analysis, we find ≈5-fold protection against confirmed infection.</p>\n<p><a href=\"https://i.stack.imgur.com/uZYhA.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/uZYhA.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n", "score": 1 } ]

[ "covid-19", "vaccination", "reference-request" ]

[ { "answer_id": 28899, "body": "<p>It's unclear to me what tissue you expect to be sampled. SARS-CoV-2 is a respiratory virus and <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3494547/\" rel=\"nofollow noreferrer\">like</a> similar viruses it's (differentially) diagnosed by &quot;nasal&quot; (more accurately: nasopharyngeal) swabs and PCR or at most by doing the same (PCR) on the more invasive (to obtain) <a href=\"https://en.wikipedia.org/wiki/Bronchoalveolar_lavage\" rel=\"nofollow noreferrer\">BAL</a> samples, which are more commonly used in pneumonia cases. (The latter samples are also used to detect bacterial co-infections etc.)</p>\n<p>Actually, SARS-CoV-2 has some affinity for cells in the digestive tract as well, but while stool sampling <a href=\"https://virologyj.biomedcentral.com/articles/10.1186/s12985-020-01359-1\" rel=\"nofollow noreferrer\">can</a> detect it, I haven't heard of it this method being very common, in practice.\n(As far as determining the aforementioned affinity, some duodenal biopsies <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7335412/\" rel=\"nofollow noreferrer\">were</a> performed, but that would be way overkill/invasive for regular diagnostics.)</p>\n<p>As for your question on the destruction of the spike protein from the vaccines... no that hasn't been tested at all in humans, as far as I know. During vaccine development, modified fluorescent proteins have been used <a href=\"https://www.sciencedirect.com/science/article/pii/S0264410X21006071#f0030\" rel=\"nofollow noreferrer\">in vitro</a> to determine how the protein spreads and how long it lasts. (For some other vaccines, I do recall seeing full-mouse fluorescent images, but I'm not sure such studies have been for SARS-CoV-2 vaccines in particular, due to the speed of development during the pandemic.) For a state-of-the-art paper on fluorescence tracking of mRNA during delivery see e.g. <a href=\"https://pubs.acs.org/doi/10.1021/jacs.1c00014\" rel=\"nofollow noreferrer\">https://pubs.acs.org/doi/10.1021/jacs.1c00014</a></p>\n<p>Below is what a &quot;kinetic biodistribution&quot; study looks like. <a href=\"https://www.nature.com/articles/s41392-021-00634-z\" rel=\"nofollow noreferrer\">This one</a> is for an experimental Chinese mRNA vaccine, using two different types on nanoparticles. (The point of the paper is to claim that their LPP is in some ways superior to &quot;traditional&quot; LNPs used in Western vaccines.)</p>\n<p><a href=\"https://i.stack.imgur.com/3Gmtw.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/3Gmtw.png\" alt=\"enter image description here\" /></a></p>\n<p>The time-graph (e) is pretty badly rendered; there's larger version <a href=\"https://www.nature.com/articles/s41392-021-00634-z/figures/2\" rel=\"nofollow noreferrer\">here</a>, but from I can see, they've only tracked up to 240 hours, after which the mRNA was mostly gone (except maybe from the lungs), so they stopped.</p>\n<p>These things are generally conducted for regulatory approval purposes, but not always published as papers in the academic press. For your purpose of knowing the trajectory of the spike protein rather than mRNA, a study like this on a protein subunit vaccine like Novavax's would be useful, but from their studies <a href=\"https://www.nature.com/articles/s41467-020-20653-8\" rel=\"nofollow noreferrer\">I know about</a>, they haven't published something like the above.</p>\n", "score": 3 }, { "answer_id": 29010, "body": "<p>Yes, there is a way to test for presence of the spike protein in organ samples. This may not be possible in human biopsies / tissue samples with the standard vaccine, but it was done by Pfizer while testing BNT162, PF-07302048, as indicated in their own test data*. Done in rats (Wistar Han strain).</p>\n<p><a href=\"https://i.stack.imgur.com/p68CD.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/p68CD.jpg\" alt=\"Mean total lipid concentration in rats over time, Pfizer Report 185350\" /></a></p>\n<ul>\n<li><a href=\"https://files.catbox.moe/0vwcmj.pdf\" rel=\"nofollow noreferrer\">Pfizer Report</a></li>\n</ul>\n<p>The highest concentrations were found in: Injection site 165, Liver 24.3, Spleen 23.4, Adrenal glands 18.2, Ovaries 12.3, Bone marrow 3.77, Small intestine 1.47, Lymph (mesenteric) 1.37, Large intestine 1.34, Lung 1.09, Thyroid 1 µg lipid equivalent/g.</p>\n", "score": 0 } ]

[ "sars-cov-2", "biopsy" ]

[ { "answer_id": 28905, "body": "<p>There is no conflict.</p>\n<blockquote>\n<p>Currently there is no evidence</p>\n</blockquote>\n<p>means <em>there is no evidence</em>. It doesn't mean there is evidence <em>against</em>, it means that there is no evidence. They don't know of a person who has caught COVID-19 through food that was not exposed in some other way. The lack of evidence is suggestive that this isn't a major route of spread, though.</p>\n<blockquote>\n<p>It may be possible that a person can get COVID-19 by touching a surface or object</p>\n</blockquote>\n<p>means <em>it may be possible</em>. Evidence for this possibility might include swabbing surfaces and finding you can culture the virus from those swabs. There are other viruses (particularly those causing gastrointestinal illness, <a href=\"https://en.wikipedia.org/wiki/Norovirus\" rel=\"nofollow noreferrer\">norovirus</a> for example) that transmit often through a hand-to-mouth route. However, you're missing the end of the sentence in seeing a conflict:</p>\n<blockquote>\n<p>this is not thought to be the main way the virus spreads.</p>\n</blockquote>\n<p>In summary, there is no evidence (no known cases of spread) COVID-19 transmits through food, and although there is a hypothetical possibility it isn't thought to be particularly important from an epidemiological standpoint.</p>\n", "score": 1 } ]

[ "covid-19", "disease-transmission", "disease" ]

[ { "answer_id": 28950, "body": "<p>The correct way to bill Medicare patients for a diabetic foot exam performed on the same calendar day as other service is <strong>no additional codes</strong>.</p>\n<p>From the <a href=\"https://www.aafp.org/fpm/2010/0300/p46.html\" rel=\"nofollow noreferrer\">American Academy of Family Physicians</a>:</p>\n<blockquote>\n<p>Medicare does not allow for separate payment of an E/M code and a diabetic foot evaluation on the same date. Should you provide a diabetic foot exam to a patient with a documented diagnosis of diabetic sensory neuropathy and loss of protective sensation and not provide significant other E/M services on the same date, it may be beneficial to report this using the codes for the diabetic foot evaluation and treatment.</p>\n</blockquote>\n<p>The payment for the diabetic foot exam is included as part of the reimbursement for the regular visit.</p>\n<p>Other payers may theoretically cover this service on the same calendar day, but in my experience, most payers follow Medicare. Thus, because Medicare does not cover paying for the extra service code, physicians are likely not in the habit of spending time applying a code that will not be reimbursed.</p>\n<p>You will have to find another way to identify this gap in care.</p>\n", "score": 3 } ]

[ "diabetes", "united-states", "medical-billing" ]

[ { "answer_id": 30633, "body": "<blockquote>\n<p><a href=\"https://aricjournal.biomedcentral.com/articles/10.1186/s13756-018-0323-3\" rel=\"nofollow noreferrer\">The predominant organism was coagulase-negative staphylococci, of which most were methicillin-resistant coagulase-negative staphylococci (MRCoNS). All were susceptible to vancomycin, linezolid, rifampicin and amoxicillin-clavulanate. Acinetobacter baumannii was the most frequent causative Gram-negative agent and was resistant to 12 out of 18 antimicrobials tested.</a></p>\n</blockquote>\n<blockquote>\n<p><a href=\"https://www.infectiousdiseaseadvisor.com/home/decision-support-in-medicine/infectious-diseases/coagulase-negative-staphylococci/\" rel=\"nofollow noreferrer\">Species of CoNS that have important traits and are more frequently associated with clinical disease are S. epidermidis (biomaterial-based and prosthetic device infections), S. lugdunensis (skin and soft-tissue infections, bacteremia, endocarditis), S. saprophyticus (uncomplicated urinary tract infections in sexually active women), and S. haemolyticus (often less-susceptible to vancomycin).</a></p>\n</blockquote>\n<p>Many of these organisms are present as commensal on the skin. They pop up in other infections as mentioned above.</p>\n<p>PJP seems to me to be an unlikely candidate because <a href=\"https://academic.oup.com/cid/article/50/3/347/393968\" rel=\"nofollow noreferrer\">most people have it already</a> without incident. It does not tend to cause harm except in immunocompromised people as mentioned on its <a href=\"https://en.wikipedia.org/wiki/Pneumocystis_jirovecii?wprov=sfla1\" rel=\"nofollow noreferrer\">wikipedia page.</a> It is also a fungus, not a bacterium.</p>\n", "score": 1 } ]

[ "infection", "brain", "neurology", "surgery", "central-nervous-system" ]

[ { "answer_id": 28947, "body": "<p>The statistic is false, though there's something meaningful behind it. From Godar et al, 2003:</p>\n<blockquote>\n<p>Since 1986, people have been informed that they get about 80% of their lifetime ultraviolet (UV) dose by the age of 18. This belief originated from the mathematical conclusion that diligent use of sunscreens (sun protection factor 15 or higher) during the first 18 years of life would reduce the lifetime incidence of nonmelanoma skin cancers by 78%. These data were misconstrued to mean that individuals also got about 80% of their lifetime dose of UV by the age of 18 (linear relationship). However, these calculations were based on the incidence of nonmelanoma skin cancers being related to the square of the UV dose. Careful analysis of UV exposure data shows that Americans actually get less than 25% of their lifetime UV dose by the age of 18.</p>\n</blockquote>\n<p>The approximately &quot;80% before 18&quot; number comes from the reduction in cancer risk of wearing sunscreens during those years, rather than actually measuring &quot;UV exposure&quot;. Cancer risks are best understood as a cumulative accumulation of cellular damage, so it does make some sense to credit earlier UV exposure as higher risk, since damage caused at an early age has a longer time to potentially accumulate further damage and result in cancer.</p>\n<p>A better way to re-write the quoted statement to be more accurate while keeping with the intended message might be:</p>\n<blockquote>\n<p>Most of an average person's cancer risk from UV exposure from the sun occurs before the age of 18.</p>\n</blockquote>\n<hr />\n<p><a href=\"https://pubmed.ncbi.nlm.nih.gov/12733658/\" rel=\"nofollow noreferrer\">Godar, D. E., Urbach, F., Gasparro, F. P., &amp; van der Leun, J. C. (2003). UV doses of young adults¶. Photochemistry and photobiology, 77(4), 453-457.</a></p>\n", "score": 5 } ]

[ "pediatrics", "public-health", "sun-exposure", "uv-rays" ]

[ { "answer_id": 29003, "body": "<p>Well, it's hard for me to say how closely this matches the Chinese testing methods, but there is <a href=\"https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0252611\" rel=\"nofollow noreferrer\">one study</a> from Nigeria that compared the methods:</p>\n<blockquote>\n<p>Diagnosis of coronavirus disease 2019 (COVID-19) is currently established with a polymerase chain reaction (PCR) test by means of oropharyngeal-, nasopharyngeal-, anal-swabs, sputum and blood plasma. However, oral and nasal swabs are more commonly used. This study, therefore, assessed sensitivity and specificity of plasma as a diagnostic in comparison with a combination of oral and nasal swab samples, and the implications for blood transfusion. Oropharyngeal (OP) and nasopharyngeal (NP) swab samples were obtained from 125 individuals suspected to have COVID-19 and stored in viral transport medium (VTM) tubes. [...]</p>\n<p>Average age of study participants was 41 years, with 74 (59.2%) being male. <strong>Out of the 125 individuals tested for COVID-19, 75 (60%) were positive by OP/NP swab. However, only 6 (4.8%) had a positive plasma result for COVID-19</strong> with median Ct value of 32.4. Sensitivity and specificity of RT-PCR SARS-CoV-2 test using plasma was 8% and 100% respectively. There was no false positive recorded, but 69 (55.2%) false negatives were obtained by plasma. SARS-CoV-2 viral RNA was detected, albeit low (4.8%) in plasma. Plasma is likely not a suitable biological sample to diagnose acute SARS-CoV-2 infection.</p>\n</blockquote>\n<p>So it does look like a lot of cases could have been missed by relying only on plasma testing.</p>\n<p>There's also <a href=\"https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-020-02693-2\" rel=\"nofollow noreferrer\">a study from China</a> that albeit just tested blood not plasma in comparison.</p>\n<blockquote>\n<p>The positive detection rate in nasopharyngeal swab was the highest (54.05%), followed by anal swab (24.32%), and the positive detection rate in saliva, blood, and urine was 16.22%, 10.81%, and 5.41%, respectively. However, some patients with negative nasopharyngeal swabs had other specimens tested positive.</p>\n</blockquote>\n<p>The ratio here is only like 5:1 instead of 12:1 as in the Nigerian study, but still there's a significant difference.</p>\n", "score": 1 } ]

[ "epidemiology", "sars-cov-2", "test" ]

[ { "answer_id": 29021, "body": "<p>The fibrovascular cushions you describe are part of normal anal anatomy and are sometimes called haemorrhoid cushions.</p>\n<p>Haemorrhoid, as a noun, is usually used to refer to a pathological condition with enlargement of this tissue and the presence of symptoms.</p>\n<p>I'm not quite sure exactly what your question &quot;I don't understand what if not blood clots prevents blood from leaving external hemorrhoid cushions after person leaves the toilet.&quot; refers to. Blood does leave the cushions, to some extent, after straining ceases and the pressure in the anal area is reduced. Some blood would remain in these tissues but the blood that built up during straining would then return to the rest of the vascular system.</p>\n<p>If you mean why would haemorrhoids remain enlarged and symptomatic if no clot is present, this would be due to relatively persistant changes to the tissue due to the swelling, with enlargement of the vascular spaces.</p>\n<p>4th Degree haemorrhoids referred to haemorrhoids that do not return spontaneously into the anus after defecation nor can they be returned by manual pressure.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342598/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342598/</a></p>\n", "score": 1 } ]

[ "anatomy" ]

[ { "answer_id": 29078, "body": "<p>I usually batch-convert DICOM files to jpegs using ImageJ (in Ubuntu). This way you can open multiple windows side-by-side. The size is also much smaller, for example, 3.9MB for all 7 upright MRI sequences of 32 slices each.</p>\n", "score": 1 } ]

[ "mri" ]

[ { "answer_id": 29131, "body": "<p>According to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004018/\" rel=\"nofollow noreferrer\">a paper</a> published by the principle investigator, Dr. Brash, who was interviewed in the article linked in the question:</p>\n<blockquote>\n<p>We document the ability of [acetyl zingerone] <em>in vitro</em> to prevent dark‐CPD formation in melanocytes within the first few hours after UVA exposure</p>\n</blockquote>\n<p>Thus, Dr. Brash appears to be investigating such compounds. In the manuscript, they also describe the existence of a naturally occurring anti-oxidant, α‐tocopherol, which is also &quot;a common ingredient added to sunscreen products.&quot; They go on to compare the effectiveness of their new acetyl zingerone and α‐tocopherol.</p>\n<p>However, I encourage you to consider these results, and Dr. Brash's motives, with a healthy dose of skepticism. The paper's acknowledgments section states:</p>\n<blockquote>\n<p>The authors would like to thank Sytheon for funding this research.</p>\n</blockquote>\n<p>A quick web search shows this company has a patent on acetyl zingerone. In <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6944110/\" rel=\"nofollow noreferrer\">a paper</a> published the same year, the authors of the manuscript report &quot;no conflicts of interest&quot;, yet they had just received research funding from a chemical manufacturer directly benefiting from the research, which in my mind at least, gives the appearance of a conflict of interest.</p>\n<p>Overall, yes, there appears to at least one compound, α‐tocopherol, which is commonly added to skin care products which has at least some theoretical activity to prevent DNA damage after-the-fact.</p>\n", "score": 3 } ]

[ "dermatology", "treatment", "uv-rays", "sun-exposure" ]

[ { "answer_id": 29146, "body": "<p>&quot;Equal viral load&quot; can be rather misleading because it refers to peak measure at one point in time and in one spot (in &quot;the nose&quot;, more precisely by nasopharyngeal probe.) There are a couple of counterpoints to this:</p>\n<ol>\n<li>At least, in monkey [models] of re-infections with SARS-CoV-2, there's <a href=\"https://www.science.org/doi/10.1126/science.abc4776\" rel=\"nofollow noreferrer\">differential response</a> in the nose and in the lungs after acquired immunity, with much less replication being observed in the lungs (where it could give severe disease) as opposed to the nose, where some replication was still noted after re-challenge:</li>\n</ol>\n<blockquote>\n<p>After rechallenge, <strong>viral RNA was higher in NS [nasal swab] compared with BAL [bronchoalveolar lavage]</strong> but exhibited dose dependence and rapid decline, and median peak viral loads in NS were still &gt;1.7 log10 compared with after the primary challenge (P = 0.0011, two-sided Mann-Whitney test; Fig. 5D).</p>\n<p><a href=\"https://i.stack.imgur.com/Ntc31.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Ntc31.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>(The groups 1-3 in the diagram are simply different challenge doses.)</p>\n<p>Alas I don't know of similar studies in humans.</p>\n<ol start=\"2\">\n<li>Equal peak viral loads <a href=\"https://www.nbcnews.com/health/health-news/vaccinated-people-are-less-likely-spread-covid-new-research-finds-n1280583\" rel=\"nofollow noreferrer\">isn't necessarily</a> just as infectious (to others) if the peak lasts less time, which seems to be the case with the vaccinated group, even in the case of breakthrough infection:</li>\n</ol>\n<blockquote>\n<p>It's likely that people who have been vaccinated clear the infectious virus from the body faster. A previous <a href=\"https://www.medrxiv.org/content/10.1101/2021.07.28.21261295v1\" rel=\"nofollow noreferrer\">study</a> from Singapore had found that although levels of the virus were initially the same in those infected with the delta variant regardless of vaccine status, by day seven, levels of the virus dropped quickly in those who were vaccinated, which may reduce the ability to spread illness.</p>\n</blockquote>\n<p>The relevant graph from this latter study:</p>\n<blockquote>\n<p><a href=\"https://i.stack.imgur.com/72MvV.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/72MvV.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<ol start=\"3\">\n<li>This situation <a href=\"https://www.acpjournals.org/doi/10.7326/M20-6169\" rel=\"nofollow noreferrer\">is not</a> really unique to Covid-19 vaccines.</li>\n</ol>\n<blockquote>\n<p>There is precedent (for example, dengue [11], influenza [12–14], pertussis [15], pneumococcal bacteremia [16], rotavirus [17], and varicella [18]) that many vaccines confer greater efficacy against severe disease than milder disease.</p>\n</blockquote>\n", "score": 2 } ]

[ "covid-19", "vaccination", "immune-system", "coronavirus" ]

[ { "answer_id": 29207, "body": "<p>I am neither a medical professional nor a statistician, so <em>caveat emptor</em> and all that</p>\n<p>Short answer is no.</p>\n<p>This is because, in the article the authors state:</p>\n<blockquote>\n<p>A total of 1,736,832 persons were eligible for inclusion in the vaccination cohort...</p>\n</blockquote>\n<blockquote>\n<p>...The vaccination cohorts included a mean of 884,828 vaccinated persons, with a median age of 38 years</p>\n</blockquote>\n<p>If you compare these to the numbers of persons in the adverse events cohort column recorded for each category, then you can see that a sum total of persons (22,080,670, if my maths is correct) would be well in excess of the enrolled cohort. This means that each reported event is not independent and it is likely that a person who had one adverse event also had at least one other reported event.</p>\n<p>Thus, a simple sum of the excess events is not something that can be performed. Indeed, if this were the case, the authors would likely have done so in the paper, but they did not, leading to the conclusion that it is not a valid technique.</p>\n<p>Now we must consider that adverse event risk ratios are calculated for vaccines and other medicines, so there must be some methodology to do so, but what that methodology is, I don't know though I suspect an <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938757/\" rel=\"nofollow noreferrer\">odds-ratio</a> calculation of some sort.</p>\n<p>Note that the authors only considered some of these events to be a significant difference, even if the risk ratio or risk difference were higher than expected, so they excluded parathesia (tingling/prickling sensation) as well as vertigo (dizziness), but it looks like the excluded ones are all minor symptoms not associated with a general morbidity/mortality:</p>\n<blockquote>\n<p>The risk was substantially higher on either the multiplicative (risk ratio) or additive (risk difference) scales in the vaccinated group than in the unvaccinated group for myocarditis (risk ratio, 3.24; 95% confidence interval [CI], 1.55 to 12.44; risk difference, 2.7 events per 100,000 persons; 95% CI, 1.0 to 4.6), lymphadenopathy (risk ratio, 2.43; 95% CI, 2.05 to 2.78; risk difference, 78.4 events per 100,000 persons; 95% CI, 64.1 to 89.3), appendicitis (risk ratio, 1.40; 95% CI, 1.02 to 2.01; risk difference, 5.0 events per 100,000 persons; 95% CI, 0.3 to 9.9), and herpes zoster infection (risk ratio, 1.43; 95% CI, 1.20 to 1.73; risk difference, 15.8 events per 100,000 persons; 95% CI, 8.2 to 24.2).</p>\n</blockquote>\n<p>They also note the risks associated with SARS-CoV-2 infection in general and in figures 3 and 4 of the paper comparing to the risk with vaccination:</p>\n<blockquote>\n<p>Infection substantially increased the risk of many different adverse events, including <strong>myocarditis</strong> (risk ratio, 18.28; 95% CI, 3.95 to 25.12; risk difference, 11.0 events per 100,000 persons; 95% CI, 5.6 to 15.8), acute kidney injury (risk ratio, 14.83; 95% CI, 9.24 to 28.75; risk difference, 125.4 events per 100,000 persons; 95% CI, 107.0 to 142.6), pulmonary embolism (risk ratio, 12.14; 95% CI, 6.89 to 29.20; risk difference, 61.7 events per 100,000 persons; 95% CI, 48.5 to 75.4), intracranial hemorrhage (risk ratio, 6.89; 95% CI, 1.90 to 19.16; risk difference, 7.6 events per 100,000 persons; 95% CI, 2.7 to 12.6), pericarditis (risk ratio, 5.39; 95% CI, 2.22 to 23.58; risk difference, 10.9 events per 100,000 persons; 95% CI, 4.9 to 16.9), myocardial infarction (risk ratio, 4.47; 95% CI, 2.47 to 9.95; risk difference, 25.1 events per 100,000 persons; 95% CI, 16.2 to 33.9), deep-vein thrombosis (risk ratio, 3.78; 95% CI, 2.50 to 6.59; risk difference, 43.0 events per 100,000 persons; 95% CI, 29.9 to 56.6), and arrhythmia (risk ratio, 3.83; 95% CI, 3.07 to 4.95; risk difference, 166.1 events per 100,000 persons; 95% CI, 139.6 to 193.2).</p>\n</blockquote>\n<p><strong>Figure 3</strong>\n<a href=\"https://i.stack.imgur.com/szNFl.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/szNFl.jpg\" alt=\"Figure 3\" /></a>\n<strong>Figure 4</strong>\n<a href=\"https://i.stack.imgur.com/E9okj.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/E9okj.jpg\" alt=\"Figure 4\" /></a></p>\n", "score": 3 }, { "answer_id": 29215, "body": "<p>I think there's some missing the forest for the trees here, in the sense that adverse events (aka adverse effects) generally do not have a strict definition beyond something <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098080/\" rel=\"nofollow noreferrer\">like</a>:</p>\n<blockquote>\n<p>untoward medical occurrences after exposure. These endpoints, which are not necessarily causally related [to the treatment], are called adverse events (or sometimes adverse effects) (AEs)</p>\n</blockquote>\n<p>AEs are often enough protocol-defined. In this Israeli study:</p>\n<blockquote>\n<p>Adverse events were defined according to diagnostic codes and short free-text phrases that accompany diagnoses in the CHS database. A complete list of the study outcomes (adverse events) and their definitions is provided in Table S2.</p>\n</blockquote>\n<p>with the stated intent to capture &quot;a broad set of potential short- and medium-term adverse events among vaccinated persons&quot;.</p>\n<p>You'll note that the most common AE in table 2 (that you've included in your question) is lymphadenopathy (inflammation of the lymph nodes) which is a common but temporary (and most often <a href=\"https://edition.cnn.com/2021/10/08/health/covid-vaccine-swollen-lymph-nodes-wellness/index.html\" rel=\"nofollow noreferrer\">benign</a>) side effect of vaccines, but almost certainly not the most common side effect spontaneusly reported... as shown e.g. in this <a href=\"https://health-infobase.canada.ca/covid-19/vaccine-safety/\" rel=\"nofollow noreferrer\">Canadian database</a>, where lymphadenopathy is somewhere in the middle of the pack of the effects reported (and even below myocarditis in the Canadian database, even though that's much, much rarer in the Israeli study):</p>\n<p><a href=\"https://i.stack.imgur.com/JA92o.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/JA92o.png\" alt=\"enter image description here\" /></a></p>\n<p>So the &quot;broad set&quot; was perhaps not so broad in the Israeli study, as if clearly excluded the commonly reported vaccine side effects like headache etc. While you can definitely sum up AEs according to one study's particular definition(s) and even express that total as a ratio to the population under study... it's an not incredibly useful sum/conclusion beyond that study. Whereas specific AEs are in a sense &quot;portable&quot; between studies, assuming they used some reasonably common definition for the individual AEs. (Myocarditis is somewhat complicated as there are [Brighton Collaboration] levels for it. Also the Canadians reported it up to 92 days after vaccination, which is a longer time window than in the Israeli study.) This is almost certainly why the Israeli paper's abstract doesn't present some sum, but the individual AEs that they found statistically significant in the vaccine's direction:</p>\n<blockquote>\n<p>Vaccination was most strongly associated with an elevated risk of myocarditis (risk ratio, 3.24; 95% confidence interval [CI], 1.55 to 12.44; risk difference, 2.7 events per 100,000 persons; 95% CI, 1.0 to 4.6), lymphadenopathy (risk ratio, 2.43; 95% CI, 2.05 to 2.78; risk difference, 78.4 events per 100,000 persons; 95% CI, 64.1 to 89.3), appendicitis (risk ratio, 1.40; 95% CI, 1.02 to 2.01; risk difference, 5.0 events per 100,000 persons; 95% CI, 0.3 to 9.9), and herpes zoster infection (risk ratio, 1.43; 95% CI, 1.20 to 1.73; risk difference, 15.8 events per 100,000 persons; 95% CI, 8.2 to 24.2).</p>\n</blockquote>\n<p>One has to wonder how herpes or appendicitis might be causally related to the vaccine, by the way. It could be simply behavioral like more kissing and going out to restaurants more often, although for appendicitis some connection via a higher likelihood of general inflammatory reaction can't be excluded. (For herpes zoster at least, reactivation from lymph nodes has been <a href=\"https://www.ijidonline.com/article/S1201-9712(21)00681-0/fulltext\" rel=\"nofollow noreferrer\">posited</a>.) The Israeli paper notes that the clinical trials have noted a trend for appendicitis too, but not statistically significant, perhaps due to undepowered sample to detect a small effect. So, it's somewhat clear that they tried do &quot;double check&quot; some such trends they noticed/suspected, useing their larger database, while excluding AEs they probably considered trivial or &quot;boring&quot;.</p>\n", "score": 2 } ]

[ "covid-19", "vaccination", "mrna", "adverse-events" ]

[ { "answer_id": 29313, "body": "<p>My estimate is <strong>~25% of lifetime incidence for tendinopathy in the general population</strong> based on the following 2 studies.</p>\n<ol>\n<li><p>The lifetime incidence for Achilles tendinopathy in 6% in the general population {2}.</p>\n</li>\n<li><p>The presentation {1} mentions the yearly symptomatic tendinopathy incidence for the most typical sites of tendon injuries:</p>\n<ul>\n<li>Achilles: 2.35/1,000 {1}</li>\n<li>Patellar: 1.6/1,000 {1}</li>\n<li>Adductor: 1.22/1,000 {1}</li>\n<li>Gluteal: 4.22/1,000 {1}</li>\n<li>Plantar Fascia: 2.44/1,000 {1}</li>\n<li>Elbow: 3/1,000 {1}</li>\n<li>Shoulder: 3/1,0003/1,000 {1}</li>\n</ul>\n</li>\n</ol>\n<p>Given that there exist at least 6 other joints where tendon injuries happen with a similar incidence as in the Achilles tendon, the lifetime incidence for tendinopathy is ~25% (7 injury locations*6% of lifetime incidence for each of them = 36% lifetime incidence for any, lifetime incidence But some people may have more than 1 injured location, hence ~25%).</p>\n<p>As a result, unsurprisingly, tendon injuries account for at least 7% of physician visits in the United States {3}.</p>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} Dry Needling for Tendinopathy 1.16.18 - Academy of Orthopaedics <a href=\"https://www.orthopt.org/uploads/content_files/files/Dry%20Needling%20for%20Tendinopathy%201.16.18.pdf\" rel=\"nofollow noreferrer\">https://www.orthopt.org/uploads/content_files/files/Dry%20Needling%20for%20Tendinopathy%201.16.18.pdf</a> (<a href=\"https://web.archive.org/web/20190406233117/https://www.orthopt.org/uploads/content_files/files/Dry%20Needling%20for%20Tendinopathy%201.16.18.pdf\" rel=\"nofollow noreferrer\">mirror</a>)</li>\n<li>{2} Florit D, Pedret C, Casals M, Malliaras P, Sugimoto D, Rodas G. Incidence of Tendinopathy in Team Sports in a Multidisciplinary Sports Club Over 8 Seasons. J Sports Sci Med. 2019 Nov 19;18(4):780-788. PMID: 31827363; PMCID: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873129/\" rel=\"nofollow noreferrer\">PMC6873129</a>.</li>\n<li>{3} Kane SF, Olewinski LH, Tamminga KS. Management of Chronic Tendon Injuries. Am Fam Physician. 2019 Aug 1;100(3):147-157. PMID: 31361101.\n<a href=\"https://www.aafp.org/afp/2019/0801/p147.html\" rel=\"nofollow noreferrer\">https://www.aafp.org/afp/2019/0801/p147.html</a></li>\n</ul>\n", "score": 2 } ]

[ "statistics", "tendinopathy" ]

[ { "answer_id": 30635, "body": "<p>There is no general answer to this question -- it depends on the viruses involved, the antibodies in question and the specific immune system gene versions of an infectee.</p>\n<p>Unlike with monoclonal antibodies, the population of antibodies to a given protein generated by a natural immune response is enormous. That population includes antibodies targeted to different parts of the protein, as the immune system chops up the protein into short (8-20 aa long) peptides in order to &quot;present&quot; those to the various antigen-recognizing immune cells. <a href=\"https://dx.doi.org/10.1186%2F1745-7580-4-6\" rel=\"nofollow noreferrer\">&quot;Peptide length significantly influences in vitro affinity for MHC class II molecules&quot; doi: 10.1186/1745-7580-4-6</a></p>\n<p>Any given change to the original target protein may directly or indirectly affect from just one to many of its recognized peptides. Thus, a given antibody may have an affinity for the new protein ranging from unchanged (if its target antigen region was unchanged) all the way to essentially no binding (if its target region was greatly changed or eliminated). An individual's overall Ab &quot;neutralizing titer&quot; against the new protein will depend both on the affinity of individual Abs to the new protein and on the number of each Ab present.</p>\n", "score": 4 }, { "answer_id": 30624, "body": "<p>In vitro research suggests that the multiple changes associated with the S- (Spike) protein and for that matter, the N- (nucleocapsid) protein attributed to omicron that has demonstrated some ability to evade current vaccine-induced immunity, but also, and more markedly, can evade infection-conferred immunity. Or, to put it another way, recent infection with the delta variant is little protection against a breakthrough infection with omicron. Recent prior infection appears to moderate the potential severity in some unvaccinated, but previously infected patients. Persons who have been fully vaccinated and boosted may also experience breakthrough infection but the majority are mild symptomatically,with a much lower predisposition toward requiring hospitalization. Persons previously infected and subsequently fully vaccinated, or fully vaccinated but who still experienced breakthrough infection are much less likely to contract a breakthrough infection and much more likely, if they are reinfected, to have asymptomatic or very mild disease.</p>\n<p>I'm not sure I've seen any research, peer-reviewed or preprint, that discusses the IgG binding affinity for the case you describe.</p>\n<p>(<a href=\"https://www.imperial.ac.uk/mrc-global-infectious-disease-analysis/covid-19/report-49-Omicron/\" rel=\"nofollow noreferrer\">https://www.imperial.ac.uk/mrc-global-infectious-disease-analysis/covid-19/report-49-Omicron/</a>)</p>\n", "score": 1 } ]

[ "covid-19", "antibodies" ]

[ { "answer_id": 29330, "body": "<p>You have the data a little wrong. Here's a screenshot of the figures:</p>\n<p><a href=\"https://i.stack.imgur.com/M4RXy.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/M4RXy.png\" alt=\"totals\" /></a></p>\n<p>From this you can see that your figures show the total hospitalizations over the period, rather than the fully vaccinated. So the total hospitalizations for the fully vaccinated are 389 and 393 respectively for pre-delta and delta (that's interesting of itself, but not relevant here).</p>\n<p>You have the data correct for the ICU admission, ≥ 18 category:</p>\n<p><a href=\"https://i.stack.imgur.com/QHWtl.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/QHWtl.png\" alt=\"&lt;18\" /></a></p>\n<ol>\n<li>Correct - you can't say that the populations are different, however, incorrect on sample size. The general way to phrase this is:</li>\n</ol>\n<blockquote>\n<p>If, in the population from which this sample was drawn, there was no effect, how likely is it that we would get, in a sample of this size, get a test statistic this large or larger</p>\n</blockquote>\n<p>Based on a p-value of &gt;0.99, there is no difference in these populations, however, the sample sizes are probably large enough to see some variation if it existed. Generally (at least when I was taught) you need at least 30 samples for statistical validity - they have many more than this. However, this depends on what sort of effect they are trying to find. It could still be that the sample sizes are too small, particularly in the fully vaccinated when broken down into age groups.</p>\n<ol start=\"2\">\n<li><p>The sample sizes are not weighted - i.e. they presented total numbers (as you might expect). They did weight the percentage in each group (age, sex, etc) and the CI correspondingly.</p>\n</li>\n<li><p>I don't know for sure, but based on this line in the text:</p>\n</li>\n</ol>\n<blockquote>\n<p>Unadjusted age-specific monthly population-based hospitalization rates (hospitalizations per 100,000 persons) among all adults aged ≥18 years irrespective of pregnancy status during January–August 2021 were calculated by dividing the total number of hospitalized COVID-19 patients by population estimates within each age group in the surveillance catchment area.¶</p>\n</blockquote>\n<p>It sounds like weighted relative to the estimated age proportion in the general population.</p>\n<ol start=\"4\">\n<li><p>Yes, but you can't calculate the numbers like that, you would have to adjust for the age weighting in the calculation, but we aren't given the age weighting in the data provided.</p>\n</li>\n<li><p>Yes, comparing rates pre- and post-delta. They used a χ-square test for all groups in the corresponding cells, hence the single value for some of the groups (e.g. ethnicity). Where they have looked closer at the differences they have provided tests for each sub-group (e.g. comparing age 18-49 with other 18-49, but not to 50-64).</p>\n</li>\n<li><p>see 5.</p>\n</li>\n<li><p>Nothing. Because of the age weighting in applying the percentages you can't simply sum the percentages for each age group to reach 100% of the total population. This is why the calculation in 4. doesn't work.</p>\n</li>\n</ol>\n", "score": 1 } ]

[ "covid-19", "vaccination", "statistics", "clinical-study" ]

[ { "answer_id": 29383, "body": "<p>Although such cases are undoubtedly rare, they are not impossible. Here's <a href=\"https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-3148.2005.00603.x\" rel=\"noreferrer\">a case report from 2005</a>:</p>\n<blockquote>\n<p>Apparent deviation from Mendelian rules of blood group inheritance is rarely observed. Blood group O parents with children expressing weak A subgroups have occasionally been described but not explained. A detailed serological investigation of such a family is described here. [...]</p>\n<p>The propositus' RBCs were very weakly agglutinated with monoclonal anti-A but distinctly with polyclonal anti-A,B, i.e. typical for Ax. Serum anti-A1 (titre 4) and -B were present. Her parents' blood groups were both clearly O, with titres of serum anti-A1, and -A at 16 and 4, respectively. Adsorption/elution studies demonstrated A antigen on the daughter's cells only. The ABO genotypes were: mother, AxO1; father, O1vO2; and propositus, AxO2. The Ax allele was an A1-O1v hybrid allele with a crossing-over breakpoint between positions 235 and 446 in intron 6 (Ax-4). Compared to the A1 glycosyltransferase, this allele predicts a protein with two amino acid substitutions (Phe216Ile and Met277Val) known to yield either weakly expressed or no A antigen on RBCs.</p>\n<p>This study suggests that the nature of the ABO allele in trans can influence A antigen expression, a phenomenon previously described as allelic enhancement (or reinforcement).</p>\n</blockquote>\n", "score": 5 } ]

[ "blood", "genetics" ]