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http://www.ncbi.nlm.nih.gov/pubmed/17989259,http://www.ncbi.nlm.nih.gov/pubmed/17387144,http://www.ncbi.nlm.nih.gov/pubmed/19374772,http://www.ncbi.nlm.nih.gov/pubmed/21619633,http://www.ncbi.nlm.nih.gov/pubmed/19969543 | Elaborate on the association between Genomic Regulatory Blocks (GRBs) and target genes | Genomic regulatory blocks (GRBs) are chromosomal regions spanned by highly conserved non-coding elements (HCNEs), most of which serve as regulatory inputs of one target gene in the region. The target genes are most often transcription factors involved in embryonic development and differentiation. GRBs often contain extensive gene deserts, as well as additional 'bystander' genes intertwined with HCNEs but whose expression and function are unrelated to those of the target gene. GRB target genes have properties that set them apart from their bystanders as well as other genes in the genome: longer CpG islands, a higher number and wider spacing of alternative transcription start sites, and a distinct composition of transcription factor binding sites in their core/proximal promoters. Target gene expression correlates with the acetylation state of HCNEs in the region. |
http://www.ncbi.nlm.nih.gov/pubmed/20852673,http://www.ncbi.nlm.nih.gov/pubmed/20223299,http://www.ncbi.nlm.nih.gov/pubmed/24079768 | Which therapeutic interventions for sarcopenia have been applied | The main bulk of experimental pharmacological interventions addressing the clinical problem of frailty have been focused on the use of hormones, as replacement therapy in subjects with low or normal circulating basal levels of the hormone. Results have been disappointing, except for the case of testosterone that have shown some benefits. The effectiveness of other potential therapeutic interventions (antioxidants, anti-inflammatory agents, nutritional supplements) appears to be limited or has not been explored in detail until now. |
http://www.ncbi.nlm.nih.gov/pubmed/24019745,http://www.ncbi.nlm.nih.gov/pubmed/17677003,http://www.ncbi.nlm.nih.gov/pubmed/2687104,http://www.ncbi.nlm.nih.gov/pubmed/6214719,http://www.ncbi.nlm.nih.gov/pubmed/21217880,http://www.ncbi.nlm.nih.gov/pubmed/18256394,http://www.ncbi.nlm.nih.gov/pubmed/9309268,http://www.ncbi.nlm.nih.gov/pubmed/1128606 | What is the genetic basis of progeria? | Hutchinson-Gilford progeria syndrome is a rare, sporadic, autosomal dominant syndrome that involves premature aging, generally leading to death at approximately 13 years of age due to myocardial infarction or stroke. The genetic basis of most cases of this syndrome is a change from glycine GGC to glycine GGT in codon 608 of the lamin A (LMNA) gene, which activates a cryptic splice donor site to produce abnormal lamin A; this disrupts the nuclear membrane and alters transcription. |
http://www.ncbi.nlm.nih.gov/pubmed/19858287,http://www.ncbi.nlm.nih.gov/pubmed/16731656,http://www.ncbi.nlm.nih.gov/pubmed/12381662,http://www.ncbi.nlm.nih.gov/pubmed/16061665,http://www.ncbi.nlm.nih.gov/pubmed/19833968,http://www.ncbi.nlm.nih.gov/pubmed/12495442,http://www.ncbi.nlm.nih.gov/pubmed/15047890,http://www.ncbi.nlm.nih.gov/pubmed/23471982,http://www.ncbi.nlm.nih.gov/pubmed/16777965,http://www.ncbi.nlm.nih.gov/pubmed/21236481,http://www.ncbi.nlm.nih.gov/pubmed/19405859,http://www.ncbi.nlm.nih.gov/pubmed/22952936,http://www.ncbi.nlm.nih.gov/pubmed/22140039,http://www.ncbi.nlm.nih.gov/pubmed/22170608,http://www.ncbi.nlm.nih.gov/pubmed/18974860,http://www.ncbi.nlm.nih.gov/pubmed/20100521,http://www.ncbi.nlm.nih.gov/pubmed/15980066,http://www.ncbi.nlm.nih.gov/pubmed/20825493,http://www.ncbi.nlm.nih.gov/pubmed/12121621,http://www.ncbi.nlm.nih.gov/pubmed/20023637,http://www.ncbi.nlm.nih.gov/pubmed/22669941,http://www.ncbi.nlm.nih.gov/pubmed/14712914 | What is the function of cryptochrome-1 in mouse? | Cryptochrome-1 (Cry1) is an essential component of the central and peripheral circadian clocks for generation of circadian rhythms in mice. |
http://www.ncbi.nlm.nih.gov/pubmed/20145785,http://www.ncbi.nlm.nih.gov/pubmed/24152859,http://www.ncbi.nlm.nih.gov/pubmed/23737378,http://www.ncbi.nlm.nih.gov/pubmed/20512532,http://www.ncbi.nlm.nih.gov/pubmed/24578770,http://www.ncbi.nlm.nih.gov/pubmed/25374038,http://www.ncbi.nlm.nih.gov/pubmed/25633735,http://www.ncbi.nlm.nih.gov/pubmed/25542761,http://www.ncbi.nlm.nih.gov/pubmed/24384663,http://www.ncbi.nlm.nih.gov/pubmed/25860519,http://www.ncbi.nlm.nih.gov/pubmed/24059450 | Describe July Effect. | The July effect is the hypothetical increase in morbidity and mortality thought to be associated with the influx of new (or newly promoted) trainees during the first portion of the academic year (in July). |
http://www.ncbi.nlm.nih.gov/pubmed/21527990,http://www.ncbi.nlm.nih.gov/pubmed/23131160,http://www.ncbi.nlm.nih.gov/pubmed/20552272,http://www.ncbi.nlm.nih.gov/pubmed/15458607,http://www.ncbi.nlm.nih.gov/pubmed/16567040,http://www.ncbi.nlm.nih.gov/pubmed/16647786,http://www.ncbi.nlm.nih.gov/pubmed/17717696,http://www.ncbi.nlm.nih.gov/pubmed/11294470,http://www.ncbi.nlm.nih.gov/pubmed/22027098,http://www.ncbi.nlm.nih.gov/pubmed/10802345,http://www.ncbi.nlm.nih.gov/pubmed/15056462,http://www.ncbi.nlm.nih.gov/pubmed/11078926,http://www.ncbi.nlm.nih.gov/pubmed/23407958,http://www.ncbi.nlm.nih.gov/pubmed/14715941,http://www.ncbi.nlm.nih.gov/pubmed/12812760 | Which intermediate filament (IF) protein can be used as a non-specific marker of the neuronal precursor cells of the subventricular zone? | Nestin can be used as a nonspecific marker protein for precursor cells in the subventricular zone (SVZ). Nestin is a unique intermediate filament protein. While it is robustly expressed in developing brain, postnatal expression is limited to the brain's SVZ. |
http://www.ncbi.nlm.nih.gov/pubmed/21268065,http://www.ncbi.nlm.nih.gov/pubmed/19468253,http://www.ncbi.nlm.nih.gov/pubmed/7638194,http://www.ncbi.nlm.nih.gov/pubmed/20506537,http://www.ncbi.nlm.nih.gov/pubmed/18536530,http://www.ncbi.nlm.nih.gov/pubmed/17312023,http://www.ncbi.nlm.nih.gov/pubmed/19789556,http://www.ncbi.nlm.nih.gov/pubmed/22704242,http://www.ncbi.nlm.nih.gov/pubmed/23393137,http://www.ncbi.nlm.nih.gov/pubmed/19778587,http://www.ncbi.nlm.nih.gov/pubmed/19923434,http://www.ncbi.nlm.nih.gov/pubmed/19282482,http://www.ncbi.nlm.nih.gov/pubmed/22072770,http://www.ncbi.nlm.nih.gov/pubmed/18665914,http://www.ncbi.nlm.nih.gov/pubmed/22967183,http://www.ncbi.nlm.nih.gov/pubmed/15799776,http://www.ncbi.nlm.nih.gov/pubmed/22761581,http://www.ncbi.nlm.nih.gov/pubmed/22064703,http://www.ncbi.nlm.nih.gov/pubmed/22278882,http://www.ncbi.nlm.nih.gov/pubmed/20940144,http://www.ncbi.nlm.nih.gov/pubmed/21559294,http://www.ncbi.nlm.nih.gov/pubmed/18922972,http://www.ncbi.nlm.nih.gov/pubmed/19417133,http://www.ncbi.nlm.nih.gov/pubmed/18302924,http://www.ncbi.nlm.nih.gov/pubmed/16963560,http://www.ncbi.nlm.nih.gov/pubmed/17989773,http://www.ncbi.nlm.nih.gov/pubmed/20007090,http://www.ncbi.nlm.nih.gov/pubmed/22898819,http://www.ncbi.nlm.nih.gov/pubmed/17965600,http://www.ncbi.nlm.nih.gov/pubmed/22284370,http://www.ncbi.nlm.nih.gov/pubmed/19825994,http://www.ncbi.nlm.nih.gov/pubmed/19966177,http://www.ncbi.nlm.nih.gov/pubmed/22934696,http://www.ncbi.nlm.nih.gov/pubmed/20864525,http://www.ncbi.nlm.nih.gov/pubmed/21625467,http://www.ncbi.nlm.nih.gov/pubmed/23029374,http://www.ncbi.nlm.nih.gov/pubmed/22633409,http://www.ncbi.nlm.nih.gov/pubmed/20139415,http://www.ncbi.nlm.nih.gov/pubmed/20364115,http://www.ncbi.nlm.nih.gov/pubmed/16500889,http://www.ncbi.nlm.nih.gov/pubmed/21553025,http://www.ncbi.nlm.nih.gov/pubmed/20071334,http://www.ncbi.nlm.nih.gov/pubmed/22323818,http://www.ncbi.nlm.nih.gov/pubmed/22073356,http://www.ncbi.nlm.nih.gov/pubmed/21389349,http://www.ncbi.nlm.nih.gov/pubmed/22088914,http://www.ncbi.nlm.nih.gov/pubmed/21163962,http://www.ncbi.nlm.nih.gov/pubmed/17033890,http://www.ncbi.nlm.nih.gov/pubmed/17576694,http://www.ncbi.nlm.nih.gov/pubmed/21507353,http://www.ncbi.nlm.nih.gov/pubmed/21913078,http://www.ncbi.nlm.nih.gov/pubmed/16807237,http://www.ncbi.nlm.nih.gov/pubmed/22538524,http://www.ncbi.nlm.nih.gov/pubmed/21518897,http://www.ncbi.nlm.nih.gov/pubmed/19932585,http://www.ncbi.nlm.nih.gov/pubmed/18297739,http://www.ncbi.nlm.nih.gov/pubmed/22048250,http://www.ncbi.nlm.nih.gov/pubmed/20348135,http://www.ncbi.nlm.nih.gov/pubmed/17929180,http://www.ncbi.nlm.nih.gov/pubmed/19016755,http://www.ncbi.nlm.nih.gov/pubmed/21532572,http://www.ncbi.nlm.nih.gov/pubmed/19819843,http://www.ncbi.nlm.nih.gov/pubmed/20820192,http://www.ncbi.nlm.nih.gov/pubmed/19173286,http://www.ncbi.nlm.nih.gov/pubmed/19450230,http://www.ncbi.nlm.nih.gov/pubmed/22563479,http://www.ncbi.nlm.nih.gov/pubmed/20035856,http://www.ncbi.nlm.nih.gov/pubmed/22413869 | Which enzyme is involved in the maintenance of DNA (cytosine-5-)-methylation? | The mammalian DNA (cytosine-5) methyltransferase 1, DNMT1 is the major enzyme responsible for the maintenance of the DNA methylation patterns on the newly synthesized strand after DNA replication. DNMT1 prefers hemimethylated DNA and during DNA replication methylates hemimethylated CpG sites by copying methylation patterns from the parental DNA strand to the newly synthesized daughter strand. The equivalent of DNMT1 in plants is MET1. |
http://www.ncbi.nlm.nih.gov/pubmed/2060321,http://www.ncbi.nlm.nih.gov/pubmed/21219847,http://www.ncbi.nlm.nih.gov/pubmed/15616033,http://www.ncbi.nlm.nih.gov/pubmed/2951101,http://www.ncbi.nlm.nih.gov/pubmed/2949917,http://www.ncbi.nlm.nih.gov/pubmed/3522326,http://www.ncbi.nlm.nih.gov/pubmed/10922975,http://www.ncbi.nlm.nih.gov/pubmed/7579054,http://www.ncbi.nlm.nih.gov/pubmed/22950063,http://www.ncbi.nlm.nih.gov/pubmed/6642091,http://www.ncbi.nlm.nih.gov/pubmed/1619500,http://www.ncbi.nlm.nih.gov/pubmed/18347777,http://www.ncbi.nlm.nih.gov/pubmed/10703889,http://www.ncbi.nlm.nih.gov/pubmed/3569694,http://www.ncbi.nlm.nih.gov/pubmed/10027580,http://www.ncbi.nlm.nih.gov/pubmed/2210073,http://www.ncbi.nlm.nih.gov/pubmed/11395874,http://www.ncbi.nlm.nih.gov/pubmed/8712223,http://www.ncbi.nlm.nih.gov/pubmed/10405209,http://www.ncbi.nlm.nih.gov/pubmed/2970919,http://www.ncbi.nlm.nih.gov/pubmed/378740,http://www.ncbi.nlm.nih.gov/pubmed/1547928,http://www.ncbi.nlm.nih.gov/pubmed/9536925,http://www.ncbi.nlm.nih.gov/pubmed/8960847,http://www.ncbi.nlm.nih.gov/pubmed/22516624,http://www.ncbi.nlm.nih.gov/pubmed/7698029,http://www.ncbi.nlm.nih.gov/pubmed/8187356,http://www.ncbi.nlm.nih.gov/pubmed/18712042,http://www.ncbi.nlm.nih.gov/pubmed/8436254,http://www.ncbi.nlm.nih.gov/pubmed/15581746,http://www.ncbi.nlm.nih.gov/pubmed/15019550 | Is transcapillary albumin escape altered in diabetic patients? | An altered TERalb is present in type 2 diabetic patients, both with normal and altered patterns of AER.
TERalb is increased also in normo-albuminuric type 1 diabetic patients. |
http://www.ncbi.nlm.nih.gov/pubmed/19324998,http://www.ncbi.nlm.nih.gov/pubmed/9224811,http://www.ncbi.nlm.nih.gov/pubmed/9832432,http://www.ncbi.nlm.nih.gov/pubmed/19916081,http://www.ncbi.nlm.nih.gov/pubmed/10319950 | Which genes does thyroid hormone receptor beta1 regulate in the liver? | LDL receptor"//
"ChREBP"//
"ME", "malic enzyme"//
"cytochrome P450 oxidoreductase"// |
http://www.ncbi.nlm.nih.gov/pubmed/18282512,http://www.ncbi.nlm.nih.gov/pubmed/16630819,http://www.ncbi.nlm.nih.gov/pubmed/16859531,http://www.ncbi.nlm.nih.gov/pubmed/19562753,http://www.ncbi.nlm.nih.gov/pubmed/21175683,http://www.ncbi.nlm.nih.gov/pubmed/18279518,http://www.ncbi.nlm.nih.gov/pubmed/16533910,http://www.ncbi.nlm.nih.gov/pubmed/17387144,http://www.ncbi.nlm.nih.gov/pubmed/19698106,http://www.ncbi.nlm.nih.gov/pubmed/19073165 | Are conserved noncoding elements associated with developmental genes? | Yes. Numerous studies suggest that conserved noncoding elements span developmental regulatory genes and define regulatory domains. |
http://www.ncbi.nlm.nih.gov/pubmed/1318542,http://www.ncbi.nlm.nih.gov/pubmed/23124387,http://www.ncbi.nlm.nih.gov/pubmed/8110005,http://www.ncbi.nlm.nih.gov/pubmed/12530495,http://www.ncbi.nlm.nih.gov/pubmed/9315539,http://www.ncbi.nlm.nih.gov/pubmed/7576410,http://www.ncbi.nlm.nih.gov/pubmed/8512763,http://www.ncbi.nlm.nih.gov/pubmed/14990637,http://www.ncbi.nlm.nih.gov/pubmed/9381720,http://www.ncbi.nlm.nih.gov/pubmed/12454107 | In what proportion of children with heart failure has Enalapril been shown to be safe and effective? | In children with heart failure evidence of the effect of enalapril is empirical. Enalapril was clinically safe and effective in 50% to 80% of for children with cardiac failure secondary to congenital heart malformations before and after cardiac surgery, impaired ventricular function , valvar regurgitation, congestive cardiomyopathy, , arterial hypertension, life-threatening arrhythmias coexisting with circulatory insufficiency.
ACE inhibitors have shown a transient beneficial effect on heart failure due to anticancer drugs and possibly a beneficial effect in muscular dystrophy-associated cardiomyopathy, which deserves further studies. |
http://www.ncbi.nlm.nih.gov/pubmed/15168159,http://www.ncbi.nlm.nih.gov/pubmed/25122205,http://www.ncbi.nlm.nih.gov/pubmed/25285145,http://www.ncbi.nlm.nih.gov/pubmed/22531999,http://www.ncbi.nlm.nih.gov/pubmed/23543381,http://www.ncbi.nlm.nih.gov/pubmed/22840813,http://www.ncbi.nlm.nih.gov/pubmed/15003307,http://www.ncbi.nlm.nih.gov/pubmed/11328209,http://www.ncbi.nlm.nih.gov/pubmed/24935165,http://www.ncbi.nlm.nih.gov/pubmed/2237235,http://www.ncbi.nlm.nih.gov/pubmed/16690366 | Is myasthenia gravis associated with osteoporosis? | Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased risk of glucocorticoid-induced osteoporosis. Thymectomy can also increase risk for osteoporosis. Appropriate osteoporosis preventive measures can reduce osteoporosis risk in MG patients. |
http://www.ncbi.nlm.nih.gov/pubmed/25532001,http://www.ncbi.nlm.nih.gov/pubmed/25294372,http://www.ncbi.nlm.nih.gov/pubmed/25294889,http://www.ncbi.nlm.nih.gov/pubmed/25394660,http://www.ncbi.nlm.nih.gov/pubmed/24888775,http://www.ncbi.nlm.nih.gov/pubmed/24897131,http://www.ncbi.nlm.nih.gov/pubmed/25177680,http://www.ncbi.nlm.nih.gov/pubmed/25099181,http://www.ncbi.nlm.nih.gov/pubmed/25220535,http://www.ncbi.nlm.nih.gov/pubmed/25501094 | Which cell type has the protein Chromogranin A as marker? | Chromogranin A is a marker for neuroendocrine cells |
http://www.ncbi.nlm.nih.gov/pubmed/17396267,http://www.ncbi.nlm.nih.gov/pubmed/16367838,http://www.ncbi.nlm.nih.gov/pubmed/21624997,http://www.ncbi.nlm.nih.gov/pubmed/21076829,http://www.ncbi.nlm.nih.gov/pubmed/16951057,http://www.ncbi.nlm.nih.gov/pubmed/20352120,http://www.ncbi.nlm.nih.gov/pubmed/22087274,http://www.ncbi.nlm.nih.gov/pubmed/24075201,http://www.ncbi.nlm.nih.gov/pubmed/16322515,http://www.ncbi.nlm.nih.gov/pubmed/24465214,http://www.ncbi.nlm.nih.gov/pubmed/24126360,http://www.ncbi.nlm.nih.gov/pubmed/21705748,http://www.ncbi.nlm.nih.gov/pubmed/20140188,http://www.ncbi.nlm.nih.gov/pubmed/22491190,http://www.ncbi.nlm.nih.gov/pubmed/21385389,http://www.ncbi.nlm.nih.gov/pubmed/20978039,http://www.ncbi.nlm.nih.gov/pubmed/18346126,http://www.ncbi.nlm.nih.gov/pubmed/16339379,http://www.ncbi.nlm.nih.gov/pubmed/24282552 | Does a selective sweep increase genetic variation? | Selective sweep is a phenomenon in which the fixation of strongly beneficial alleles within a population reduces genetic diversity at partially linked neutral loci. Reduced variation or deviations from neutrality, along with an excess of fixed replacement sites, are indicative of selective sweep. |
http://www.ncbi.nlm.nih.gov/pubmed/24528855,http://www.ncbi.nlm.nih.gov/pubmed/23190330,http://www.ncbi.nlm.nih.gov/pubmed/20380929,http://www.ncbi.nlm.nih.gov/pubmed/24961627,http://www.ncbi.nlm.nih.gov/pubmed/24285972 | Which disease phenotypes are associated to PRPS1 mutations? | X-linked Charcot-Marie-Tooth disease type 5 (CMTX5), Arts syndrome, and non-syndromic sensorineural deafness (DFN2) are allelic syndromes, caused by reduced activity of phosphoribosylpyrophosphate synthetase 1 (PRS-I) due to loss-of-function mutations in PRPS1. |
http://www.ncbi.nlm.nih.gov/pubmed/19774218,http://www.ncbi.nlm.nih.gov/pubmed/10575394,http://www.ncbi.nlm.nih.gov/pubmed/8164066,http://www.ncbi.nlm.nih.gov/pubmed/8650957,http://www.ncbi.nlm.nih.gov/pubmed/23877741,http://www.ncbi.nlm.nih.gov/pubmed/11944023,http://www.ncbi.nlm.nih.gov/pubmed/9430400,http://www.ncbi.nlm.nih.gov/pubmed/10329064,http://www.ncbi.nlm.nih.gov/pubmed/12069675,http://www.ncbi.nlm.nih.gov/pubmed/9877124,http://www.ncbi.nlm.nih.gov/pubmed/18277182,http://www.ncbi.nlm.nih.gov/pubmed/22342390,http://www.ncbi.nlm.nih.gov/pubmed/7695869,http://www.ncbi.nlm.nih.gov/pubmed/10987596,http://www.ncbi.nlm.nih.gov/pubmed/9193380,http://www.ncbi.nlm.nih.gov/pubmed/8472392,http://www.ncbi.nlm.nih.gov/pubmed/9746269,http://www.ncbi.nlm.nih.gov/pubmed/9723625,http://www.ncbi.nlm.nih.gov/pubmed/9849356,http://www.ncbi.nlm.nih.gov/pubmed/10077397,http://www.ncbi.nlm.nih.gov/pubmed/22645453,http://www.ncbi.nlm.nih.gov/pubmed/22293859,http://www.ncbi.nlm.nih.gov/pubmed/15531665,http://www.ncbi.nlm.nih.gov/pubmed/8479464,http://www.ncbi.nlm.nih.gov/pubmed/18548846,http://www.ncbi.nlm.nih.gov/pubmed/15567903,http://www.ncbi.nlm.nih.gov/pubmed/15302616,http://www.ncbi.nlm.nih.gov/pubmed/8602181,http://www.ncbi.nlm.nih.gov/pubmed/11192356,http://www.ncbi.nlm.nih.gov/pubmed/9659191,http://www.ncbi.nlm.nih.gov/pubmed/10386507,http://www.ncbi.nlm.nih.gov/pubmed/7977015,http://www.ncbi.nlm.nih.gov/pubmed/8479463,http://www.ncbi.nlm.nih.gov/pubmed/12204790,http://www.ncbi.nlm.nih.gov/pubmed/18377792,http://www.ncbi.nlm.nih.gov/pubmed/12090883,http://www.ncbi.nlm.nih.gov/pubmed/23335472,http://www.ncbi.nlm.nih.gov/pubmed/19033020,http://www.ncbi.nlm.nih.gov/pubmed/10711786,http://www.ncbi.nlm.nih.gov/pubmed/8946266,http://www.ncbi.nlm.nih.gov/pubmed/16603825,http://www.ncbi.nlm.nih.gov/pubmed/15153272,http://www.ncbi.nlm.nih.gov/pubmed/11089430,http://www.ncbi.nlm.nih.gov/pubmed/12741415,http://www.ncbi.nlm.nih.gov/pubmed/12968298,http://www.ncbi.nlm.nih.gov/pubmed/12732794,http://www.ncbi.nlm.nih.gov/pubmed/22254063,http://www.ncbi.nlm.nih.gov/pubmed/20400494,http://www.ncbi.nlm.nih.gov/pubmed/20350251,http://www.ncbi.nlm.nih.gov/pubmed/10656300,http://www.ncbi.nlm.nih.gov/pubmed/9164706,http://www.ncbi.nlm.nih.gov/pubmed/19859067,http://www.ncbi.nlm.nih.gov/pubmed/24489984,http://www.ncbi.nlm.nih.gov/pubmed/15117174,http://www.ncbi.nlm.nih.gov/pubmed/23055813,http://www.ncbi.nlm.nih.gov/pubmed/12675072,http://www.ncbi.nlm.nih.gov/pubmed/15585762,http://www.ncbi.nlm.nih.gov/pubmed/17275460,http://www.ncbi.nlm.nih.gov/pubmed/10812586,http://www.ncbi.nlm.nih.gov/pubmed/23833580,http://www.ncbi.nlm.nih.gov/pubmed/21996047,http://www.ncbi.nlm.nih.gov/pubmed/12492632,http://www.ncbi.nlm.nih.gov/pubmed/18460663,http://www.ncbi.nlm.nih.gov/pubmed/10498115,http://www.ncbi.nlm.nih.gov/pubmed/8570438,http://www.ncbi.nlm.nih.gov/pubmed/10696633,http://www.ncbi.nlm.nih.gov/pubmed/10639540,http://www.ncbi.nlm.nih.gov/pubmed/10600089,http://www.ncbi.nlm.nih.gov/pubmed/11702901,http://www.ncbi.nlm.nih.gov/pubmed/23022248,http://www.ncbi.nlm.nih.gov/pubmed/21115589,http://www.ncbi.nlm.nih.gov/pubmed/15693087 | Is indicated the use of antioxidant supplements in patients at risk for coronary artery disease? | antioxidant supplementation
However there are no clear evidencies on the clinical and prognostic benefit of this supplementation.
Currently there areno recommendation for the antioxidant therapy in patients with coronary artery disease.
Currently the American Heart Association recommends consumption of a balanced diet with emphasis on antioxidant-rich fruits and vegetables but does not recommend antioxidant supplementation for the general population. |
http://www.ncbi.nlm.nih.gov/pubmed/12242302,http://www.ncbi.nlm.nih.gov/pubmed/21816340,http://www.ncbi.nlm.nih.gov/pubmed/20007147,http://www.ncbi.nlm.nih.gov/pubmed/23837869,http://www.ncbi.nlm.nih.gov/pubmed/11486028,http://www.ncbi.nlm.nih.gov/pubmed/19252527,http://www.ncbi.nlm.nih.gov/pubmed/10673359,http://www.ncbi.nlm.nih.gov/pubmed/23155001,http://www.ncbi.nlm.nih.gov/pubmed/24152440,http://www.ncbi.nlm.nih.gov/pubmed/19345675,http://www.ncbi.nlm.nih.gov/pubmed/9155038,http://www.ncbi.nlm.nih.gov/pubmed/19884656,http://www.ncbi.nlm.nih.gov/pubmed/17317627,http://www.ncbi.nlm.nih.gov/pubmed/14530362,http://www.ncbi.nlm.nih.gov/pubmed/23223443,http://www.ncbi.nlm.nih.gov/pubmed/15036402,http://www.ncbi.nlm.nih.gov/pubmed/12605686,http://www.ncbi.nlm.nih.gov/pubmed/21164076,http://www.ncbi.nlm.nih.gov/pubmed/9860962,http://www.ncbi.nlm.nih.gov/pubmed/15863502,http://www.ncbi.nlm.nih.gov/pubmed/12730239,http://www.ncbi.nlm.nih.gov/pubmed/23401122,http://www.ncbi.nlm.nih.gov/pubmed/10075998,http://www.ncbi.nlm.nih.gov/pubmed/22446588,http://www.ncbi.nlm.nih.gov/pubmed/15861128,http://www.ncbi.nlm.nih.gov/pubmed/17288991,http://www.ncbi.nlm.nih.gov/pubmed/9628881,http://www.ncbi.nlm.nih.gov/pubmed/22310293,http://www.ncbi.nlm.nih.gov/pubmed/21515253,http://www.ncbi.nlm.nih.gov/pubmed/9763509,http://www.ncbi.nlm.nih.gov/pubmed/22201738,http://www.ncbi.nlm.nih.gov/pubmed/16639702,http://www.ncbi.nlm.nih.gov/pubmed/15543229,http://www.ncbi.nlm.nih.gov/pubmed/15824116,http://www.ncbi.nlm.nih.gov/pubmed/19289500,http://www.ncbi.nlm.nih.gov/pubmed/21745814,http://www.ncbi.nlm.nih.gov/pubmed/17392515,http://www.ncbi.nlm.nih.gov/pubmed/23508105 | Which are the main functions of the human HuR (ELAVL1) protein in fibroblasts? | HuR is an RNA-binding protein that can stabilize labile mRNAs containing AU-rich elements in their 3' untranslated regions and has been shown to shuttle between the nucleus and cytoplasm. HuR function was previously shown to be implicated in the maintenance of a "young cell" phenotype in models of replicative cellular senescence. Loss of HuR is linked to reduced expression of proliferative genes during replicative senescence. Importantly, overexpression of HuR in senescent cells restored a "younger" phenotype, while a reduction in HuR expression accentuated the senescent phenotype. HuR associated with the 3' untranslated region of the mRNA encoding the longevity and stress-response protein SIRT1, stabilized the SIRT1 mRNA, and increased SIRT1 expression levels. In mesenchymal cells HuR plays a dominant role in lung development and as a key post-transcriptional regulator of networks guiding tissue remodeling during branching morphogenesis. In fibroblasts knockdown of HuR decreased the endogenous expression of TGFβ1 under exogenous TGFβ1 treatment, simultaneously with the decrease of Col1a, Col3a and fibronectin expression. HuR (human antigen R), represses ARF mRNA translation, thereby maintaining the replicative life span of mouse embryonic fibroblasts (MEFs). HuR is considered a global regulator of cell-cycle progression and tumorigenesis. Through its post-transcriptional influence on specific target mRNAs, HuR can alter the cellular response to proliferative, stress, apoptotic, differentiation, senescence, inflammatory and immune stimuli. |
http://www.ncbi.nlm.nih.gov/pubmed/24965573,http://www.ncbi.nlm.nih.gov/pubmed/25431052,http://www.ncbi.nlm.nih.gov/pubmed/26137574,http://www.ncbi.nlm.nih.gov/pubmed/24818516,http://www.ncbi.nlm.nih.gov/pubmed/23492738 | Which kinases does baricitinib inhibit? | Baricitinib is an inhibitor of Janus kinase family of enzymes (JAKs) with selectivity for JAK1 and JAK2. |
http://www.ncbi.nlm.nih.gov/pubmed/9681483,http://www.ncbi.nlm.nih.gov/pubmed/11719005,http://www.ncbi.nlm.nih.gov/pubmed/12445968,http://www.ncbi.nlm.nih.gov/pubmed/6798220,http://www.ncbi.nlm.nih.gov/pubmed/23313345,http://www.ncbi.nlm.nih.gov/pubmed/23601250,http://www.ncbi.nlm.nih.gov/pubmed/839237,http://www.ncbi.nlm.nih.gov/pubmed/7804793 | Is there evidence to suggest that triiodothyronine has neuroprotective properties in traumatic brain injury? | Yes, it has been demonstrated that triiodothyronine exerts neuroprotective properties in traumatic brain injury setting. |
http://www.ncbi.nlm.nih.gov/pubmed/20644257 | What is the role played by mTOR in hypertrophic response and heart failure? | When subjected to pressure overload, mTOR-ablated mice demonstrated an impaired hypertrophic response and accelerated heart failure progression. Thus, mTOR complex 1 signaling plays an important role in myocardial response to stress, to regulate cardiomyocyte viability and heart failure. |
http://www.ncbi.nlm.nih.gov/pubmed/19497860,http://www.ncbi.nlm.nih.gov/pubmed/19736520,http://www.ncbi.nlm.nih.gov/pubmed/22699452,http://www.ncbi.nlm.nih.gov/pubmed/22801375,http://www.ncbi.nlm.nih.gov/pubmed/23795291,http://www.ncbi.nlm.nih.gov/pubmed/22310283,http://www.ncbi.nlm.nih.gov/pubmed/17707228,http://www.ncbi.nlm.nih.gov/pubmed/23147254,http://www.ncbi.nlm.nih.gov/pubmed/24163373,http://www.ncbi.nlm.nih.gov/pubmed/22399799 | Is Lysine-specific demethylase 1 (LSD1) a critical regulator of hematopoiesis? | Yes. Lysine-specific demethylase 1 restricts hematopoietic progenitor proliferation and is essential for terminal differentiation of erythroid, granulomonocytic and megakaryocytic progenitors. |
http://www.ncbi.nlm.nih.gov/pubmed/18042044,http://www.ncbi.nlm.nih.gov/pubmed/21737094,http://www.ncbi.nlm.nih.gov/pubmed/19091944,http://www.ncbi.nlm.nih.gov/pubmed/21071436,http://www.ncbi.nlm.nih.gov/pubmed/15728425,http://www.ncbi.nlm.nih.gov/pubmed/20663875 | Is K-63 linked protein ubiquitination related to proteasomal degradation? | Ubiquitination is best known for its role in targeting proteins for degradation by the proteasome, but evidence of the nonproteolytic functions of ubiquitin is also rapidly accumulating. One example of the regulatory, rather than proteolytic, function of ubiquitin is provided by study of the tumor necrosis factor (TNF) receptor-associated factor (TRAF) proteins, which function as ubiquitin ligases to synthesize lysine 63 (K(63))-linked polyubiquitin chains to mediate protein kinase activation through a proteasome-independent mechanism. Some TRAF proteins, such as TRAF2 and TRAF3, have recently been shown to have a positive role in the canonical pathway that activates nuclear factor kappaB (NF-kappaB) through IkappaB kinase beta (IKKbeta), but a negative role in the noncanonical pathway that activates NF-kappaB through IKKalpha. These opposing roles of TRAF proteins may be linked to their ability to synthesize distinct forms of polyubiquitin chains. Indeed, the TRAF2-interacting protein RIP can mediate IKK activation when it is modified by K(63) polyubiquitin chains, but is targeted to degradation by the proteasome when it is K(48)-polyubiquitinted by the NF-kappaB inhibitor A20. Thus, ubiquitin chains are dynamic switches that can influence signaling outputs in dramatically different ways.In contrast to K48-linked polyubiquitin chains, K63-linked polyubiquitin chains function in nonproteasomal biological processes.In contrast to K48-linked polyubiquitin chains, K63-linked polyubiquitin chains function in nonproteasomal biological processes. Modification of proteins by the addition of lysine (K)-63-linked polyubiquitin (polyUb) chains is suggested to play important roles in a variety of cellular events, including DNA repair, signal transduction, and receptor endocytosis. One example of the regulatory, rather than proteolytic, function of ubiquitin is provided by study of the tumor necrosis factor (TNF) receptor-associated factor (TRAF) proteins, which function as ubiquitin ligases to synthesize lysine 63 (K(63))-linked polyubiquitin chains to mediate protein kinase activation through a proteasome-independent mechanism.One example of the regulatory, rather than proteolytic, function of ubiquitin is provided by study of the tumor necrosis factor (TNF) receptor-associated factor (TRAF) proteins, which function as ubiquitin ligases to synthesize lysine 63 (K(63))-linked polyubiquitin chains to mediate protein kinase activation through a proteasome-independent mechanismModification of proteins by the addition of lysine (K)-63-linked polyubiquitin (polyUb) chains is suggested to play important roles in a variety of cellular events, including DNA repair, signal transduction, and receptor endocytosis. In contrast to K48-linked polyubiquitin chains, K63-linked polyubiquitin chains function in nonproteasomal biological processes. |
http://www.ncbi.nlm.nih.gov/pubmed/14570063,http://www.ncbi.nlm.nih.gov/pubmed/12386935 | Could transcription factors act as cell-cell signalling molecules? | Yes. Recent data support the view that transcription factors - in particular, homeoproteins - can be transferred from cell to cell and have direct non-cell-autonomous (and therefore paracrine) activities.Pax6 is a transcription factor essential for the development of tissues including the eyes, central nervous system and endocrine glands of vertebrates and invertebrates. It regulates the expression of a broad range of molecules, including transcription factors, cell adhesion and short-range cell-cell signalling molecules, hormones and structural proteins |
http://www.ncbi.nlm.nih.gov/pubmed/23326761,http://www.ncbi.nlm.nih.gov/pubmed/22903707,http://www.ncbi.nlm.nih.gov/pubmed/23176741,http://www.ncbi.nlm.nih.gov/pubmed/22796092,http://www.ncbi.nlm.nih.gov/pubmed/23021809,http://www.ncbi.nlm.nih.gov/pubmed/23746403,http://www.ncbi.nlm.nih.gov/pubmed/23149231,http://www.ncbi.nlm.nih.gov/pubmed/23143268,http://www.ncbi.nlm.nih.gov/pubmed/23401153,http://www.ncbi.nlm.nih.gov/pubmed/23928048,http://www.ncbi.nlm.nih.gov/pubmed/23877419,http://www.ncbi.nlm.nih.gov/pubmed/23971905,http://www.ncbi.nlm.nih.gov/pubmed/24291643,http://www.ncbi.nlm.nih.gov/pubmed/23501439,http://www.ncbi.nlm.nih.gov/pubmed/24224000,http://www.ncbi.nlm.nih.gov/pubmed/23411631,http://www.ncbi.nlm.nih.gov/pubmed/22841112,http://www.ncbi.nlm.nih.gov/pubmed/23850993,http://www.ncbi.nlm.nih.gov/pubmed/23845492,http://www.ncbi.nlm.nih.gov/pubmed/23174509,http://www.ncbi.nlm.nih.gov/pubmed/23934803,http://www.ncbi.nlm.nih.gov/pubmed/24148457,http://www.ncbi.nlm.nih.gov/pubmed/23378340,http://www.ncbi.nlm.nih.gov/pubmed/23540244,http://www.ncbi.nlm.nih.gov/pubmed/23598134,http://www.ncbi.nlm.nih.gov/pubmed/23257838 | Magnetic beads has been used in numerous applications. List some coatings used. | aptamers
enzymes
streptavidin
concanavalin A
carboxylic-modified
TiO2
antibodies
SELEX library
synthesized DNA
C18
C8
oligo(dT) |
http://www.ncbi.nlm.nih.gov/pubmed/20807695,http://www.ncbi.nlm.nih.gov/pubmed/16259335,http://www.ncbi.nlm.nih.gov/pubmed/23559085,http://www.ncbi.nlm.nih.gov/pubmed/16542047,http://www.ncbi.nlm.nih.gov/pubmed/22529180,http://www.ncbi.nlm.nih.gov/pubmed/16026106,http://www.ncbi.nlm.nih.gov/pubmed/23369134,http://www.ncbi.nlm.nih.gov/pubmed/17636722,http://www.ncbi.nlm.nih.gov/pubmed/21823062,http://www.ncbi.nlm.nih.gov/pubmed/19463607,http://www.ncbi.nlm.nih.gov/pubmed/23252247,http://www.ncbi.nlm.nih.gov/pubmed/19006851 | is pharmacological treatment of subclinical hypothyroidism effective in reducing cardiovascular events? | whether SH confers a high risk for cardiovascular disease, and whether LT4 therapy has a long-term benefit that clearly outweighs the risks of overzealous treatment in these individuals, remain topics of controversy. |
http://www.ncbi.nlm.nih.gov/pubmed/24076290,http://www.ncbi.nlm.nih.gov/pubmed/22050625,http://www.ncbi.nlm.nih.gov/pubmed/18684293,http://www.ncbi.nlm.nih.gov/pubmed/19601860,http://www.ncbi.nlm.nih.gov/pubmed/19564966,http://www.ncbi.nlm.nih.gov/pubmed/15890976,http://www.ncbi.nlm.nih.gov/pubmed/18483626,http://www.ncbi.nlm.nih.gov/pubmed/19575158,http://www.ncbi.nlm.nih.gov/pubmed/19568611,http://www.ncbi.nlm.nih.gov/pubmed/19631908,http://www.ncbi.nlm.nih.gov/pubmed/20513597,http://www.ncbi.nlm.nih.gov/pubmed/17959506,http://www.ncbi.nlm.nih.gov/pubmed/24011300,http://www.ncbi.nlm.nih.gov/pubmed/20361477,http://www.ncbi.nlm.nih.gov/pubmed/22995932,http://www.ncbi.nlm.nih.gov/pubmed/20143088,http://www.ncbi.nlm.nih.gov/pubmed/19781797,http://www.ncbi.nlm.nih.gov/pubmed/21616285,http://www.ncbi.nlm.nih.gov/pubmed/22524859,http://www.ncbi.nlm.nih.gov/pubmed/20091251,http://www.ncbi.nlm.nih.gov/pubmed/22119737,http://www.ncbi.nlm.nih.gov/pubmed/21893508,http://www.ncbi.nlm.nih.gov/pubmed/22307399,http://www.ncbi.nlm.nih.gov/pubmed/21872879,http://www.ncbi.nlm.nih.gov/pubmed/19345240,http://www.ncbi.nlm.nih.gov/pubmed/22749309,http://www.ncbi.nlm.nih.gov/pubmed/23286974,http://www.ncbi.nlm.nih.gov/pubmed/12837242,http://www.ncbi.nlm.nih.gov/pubmed/23040497,http://www.ncbi.nlm.nih.gov/pubmed/12574890,http://www.ncbi.nlm.nih.gov/pubmed/22993115,http://www.ncbi.nlm.nih.gov/pubmed/15749201,http://www.ncbi.nlm.nih.gov/pubmed/17052226,http://www.ncbi.nlm.nih.gov/pubmed/21135804,http://www.ncbi.nlm.nih.gov/pubmed/21292648,http://www.ncbi.nlm.nih.gov/pubmed/11807805,http://www.ncbi.nlm.nih.gov/pubmed/23094885,http://www.ncbi.nlm.nih.gov/pubmed/12386154 | Could Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
cause sudden cardiac death? | Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) can cause sudden cardiac death. |
http://www.ncbi.nlm.nih.gov/pubmed/8824770,http://www.ncbi.nlm.nih.gov/pubmed/23715267 | What is the mechanism of action of DNA topoisomerase II inhibitors? | DNA topoisomerase II inhibitors eliminate cancer cells by causing DNA double-strand breaks, finally leading to apoptotic cell death. Moreover, drug-induced histone eviction was also shown to be associated with attenuated DNA repair, epigenetic changes and transcpription deregulation. |
http://www.ncbi.nlm.nih.gov/pubmed/19417021,http://www.ncbi.nlm.nih.gov/pubmed/20884621,http://www.ncbi.nlm.nih.gov/pubmed/22279574,http://www.ncbi.nlm.nih.gov/pubmed/21041383,http://www.ncbi.nlm.nih.gov/pubmed/22038994,http://www.ncbi.nlm.nih.gov/pubmed/22811583,http://www.ncbi.nlm.nih.gov/pubmed/10893438,http://www.ncbi.nlm.nih.gov/pubmed/15800932,http://www.ncbi.nlm.nih.gov/pubmed/21452015,http://www.ncbi.nlm.nih.gov/pubmed/22161747,http://www.ncbi.nlm.nih.gov/pubmed/19789319,http://www.ncbi.nlm.nih.gov/pubmed/19509253,http://www.ncbi.nlm.nih.gov/pubmed/18981013,http://www.ncbi.nlm.nih.gov/pubmed/19861438,http://www.ncbi.nlm.nih.gov/pubmed/18506586,http://www.ncbi.nlm.nih.gov/pubmed/15318170 | Are histone deacetylase (HDAC) inhibitors good candidates to control metastasis of solid tumors? | Yes, some HDAC inhibitors, such as Vorinostat, are on trial for human treatment after proving successful in animal models. Combination with other drugs is likely to be needed to control metastasis. |
http://www.ncbi.nlm.nih.gov/pubmed/16228909,http://www.ncbi.nlm.nih.gov/pubmed/22421737,http://www.ncbi.nlm.nih.gov/pubmed/15978612,http://www.ncbi.nlm.nih.gov/pubmed/15639480,http://www.ncbi.nlm.nih.gov/pubmed/11788418,http://www.ncbi.nlm.nih.gov/pubmed/21562304,http://www.ncbi.nlm.nih.gov/pubmed/21484537,http://www.ncbi.nlm.nih.gov/pubmed/15205937,http://www.ncbi.nlm.nih.gov/pubmed/18083727,http://www.ncbi.nlm.nih.gov/pubmed/22371524,http://www.ncbi.nlm.nih.gov/pubmed/14567970,http://www.ncbi.nlm.nih.gov/pubmed/16352453,http://www.ncbi.nlm.nih.gov/pubmed/12642359,http://www.ncbi.nlm.nih.gov/pubmed/18505755,http://www.ncbi.nlm.nih.gov/pubmed/12397030,http://www.ncbi.nlm.nih.gov/pubmed/17535853,http://www.ncbi.nlm.nih.gov/pubmed/24860983 | Is muscle lim protein (MLP) involved in cardiomyopathies? | The skeletal muscle LIM protein 1 (SLIM1) is highly expressed in skeletal and cardiac muscle, and its expression is downregulated significantly in dilated human cardiomyopathy. Loss of murine MLP results in dilated cardiomyopathy, and mutations in human MLP lead to cardiac hypertrophy, indicating a critical role for MLP in maintaining normal cardiac function.Yes, Muscle LIM protein is involved in cardiomyopathies. In specific, the skeletal muscle LIM protein 1 (SLIM1) is highly expressed in skeletal and cardiac muscle, and its expression is downregulated significantly in dilated human cardiomyopathy. Mutations in the human MLP gene are associated with hypertrophic and dilated cardiomyopathy. MLP became an important model for experimental cardiology when it was first demonstrated that MLP deficiency leads to myocardial hypertrophy followed by a dilated cardiomyopathy and heart failure phenotype. |
http://www.ncbi.nlm.nih.gov/pubmed/25667490,http://www.ncbi.nlm.nih.gov/pubmed/25384171,http://www.ncbi.nlm.nih.gov/pubmed/26056478,http://www.ncbi.nlm.nih.gov/pubmed/25682017,http://www.ncbi.nlm.nih.gov/pubmed/25806347,http://www.ncbi.nlm.nih.gov/pubmed/25483995,http://www.ncbi.nlm.nih.gov/pubmed/25323938,http://www.ncbi.nlm.nih.gov/pubmed/25939061,http://www.ncbi.nlm.nih.gov/pubmed/26124670,http://www.ncbi.nlm.nih.gov/pubmed/26058074,http://www.ncbi.nlm.nih.gov/pubmed/26396685,http://www.ncbi.nlm.nih.gov/pubmed/25382705 | Which gene harbors the mutation T790M? | The T790M mutation refers to the mutation in exon 20 of the EGFR gene |
http://www.ncbi.nlm.nih.gov/pubmed/17693930,http://www.ncbi.nlm.nih.gov/pubmed/22146760,http://www.ncbi.nlm.nih.gov/pubmed/16581974,http://www.ncbi.nlm.nih.gov/pubmed/21422919,http://www.ncbi.nlm.nih.gov/pubmed/12580776,http://www.ncbi.nlm.nih.gov/pubmed/12091808 | what is the role of FGF-2 in cardiac regeneration after myocardial infarction? | Exogenous FGF-2 was shown to increase angiogenesis and myocardial perfusion, promote myocardial regeneration by activating the SDF-1α/CXCR4 axis, and thereby improve the cardiac function after myocardial infarction. Furthermore, prevascularization with basic FGF-incorporated microspheres enhances the benefits of cardiomyocyte transplantation. In another study, transmyocardial drilling revascularization combined with heparinized basic fibroblast growth factor (bFGF)-incorporating degradable stent implantation (TMDRSI) was shown to promote Cardiac Progenitor Cells proliferation and differentiation into cardiomyocytes through activating the SDF-1/CXCR4 axis, while inhibiting myocardial apoptosis, thereby enhancing myocardial regeneration following myocardial infarction and improving cardiac function. |
http://www.ncbi.nlm.nih.gov/pubmed/25510705,http://www.ncbi.nlm.nih.gov/pubmed/18505455,http://www.ncbi.nlm.nih.gov/pubmed/12900893,http://www.ncbi.nlm.nih.gov/pubmed/16140999,http://www.ncbi.nlm.nih.gov/pubmed/23190751,http://www.ncbi.nlm.nih.gov/pubmed/15805156,http://www.ncbi.nlm.nih.gov/pubmed/24670087,http://www.ncbi.nlm.nih.gov/pubmed/24192683,http://www.ncbi.nlm.nih.gov/pubmed/22012791,http://www.ncbi.nlm.nih.gov/pubmed/23913520 | Have 5q35 microdeletions been implicated in Sotos syndrome development? | Loss-of-function mutations of NSD1 and 5q35 microdeletions encompassing NSD1 are a major cause of Sotos syndrome (Sos), which is characterized by overgrowth, macrocephaly, characteristic facies, and variable intellectual disability (ID).Loss-of-function mutations of NSD1 and 5q35 microdeletions encompassing NSD1 are a major cause of Sotos syndrome (Sos), which is characterized by overgrowth, macrocephaly, characteristic facies, and variable intellectual disability (ID) |
http://www.ncbi.nlm.nih.gov/pubmed/23279763,http://www.ncbi.nlm.nih.gov/pubmed/10664520,http://www.ncbi.nlm.nih.gov/pubmed/9820618,http://www.ncbi.nlm.nih.gov/pubmed/17455252,http://www.ncbi.nlm.nih.gov/pubmed/23024266,http://www.ncbi.nlm.nih.gov/pubmed/20175448,http://www.ncbi.nlm.nih.gov/pubmed/11914929,http://www.ncbi.nlm.nih.gov/pubmed/18172277,http://www.ncbi.nlm.nih.gov/pubmed/9236523,http://www.ncbi.nlm.nih.gov/pubmed/21302639,http://www.ncbi.nlm.nih.gov/pubmed/23435440,http://www.ncbi.nlm.nih.gov/pubmed/10614532,http://www.ncbi.nlm.nih.gov/pubmed/7962349,http://www.ncbi.nlm.nih.gov/pubmed/21613051,http://www.ncbi.nlm.nih.gov/pubmed/9735087,http://www.ncbi.nlm.nih.gov/pubmed/10496602,http://www.ncbi.nlm.nih.gov/pubmed/10502325 | Tumors of which three organs are classically associated with the multiple endocrine neoplasia type 1 syndrome? | Multiple endocrine neoplasia type 1 syndrome is an inherited cancer syndrome defined by occurrence of multiple neuro-endocrine tumors and is classically associated with the combined occurrence of two or more tumors involving parathyroid gland, pancreas and pituitary gland. Other tumors, including but not limited to adrenal cortical tumor, carcinoid tumors lipoma, leiomyoma, duodenal gastrinoma, hepatic focal nodular hyperplasia, and renal angiomyolipoma, angiofibroma, colagenoma, thyroid tumor and meningioma, may also be present. |
http://www.ncbi.nlm.nih.gov/pubmed/20943656,http://www.ncbi.nlm.nih.gov/pubmed/21827905,http://www.ncbi.nlm.nih.gov/pubmed/24293103,http://www.ncbi.nlm.nih.gov/pubmed/24272589,http://www.ncbi.nlm.nih.gov/pubmed/9292723,http://www.ncbi.nlm.nih.gov/pubmed/23659897,http://www.ncbi.nlm.nih.gov/pubmed/20865150,http://www.ncbi.nlm.nih.gov/pubmed/16389311,http://www.ncbi.nlm.nih.gov/pubmed/21653538,http://www.ncbi.nlm.nih.gov/pubmed/23617879,http://www.ncbi.nlm.nih.gov/pubmed/20007218,http://www.ncbi.nlm.nih.gov/pubmed/24685680 | Which is the protein implicated in Spinocerebellar ataxia type 3? | Ataxin-3 is a ubiquitously expressed deubiqutinating enzyme with important functions in the proteasomal protein degradation pathway and regulation of transcription. The C-terminus of the ataxin-3 protein contains a polyglutamine (PolyQ) region that, when mutationally expanded to over 52 glutamines, causes the neurodegenerative disease spinocerebellar ataxia 3 (SCA3).Spinocerebellar ataxia type 3 (SCA3) is the most frequent inherited cerebellar ataxia in Europe, the US and Japan, leading to disability and death through motor complications. Although the affected protein ataxin-3 is found ubiquitously in the brain, grey matter atrophy is predominant in the cerebellum and the brainstem |
http://www.ncbi.nlm.nih.gov/pubmed/21253457,http://www.ncbi.nlm.nih.gov/pubmed/19767758,http://www.ncbi.nlm.nih.gov/pubmed/25636611,http://www.ncbi.nlm.nih.gov/pubmed/22925268,http://www.ncbi.nlm.nih.gov/pubmed/24077707,http://www.ncbi.nlm.nih.gov/pubmed/25139902,http://www.ncbi.nlm.nih.gov/pubmed/23990803,http://www.ncbi.nlm.nih.gov/pubmed/21053251 | What is Tn-seq? | The transposon mutagenesis and high-throughput sequencing (Tn-seq) is a technique that allows for quantitative assessment of individual mutants within a transposon mutant library by sequencing the transposon-genome junctions and then compiling mutant presence by mapping to a base genome. Using Tn-seq, it is possible to quickly define all the insertional mutants in a library and thus identify nonessential genes under the conditions in which the library was produced. Identification of fitness of individual mutants under specific conditions can be performed by exposing the library to selective pressures. |
http://www.ncbi.nlm.nih.gov/pubmed/18945929,http://www.ncbi.nlm.nih.gov/pubmed/24247648,http://www.ncbi.nlm.nih.gov/pubmed/19196885,http://www.ncbi.nlm.nih.gov/pubmed/24320036,http://www.ncbi.nlm.nih.gov/pubmed/24320031,http://www.ncbi.nlm.nih.gov/pubmed/24287796,http://www.ncbi.nlm.nih.gov/pubmed/24328010,http://www.ncbi.nlm.nih.gov/pubmed/21234418,http://www.ncbi.nlm.nih.gov/pubmed/24320038,http://www.ncbi.nlm.nih.gov/pubmed/24290090 | Is metabolic syndrome related with cardiovascular disease? | The metabolic syndrome (MetS) is characterized by a cluster of risk factors including central obesity, hypertension, dyslipidemia and insulin resistance, The MetS is associated with an increased risk for cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). |
http://www.ncbi.nlm.nih.gov/pubmed/23463199,http://www.ncbi.nlm.nih.gov/pubmed/22040846,http://www.ncbi.nlm.nih.gov/pubmed/17319152,http://www.ncbi.nlm.nih.gov/pubmed/19951725,http://www.ncbi.nlm.nih.gov/pubmed/21946389,http://www.ncbi.nlm.nih.gov/pubmed/15917225,http://www.ncbi.nlm.nih.gov/pubmed/17660525,http://www.ncbi.nlm.nih.gov/pubmed/21898331,http://www.ncbi.nlm.nih.gov/pubmed/23157297,http://www.ncbi.nlm.nih.gov/pubmed/18179252 | Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase? | Several labs have obtained evidence for a protein complex that involves many of the nonstructural (NS) proteins encoded by the virus. NS3, NS4A, NS4B, NS5A, and NS5B appear to interact structurally and functionally. The interaction between the helicase, NS3, and the RNA polymerase, NS5B play a key role in viral replication. Pull-down experiments and surface plasmon resonance data indicate a direct interaction between NS3 and NS5B that is primarily mediated through the protease domain of NS3. This interaction reduces the basal ATPase activity of NS3. However, NS5B stimulates product formation in RNA unwinding experiments under conditions of excess nucleic acid substrate. When the concentrations of NS3 and NS5B are in excess of nucleic acid substrate, NS5B reduces the rate of NS3-catalyzed unwinding. Under pre-steady-state conditions, in which NS3 and substrate concentrations are similar, product formation increased in the presence of NS5B. The increase was consistent with 1:1 complex formed between the two proteins. |
http://www.ncbi.nlm.nih.gov/pubmed/22276468,http://www.ncbi.nlm.nih.gov/pubmed/11178982,http://www.ncbi.nlm.nih.gov/pubmed/23541693,http://www.ncbi.nlm.nih.gov/pubmed/21404276,http://www.ncbi.nlm.nih.gov/pubmed/24051048,http://www.ncbi.nlm.nih.gov/pubmed/23721719,http://www.ncbi.nlm.nih.gov/pubmed/19083132,http://www.ncbi.nlm.nih.gov/pubmed/17397816,http://www.ncbi.nlm.nih.gov/pubmed/12865926,http://www.ncbi.nlm.nih.gov/pubmed/12016139,http://www.ncbi.nlm.nih.gov/pubmed/12592385,http://www.ncbi.nlm.nih.gov/pubmed/17636314,http://www.ncbi.nlm.nih.gov/pubmed/12427531,http://www.ncbi.nlm.nih.gov/pubmed/12488587,http://www.ncbi.nlm.nih.gov/pubmed/22798379,http://www.ncbi.nlm.nih.gov/pubmed/21267443,http://www.ncbi.nlm.nih.gov/pubmed/17363343,http://www.ncbi.nlm.nih.gov/pubmed/22665067,http://www.ncbi.nlm.nih.gov/pubmed/23675572,http://www.ncbi.nlm.nih.gov/pubmed/12191483,http://www.ncbi.nlm.nih.gov/pubmed/20298636,http://www.ncbi.nlm.nih.gov/pubmed/10753787,http://www.ncbi.nlm.nih.gov/pubmed/16258176,http://www.ncbi.nlm.nih.gov/pubmed/24104500,http://www.ncbi.nlm.nih.gov/pubmed/11395777,http://www.ncbi.nlm.nih.gov/pubmed/23628323,http://www.ncbi.nlm.nih.gov/pubmed/23620081,http://www.ncbi.nlm.nih.gov/pubmed/16555998,http://www.ncbi.nlm.nih.gov/pubmed/23125219,http://www.ncbi.nlm.nih.gov/pubmed/15660524,http://www.ncbi.nlm.nih.gov/pubmed/21427292 | Are defects in recombination repair involved in carcinogenesis? | Yes. The breast cancer-associated BRCA1 and BRCA2 proteins are strongly implicated in recombination repair.Carcinogenesis or oncogenesis or tumorigenesis is literally the creation of cancer. It is a process by which normal cells are transformed into cancer cells. It is characterized by a progression of changes at the cellular, genetic and epigenetic level that ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a malignant mass.
Carcinogenesis is caused by mutation and epimutation of the genetic material of normal cells, which upsets the normal balance between proliferation and cell death. This results in uncontrolled cell division and the evolution of those cells by natural selection in the body. The uncontrolled and often rapid proliferation of cells can lead to benign tumors; some types of these may turn into malignant tumors (cancer). Based on studies, carcinogenesis also related with the defects in recombination repair. |
http://www.ncbi.nlm.nih.gov/pubmed/15970608,http://www.ncbi.nlm.nih.gov/pubmed/11336401,http://www.ncbi.nlm.nih.gov/pubmed/18442953,http://www.ncbi.nlm.nih.gov/pubmed/15266396,http://www.ncbi.nlm.nih.gov/pubmed/22627569,http://www.ncbi.nlm.nih.gov/pubmed/18243066 | Which is the prevalence of cystic fibrosis in the human population? | Prevalence of Cystic Fibrosis varies according to the population. A theoretical estimate of the prevalence of cystic fibrosis based on anthropological data suggested a frequency of 25 affected individuals/100,000 inhabitants. However, real data indicated that the true prevalence in the population was considerably lower (6.9 cases/100,000 inhabitants). Results of literature reviews, surveys, and registry analyses revealed a mean prevalence of 0.737/10,000 in the 27 EU countries, which is similar to the value of 0.797 in the United States, and only one outlier, namely the Republic of Ireland at 2.98.The results of literature reviews, surveys, and registry analyses revealed a mean prevalence of 0.737/10,000 in the 27 EU countries, which is similar to the value of 0.797 in the United States, and only one outlier, namely the Republic of Ireland at 2.98 (PMID: 18442953) The allelic frequency of this variant was calculated to be 0.7% for this population (PMID: 22627569) CF mutations were identified in 374 (4.0%) individuals. (PMID: 11336401) |
http://www.ncbi.nlm.nih.gov/pubmed/22564885,http://www.ncbi.nlm.nih.gov/pubmed/15127315,http://www.ncbi.nlm.nih.gov/pubmed/24682289,http://www.ncbi.nlm.nih.gov/pubmed/13679126,http://www.ncbi.nlm.nih.gov/pubmed/12437562,http://www.ncbi.nlm.nih.gov/pubmed/23622185,http://www.ncbi.nlm.nih.gov/pubmed/25238668,http://www.ncbi.nlm.nih.gov/pubmed/17990592 | Are seizures among the neurological symptoms of incontinentia pigmenti? | Incontinentia pigmenti is an X-linked dominant disorder resulting from a mutation of IKBKG. This disorder has a classic dermatologic presentation, but neurologic involvement, with seizures and cortical infarction, can arise shortly after birth. |
http://www.ncbi.nlm.nih.gov/pubmed/20519495,http://www.ncbi.nlm.nih.gov/pubmed/22391297,http://www.ncbi.nlm.nih.gov/pubmed/21167467,http://www.ncbi.nlm.nih.gov/pubmed/12967338,http://www.ncbi.nlm.nih.gov/pubmed/15645142,http://www.ncbi.nlm.nih.gov/pubmed/18612197,http://www.ncbi.nlm.nih.gov/pubmed/11044404 | Which are the different homologs or family members of the hedgehog proteins in mammals? | Hedgehog (Hh) signaling proteins stimulate cell proliferation, differentiation, and tissue patterning at multiple points in animal development. A single Hh homolog is present in Drosophila, but three Hh homologs, Sonic hedgehog (Shh), Indian hedgehog (Ihh) , and Desert hedgehog (Dhh), are present in mammals. |
http://www.ncbi.nlm.nih.gov/pubmed/24311635,http://www.ncbi.nlm.nih.gov/pubmed/24309100,http://www.ncbi.nlm.nih.gov/pubmed/24276258,http://www.ncbi.nlm.nih.gov/pubmed/24290217,http://www.ncbi.nlm.nih.gov/pubmed/24312355,http://www.ncbi.nlm.nih.gov/pubmed/24307346,http://www.ncbi.nlm.nih.gov/pubmed/24312415,http://www.ncbi.nlm.nih.gov/pubmed/24289602,http://www.ncbi.nlm.nih.gov/pubmed/24287118,http://www.ncbi.nlm.nih.gov/pubmed/24270265,http://www.ncbi.nlm.nih.gov/pubmed/24295418 | What does mTOR stands for? | mTOR stands for: mammalian target of rapamycin. |
http://www.ncbi.nlm.nih.gov/pubmed/24946806 | Which is the most common genetic lesion among patients with Joubert Syndrome and a cerebello-oculo-renal phenotype? | Joubert syndrome (JBTS) is an inherited ciliopathy giving rise to NPHP with cerebellar vermis aplasia and retinal degeneration. Among patients with JBTS and a cerebello-oculo-renal phenotype, mutations in CEP290 (NPHP6) are the most common genetic lesion.Nephronophthisis (NPHP) is the major cause of pediatric renal failure, yet the disease remains poorly understood, partly due to the lack of appropriate animal models. Joubert syndrome (JBTS) is an inherited ciliopathy giving rise to NPHP with cerebellar vermis aplasia and retinal degeneration. Among patients with JBTS and a cerebello-oculo-renal phenotype, mutations in CEP290 (NPHP6) are the most common genetic lesion |
http://www.ncbi.nlm.nih.gov/pubmed/23283084,http://www.ncbi.nlm.nih.gov/pubmed/19840561,http://www.ncbi.nlm.nih.gov/pubmed/18824640,http://www.ncbi.nlm.nih.gov/pubmed/21862720,http://www.ncbi.nlm.nih.gov/pubmed/20435186,http://www.ncbi.nlm.nih.gov/pubmed/19261139,http://www.ncbi.nlm.nih.gov/pubmed/21505152 | Which scales are recommended by the American Heart Association for depression screening in cardiovascular patients? | Patient Health Questionnaire-2 (PHQ-2) and Patient Health Questionnaire-9 (PHQ-9) are recommended by the American Heart Association for depression screening in cardiovascular patients. |
http://www.ncbi.nlm.nih.gov/pubmed/24164596,http://www.ncbi.nlm.nih.gov/pubmed/23868195,http://www.ncbi.nlm.nih.gov/pubmed/25699710,http://www.ncbi.nlm.nih.gov/pubmed/24636987,http://www.ncbi.nlm.nih.gov/pubmed/23251031,http://www.ncbi.nlm.nih.gov/pubmed/22279048 | Is there a genome-wide technique for the detection of R-loop formation? | Genome-wide analysis of fragile sites by chromatin immunoprecipitation (ChIP) and microarray (ChIP-chip) of phosphorylated H2A in these mutants supported a transcription-dependent mechanism of DNA damage characteristic of R loops. Here we show that recombination factors are required for the survival of yeast FACT mutants, consistent with an accumulation of DNA breaks that we detected by Rad52 foci and transcription-dependent hyperrecombination. The latter pathway operates on nascent transcripts that are not simultaneously translated and requires factors Rho, NusG, and NusA, each of which is essential for viability of WT Escherichia coli. DNA replication in Escherichia coli is normally initiated at a single origin, oriC, dependent on initiation protein DnaA.Genome-wide analysis of fragile sites by chromatin immunoprecipitation (ChIP) and microarray (ChIP-chip) of phosphorylated H2A in these mutants supported a transcription-dependent mechanism of DNA damage characteristic of R loops
A bisulfite-sensitivity assay may demonstrate genome-wide increase in the occurrence of RNA-DNA hybrids (R-loops). |
http://www.ncbi.nlm.nih.gov/pubmed/10779362,http://www.ncbi.nlm.nih.gov/pubmed/10671371,http://www.ncbi.nlm.nih.gov/pubmed/10202156,http://www.ncbi.nlm.nih.gov/pubmed/10516442,http://www.ncbi.nlm.nih.gov/pubmed/1543904,http://www.ncbi.nlm.nih.gov/pubmed/10581035 | How is CBX1/M31 related to position-effect variegation? | M31 is a heterochromatin component, that is concentrated in the XY body during spermatogenesis. M31 overexpression has two contrasting effects which are dependent on chromosomal context: (i) it enhanced PEV in those lines with centromeric or pericentromeric transgene locations; and (ii) it suppressed PEV when the transgene was non-centromeric. |
http://www.ncbi.nlm.nih.gov/pubmed/25130390,http://www.ncbi.nlm.nih.gov/pubmed/23197691,http://www.ncbi.nlm.nih.gov/pubmed/20811115,http://www.ncbi.nlm.nih.gov/pubmed/25242654,http://www.ncbi.nlm.nih.gov/pubmed/21504055,http://www.ncbi.nlm.nih.gov/pubmed/25047630,http://www.ncbi.nlm.nih.gov/pubmed/25457969,http://www.ncbi.nlm.nih.gov/pubmed/22436025,http://www.ncbi.nlm.nih.gov/pubmed/24695367,http://www.ncbi.nlm.nih.gov/pubmed/23411530,http://www.ncbi.nlm.nih.gov/pubmed/24157694,http://www.ncbi.nlm.nih.gov/pubmed/24334142,http://www.ncbi.nlm.nih.gov/pubmed/24188635,http://www.ncbi.nlm.nih.gov/pubmed/25384685,http://www.ncbi.nlm.nih.gov/pubmed/23380571,http://www.ncbi.nlm.nih.gov/pubmed/23719889,http://www.ncbi.nlm.nih.gov/pubmed/24439284,http://www.ncbi.nlm.nih.gov/pubmed/22508498,http://www.ncbi.nlm.nih.gov/pubmed/25093879,http://www.ncbi.nlm.nih.gov/pubmed/22767299,http://www.ncbi.nlm.nih.gov/pubmed/23260439,http://www.ncbi.nlm.nih.gov/pubmed/23575660,http://www.ncbi.nlm.nih.gov/pubmed/24961492,http://www.ncbi.nlm.nih.gov/pubmed/24903714,http://www.ncbi.nlm.nih.gov/pubmed/23562089,http://www.ncbi.nlm.nih.gov/pubmed/23015540,http://www.ncbi.nlm.nih.gov/pubmed/20353253,http://www.ncbi.nlm.nih.gov/pubmed/22394017,http://www.ncbi.nlm.nih.gov/pubmed/21527813,http://www.ncbi.nlm.nih.gov/pubmed/24758832,http://www.ncbi.nlm.nih.gov/pubmed/24998183,http://www.ncbi.nlm.nih.gov/pubmed/24887553,http://www.ncbi.nlm.nih.gov/pubmed/23184715,http://www.ncbi.nlm.nih.gov/pubmed/20546891,http://www.ncbi.nlm.nih.gov/pubmed/25048797,http://www.ncbi.nlm.nih.gov/pubmed/21358040 | Can bioprinting use human cells? | Yes, human cells can be used for bioprinting |
http://www.ncbi.nlm.nih.gov/pubmed/23146897,http://www.ncbi.nlm.nih.gov/pubmed/21177427,http://www.ncbi.nlm.nih.gov/pubmed/21177431,http://www.ncbi.nlm.nih.gov/pubmed/17398168,http://www.ncbi.nlm.nih.gov/pubmed/23055242,http://www.ncbi.nlm.nih.gov/pubmed/10628973,http://www.ncbi.nlm.nih.gov/pubmed/23564176,http://www.ncbi.nlm.nih.gov/pubmed/20435731,http://www.ncbi.nlm.nih.gov/pubmed/15143174 | Is transcription-associated mutagenesis (TAM) related to gene expression levels? | Spontaneous point mutation rate in a gene increases with its transcription level, suggesting that movement of RNA polymerase through the target initiates a mutagenic process(es). This phenomenon is termed transcription-associated mutation (TAM). Transcription-associated mutagenesis is directly proportional to the level of gene expression. |
http://www.ncbi.nlm.nih.gov/pubmed/20590449,http://www.ncbi.nlm.nih.gov/pubmed/16809727,http://www.ncbi.nlm.nih.gov/pubmed/11838648,http://www.ncbi.nlm.nih.gov/pubmed/17785760,http://www.ncbi.nlm.nih.gov/pubmed/11265171,http://www.ncbi.nlm.nih.gov/pubmed/15970231,http://www.ncbi.nlm.nih.gov/pubmed/16235569,http://www.ncbi.nlm.nih.gov/pubmed/15217485,http://www.ncbi.nlm.nih.gov/pubmed/15510616,http://www.ncbi.nlm.nih.gov/pubmed/21632460,http://www.ncbi.nlm.nih.gov/pubmed/17159499,http://www.ncbi.nlm.nih.gov/pubmed/17947471,http://www.ncbi.nlm.nih.gov/pubmed/17184417,http://www.ncbi.nlm.nih.gov/pubmed/11579337,http://www.ncbi.nlm.nih.gov/pubmed/11097337,http://www.ncbi.nlm.nih.gov/pubmed/22112244,http://www.ncbi.nlm.nih.gov/pubmed/22461093,http://www.ncbi.nlm.nih.gov/pubmed/22065003 | Is there a pharmacogenetic test for trastuzumab? | Yes. HER2 testing is performed in breast cancer patients to determine suitability for trastuzumab (Herceptin therapy). |
http://www.ncbi.nlm.nih.gov/pubmed/21596106,http://www.ncbi.nlm.nih.gov/pubmed/15078185,http://www.ncbi.nlm.nih.gov/pubmed/15638774,http://www.ncbi.nlm.nih.gov/pubmed/17291698,http://www.ncbi.nlm.nih.gov/pubmed/24933286,http://www.ncbi.nlm.nih.gov/pubmed/11641441,http://www.ncbi.nlm.nih.gov/pubmed/10882031,http://www.ncbi.nlm.nih.gov/pubmed/19005061,http://www.ncbi.nlm.nih.gov/pubmed/26089446,http://www.ncbi.nlm.nih.gov/pubmed/22924591,http://www.ncbi.nlm.nih.gov/pubmed/21112351,http://www.ncbi.nlm.nih.gov/pubmed/16171802,http://www.ncbi.nlm.nih.gov/pubmed/21148095 | Which calcium channels does ethosuximide target? | Ethosuximide blocks the T-type calcium channels. |
http://www.ncbi.nlm.nih.gov/pubmed/11402041,http://www.ncbi.nlm.nih.gov/pubmed/15966747,http://www.ncbi.nlm.nih.gov/pubmed/11943462,http://www.ncbi.nlm.nih.gov/pubmed/14757048,http://www.ncbi.nlm.nih.gov/pubmed/6284743,http://www.ncbi.nlm.nih.gov/pubmed/19567276 | What is the sedimentation coefficient of the mammalian mitoribosome? | The mammalian mitochondrial ribosome (mitoribosome) has a highly protein-rich composition with a small sedimentation coefficient of 55 S, consisting of 39 S large and 28 S small subunits. |
http://www.ncbi.nlm.nih.gov/pubmed/19183745,http://www.ncbi.nlm.nih.gov/pubmed/19895758,http://www.ncbi.nlm.nih.gov/pubmed/23355128,http://www.ncbi.nlm.nih.gov/pubmed/20812878,http://www.ncbi.nlm.nih.gov/pubmed/23087256,http://www.ncbi.nlm.nih.gov/pubmed/20467589,http://www.ncbi.nlm.nih.gov/pubmed/25534713,http://www.ncbi.nlm.nih.gov/pubmed/21687346,http://www.ncbi.nlm.nih.gov/pubmed/23438929,http://www.ncbi.nlm.nih.gov/pubmed/23723254,http://www.ncbi.nlm.nih.gov/pubmed/18374681,http://www.ncbi.nlm.nih.gov/pubmed/20380486,http://www.ncbi.nlm.nih.gov/pubmed/21285669,http://www.ncbi.nlm.nih.gov/pubmed/23418282,http://www.ncbi.nlm.nih.gov/pubmed/22522051,http://www.ncbi.nlm.nih.gov/pubmed/19337534,http://www.ncbi.nlm.nih.gov/pubmed/24003484,http://www.ncbi.nlm.nih.gov/pubmed/20019471,http://www.ncbi.nlm.nih.gov/pubmed/20019472,http://www.ncbi.nlm.nih.gov/pubmed/19066408,http://www.ncbi.nlm.nih.gov/pubmed/23764715,http://www.ncbi.nlm.nih.gov/pubmed/20203685,http://www.ncbi.nlm.nih.gov/pubmed/20675959,http://www.ncbi.nlm.nih.gov/pubmed/18443751,http://www.ncbi.nlm.nih.gov/pubmed/21779913,http://www.ncbi.nlm.nih.gov/pubmed/23174623,http://www.ncbi.nlm.nih.gov/pubmed/22387646,http://www.ncbi.nlm.nih.gov/pubmed/19279548,http://www.ncbi.nlm.nih.gov/pubmed/21628356,http://www.ncbi.nlm.nih.gov/pubmed/20957132 | Describe the mechanism of action of aliskiren. | Aliskiren is a low-molecular-weight, orally active, hydrophilic non-peptide molecule that blocks renin and consequential angiotensin I generation. Renin inhibition interrupts the renin-angiotensin-aldosterone system (RAAS). |
http://www.ncbi.nlm.nih.gov/pubmed/14596799,http://www.ncbi.nlm.nih.gov/pubmed/6253884,http://www.ncbi.nlm.nih.gov/pubmed/23818873,http://www.ncbi.nlm.nih.gov/pubmed/12220682,http://www.ncbi.nlm.nih.gov/pubmed/3282561,http://www.ncbi.nlm.nih.gov/pubmed/9016640,http://www.ncbi.nlm.nih.gov/pubmed/11278072,http://www.ncbi.nlm.nih.gov/pubmed/1925023,http://www.ncbi.nlm.nih.gov/pubmed/15556475,http://www.ncbi.nlm.nih.gov/pubmed/10645441,http://www.ncbi.nlm.nih.gov/pubmed/16911001,http://www.ncbi.nlm.nih.gov/pubmed/1549572,http://www.ncbi.nlm.nih.gov/pubmed/656568,http://www.ncbi.nlm.nih.gov/pubmed/14711120,http://www.ncbi.nlm.nih.gov/pubmed/8339930,http://www.ncbi.nlm.nih.gov/pubmed/667214,http://www.ncbi.nlm.nih.gov/pubmed/6294066,http://www.ncbi.nlm.nih.gov/pubmed/15102446,http://www.ncbi.nlm.nih.gov/pubmed/18515342,http://www.ncbi.nlm.nih.gov/pubmed/7748943,http://www.ncbi.nlm.nih.gov/pubmed/11075932,http://www.ncbi.nlm.nih.gov/pubmed/12056890,http://www.ncbi.nlm.nih.gov/pubmed/21463569 | Which proteins act as histone-like molecules in prokaryotes? | Prokaryotic histone-like proteins (Hlps) or nucleoid-associated proteins (NAPs) are abundant proteins found in bacterial and plastid nucleoids. HU protein is a small, basic, heat-stable DNA-binding protein that is well-conserved in prokaryotes and is associated with the bacterial nucleoid. HU is well conserved in all prokaryotes but surprisingly, it is also homologous to another E. coli DNA-binding protein, IHF. In prokaryotes, IHF and HU are key architectural proteins present at high concentrations. Histone-like Nucleoid Structuring (H-NS) protein can facilitate correct recognition of a promoter by RNA polymerase in AT-rich gene regulatory regionsTHe histone-like proteins HU, IHF, H-NS (Nucleoid Structuring) act as histones in prokaryotes |
http://www.ncbi.nlm.nih.gov/pubmed/21350792,http://www.ncbi.nlm.nih.gov/pubmed/23196486,http://www.ncbi.nlm.nih.gov/pubmed/20416945,http://www.ncbi.nlm.nih.gov/pubmed/23480465,http://www.ncbi.nlm.nih.gov/pubmed/23975906,http://www.ncbi.nlm.nih.gov/pubmed/19157980,http://www.ncbi.nlm.nih.gov/pubmed/21070230,http://www.ncbi.nlm.nih.gov/pubmed/21480950,http://www.ncbi.nlm.nih.gov/pubmed/19036425,http://www.ncbi.nlm.nih.gov/pubmed/21110235,http://www.ncbi.nlm.nih.gov/pubmed/18808506,http://www.ncbi.nlm.nih.gov/pubmed/20099900,http://www.ncbi.nlm.nih.gov/pubmed/19795182,http://www.ncbi.nlm.nih.gov/pubmed/19770473,http://www.ncbi.nlm.nih.gov/pubmed/20954694,http://www.ncbi.nlm.nih.gov/pubmed/21054362,http://www.ncbi.nlm.nih.gov/pubmed/17914062,http://www.ncbi.nlm.nih.gov/pubmed/22816019,http://www.ncbi.nlm.nih.gov/pubmed/19551474,http://www.ncbi.nlm.nih.gov/pubmed/21383046,http://www.ncbi.nlm.nih.gov/pubmed/22512641,http://www.ncbi.nlm.nih.gov/pubmed/20826335,http://www.ncbi.nlm.nih.gov/pubmed/19939188,http://www.ncbi.nlm.nih.gov/pubmed/20120204,http://www.ncbi.nlm.nih.gov/pubmed/19796656,http://www.ncbi.nlm.nih.gov/pubmed/18590336,http://www.ncbi.nlm.nih.gov/pubmed/21457238,http://www.ncbi.nlm.nih.gov/pubmed/17929795,http://www.ncbi.nlm.nih.gov/pubmed/19737844,http://www.ncbi.nlm.nih.gov/pubmed/19914210,http://www.ncbi.nlm.nih.gov/pubmed/19469188,http://www.ncbi.nlm.nih.gov/pubmed/19779958,http://www.ncbi.nlm.nih.gov/pubmed/20573757,http://www.ncbi.nlm.nih.gov/pubmed/19219746,http://www.ncbi.nlm.nih.gov/pubmed/19084002,http://www.ncbi.nlm.nih.gov/pubmed/18039958,http://www.ncbi.nlm.nih.gov/pubmed/18799366,http://www.ncbi.nlm.nih.gov/pubmed/20188075,http://www.ncbi.nlm.nih.gov/pubmed/20078608,http://www.ncbi.nlm.nih.gov/pubmed/21221171,http://www.ncbi.nlm.nih.gov/pubmed/25107879,http://www.ncbi.nlm.nih.gov/pubmed/21070229,http://www.ncbi.nlm.nih.gov/pubmed/22090312,http://www.ncbi.nlm.nih.gov/pubmed/20855369,http://www.ncbi.nlm.nih.gov/pubmed/20173082,http://www.ncbi.nlm.nih.gov/pubmed/19579177,http://www.ncbi.nlm.nih.gov/pubmed/22278333,http://www.ncbi.nlm.nih.gov/pubmed/20974601,http://www.ncbi.nlm.nih.gov/pubmed/21631478,http://www.ncbi.nlm.nih.gov/pubmed/18217201,http://www.ncbi.nlm.nih.gov/pubmed/23798725,http://www.ncbi.nlm.nih.gov/pubmed/20164785,http://www.ncbi.nlm.nih.gov/pubmed/20433208,http://www.ncbi.nlm.nih.gov/pubmed/19346171,http://www.ncbi.nlm.nih.gov/pubmed/18991732,http://www.ncbi.nlm.nih.gov/pubmed/20937606,http://www.ncbi.nlm.nih.gov/pubmed/22221076 | Which receptor is targeted by telcagepant? | Telcagepant (MK-0974) is a novel calcitonin gene-related peptide (CGRP) receptor antagonist currently undergoing clinical trials for migraine. |
http://www.ncbi.nlm.nih.gov/pubmed/1388826,http://www.ncbi.nlm.nih.gov/pubmed/24486853,http://www.ncbi.nlm.nih.gov/pubmed/23465372,http://www.ncbi.nlm.nih.gov/pubmed/1984490,http://www.ncbi.nlm.nih.gov/pubmed/8672259,http://www.ncbi.nlm.nih.gov/pubmed/10327048,http://www.ncbi.nlm.nih.gov/pubmed/2176016,http://www.ncbi.nlm.nih.gov/pubmed/21073472,http://www.ncbi.nlm.nih.gov/pubmed/16788926,http://www.ncbi.nlm.nih.gov/pubmed/8384325,http://www.ncbi.nlm.nih.gov/pubmed/2855780 | What is the role of photodynamic therapy for meningioma treatment? | Photodynamic therapy was shown to have activity againt meningioma treatment. Gefitinib and ciprofloxacin enhance efficacy of photodynamic therapy. |
http://www.ncbi.nlm.nih.gov/pubmed/18366283,http://www.ncbi.nlm.nih.gov/pubmed/23118709,http://www.ncbi.nlm.nih.gov/pubmed/18240917,http://www.ncbi.nlm.nih.gov/pubmed/15937647,http://www.ncbi.nlm.nih.gov/pubmed/21983866,http://www.ncbi.nlm.nih.gov/pubmed/16482400,http://www.ncbi.nlm.nih.gov/pubmed/25054300,http://www.ncbi.nlm.nih.gov/pubmed/17938702,http://www.ncbi.nlm.nih.gov/pubmed/21390826,http://www.ncbi.nlm.nih.gov/pubmed/21344976,http://www.ncbi.nlm.nih.gov/pubmed/23662801,http://www.ncbi.nlm.nih.gov/pubmed/18035958,http://www.ncbi.nlm.nih.gov/pubmed/12074689,http://www.ncbi.nlm.nih.gov/pubmed/22715955,http://www.ncbi.nlm.nih.gov/pubmed/25085219,http://www.ncbi.nlm.nih.gov/pubmed/22718138,http://www.ncbi.nlm.nih.gov/pubmed/21479583,http://www.ncbi.nlm.nih.gov/pubmed/10414561,http://www.ncbi.nlm.nih.gov/pubmed/17350791,http://www.ncbi.nlm.nih.gov/pubmed/18636295,http://www.ncbi.nlm.nih.gov/pubmed/21300471,http://www.ncbi.nlm.nih.gov/pubmed/19123896,http://www.ncbi.nlm.nih.gov/pubmed/15069758,http://www.ncbi.nlm.nih.gov/pubmed/20155992,http://www.ncbi.nlm.nih.gov/pubmed/23535992,http://www.ncbi.nlm.nih.gov/pubmed/17334672,http://www.ncbi.nlm.nih.gov/pubmed/19046047,http://www.ncbi.nlm.nih.gov/pubmed/23350777,http://www.ncbi.nlm.nih.gov/pubmed/21330749,http://www.ncbi.nlm.nih.gov/pubmed/12672279,http://www.ncbi.nlm.nih.gov/pubmed/25269031,http://www.ncbi.nlm.nih.gov/pubmed/21756557,http://www.ncbi.nlm.nih.gov/pubmed/20706757,http://www.ncbi.nlm.nih.gov/pubmed/20511192,http://www.ncbi.nlm.nih.gov/pubmed/24246204,http://www.ncbi.nlm.nih.gov/pubmed/19514083,http://www.ncbi.nlm.nih.gov/pubmed/15015668 | Do carmustine wafers improve survival of glioblastoma patients? | Yes, it has been documented that implantation of carmustine wafers improves survival of newly diagnosed and recurrent glioblastoma patients. |
http://www.ncbi.nlm.nih.gov/pubmed/23511973,http://www.ncbi.nlm.nih.gov/pubmed/23272173,http://www.ncbi.nlm.nih.gov/pubmed/24303839,http://www.ncbi.nlm.nih.gov/pubmed/23424633,http://www.ncbi.nlm.nih.gov/pubmed/23550157,http://www.ncbi.nlm.nih.gov/pubmed/23226452 | Is Dicer part of the RISC loading complex? | Yes, Dicer is part of the RISC loading complex. |
http://www.ncbi.nlm.nih.gov/pubmed/18546951,http://www.ncbi.nlm.nih.gov/pubmed/19287845,http://www.ncbi.nlm.nih.gov/pubmed/15785984,http://www.ncbi.nlm.nih.gov/pubmed/17874345 | What is the Arnold-Chiari syndrome? | Arnold Chiari syndrome is a condition characterized by herniation of the cerebellar tonsils through the foramen magnum, manifesting usually with downbeat nystagmus, palsy of the caudal cerebral nerves, headache, and vertigo. |
http://www.ncbi.nlm.nih.gov/pubmed/23710633,http://www.ncbi.nlm.nih.gov/pubmed/22679139,http://www.ncbi.nlm.nih.gov/pubmed/24225946,http://www.ncbi.nlm.nih.gov/pubmed/21900893 | What is the biological role of SERCA2 SUMOylation in cardiac physiology and pathophysiology, such as in heart failure? | Recently, the impact of small ubiquitin-related modifier 1 (SUMO-1) on the regulation and preservation of sarcoplasmic reticulum calcium adenosine triphosphatase (SERCA2a) function was discovered. The small ubiquitin-related modifier (SUMO) can be conjugated to lysine residues of target proteins, and is involved in many cellular processes. SERCA2a is SUMOylated at lysines 480 and 585 and this SUMOylation is essential for preserving SERCA2a ATPase activity and stability in mouse and human cells. The levels of SUMO1 and the SUMOylation of SERCA2a itself were greatly reduced in failing hearts. SUMO-1 gene transfer improved cardiac function supporting the critical role of SUMO-1 in SERCA2a function and underlining the therapeutic potential of SUMO-1 for HF patients. |
http://www.ncbi.nlm.nih.gov/pubmed/7998766,http://www.ncbi.nlm.nih.gov/pubmed/17417937 | Which trinucleotide repeat disorders are affecting the nervous system? | At least six neudegenerative disorders result from trinucleotide repeat expansion: X-linked spinal and bulbar muscular atrophy (SBMA), two fragile X syndromes of mental retardation (FRAXA and FRAXE), Huntington's disease (HD), spinocerebellar ataxia type 1 (SCA1), and dentatorubral-pallidoluysian atrophy (DRPLA). |
http://www.ncbi.nlm.nih.gov/pubmed/16904272,http://www.ncbi.nlm.nih.gov/pubmed/8058745,http://www.ncbi.nlm.nih.gov/pubmed/19275569,http://www.ncbi.nlm.nih.gov/pubmed/15277238,http://www.ncbi.nlm.nih.gov/pubmed/18047734,http://www.ncbi.nlm.nih.gov/pubmed/22690333,http://www.ncbi.nlm.nih.gov/pubmed/10526221,http://www.ncbi.nlm.nih.gov/pubmed/19101576,http://www.ncbi.nlm.nih.gov/pubmed/21240275,http://www.ncbi.nlm.nih.gov/pubmed/22053284,http://www.ncbi.nlm.nih.gov/pubmed/21478198,http://www.ncbi.nlm.nih.gov/pubmed/22532920,http://www.ncbi.nlm.nih.gov/pubmed/21568838,http://www.ncbi.nlm.nih.gov/pubmed/20034732,http://www.ncbi.nlm.nih.gov/pubmed/21109493,http://www.ncbi.nlm.nih.gov/pubmed/25002988,http://www.ncbi.nlm.nih.gov/pubmed/17396147,http://www.ncbi.nlm.nih.gov/pubmed/19748364,http://www.ncbi.nlm.nih.gov/pubmed/16493006,http://www.ncbi.nlm.nih.gov/pubmed/23444773,http://www.ncbi.nlm.nih.gov/pubmed/1809228,http://www.ncbi.nlm.nih.gov/pubmed/19738377,http://www.ncbi.nlm.nih.gov/pubmed/23318445,http://www.ncbi.nlm.nih.gov/pubmed/20120016,http://www.ncbi.nlm.nih.gov/pubmed/11751423,http://www.ncbi.nlm.nih.gov/pubmed/21939290 | Is hypersensitivity to DNA crosslinking agents a hallmark of Fanconi anemia? | Yes, hypersensitivity to DNA crosslinking agents is one of the hallmarks of Fanconi anemia, the others being defective FANCD2 monoubiquitination, and genomic instability. |
http://www.ncbi.nlm.nih.gov/pubmed/15887238,http://www.ncbi.nlm.nih.gov/pubmed/15844661 | Which are the cellular targets of imatinib mesylate? | The cellular targets of imatinib mesylate are BCR-ABL, platelet-derived growth factor receptor (PDGFR) and c-kit kinases. |
http://www.ncbi.nlm.nih.gov/pubmed/14716484,http://www.ncbi.nlm.nih.gov/pubmed/22791573,http://www.ncbi.nlm.nih.gov/pubmed/19889303,http://www.ncbi.nlm.nih.gov/pubmed/16210669,http://www.ncbi.nlm.nih.gov/pubmed/24304436,http://www.ncbi.nlm.nih.gov/pubmed/23219029,http://www.ncbi.nlm.nih.gov/pubmed/23007140,http://www.ncbi.nlm.nih.gov/pubmed/19133941,http://www.ncbi.nlm.nih.gov/pubmed/11520735,http://www.ncbi.nlm.nih.gov/pubmed/15221338,http://www.ncbi.nlm.nih.gov/pubmed/24180681,http://www.ncbi.nlm.nih.gov/pubmed/12618672,http://www.ncbi.nlm.nih.gov/pubmed/19239998 | Which are the clinical characteristics of Tuberous Sclerosis? | The clinical characteristics of Tuberous Sclerosis include epilepsy, subependymal giant cell astrocytomas, lymphangioleiomyomatosis, rhabdomyoma, renal angiomyolipomas, cortical tubers, neurofibromas, angiofibromas, mental retardation, and behavioral disorders. |
http://www.ncbi.nlm.nih.gov/pubmed/20625510,http://www.ncbi.nlm.nih.gov/pubmed/9204548 | What is known about MER41 repeat sequences? | We report eleven new families of MEdium Reiteration frequency (MER) interspersed repeats in the genomes of Primates, Rodentia, and Lagomorpha. Two families of the human repeats, MER 46 and MER 47, represent non-autonomous DNA transposons. These sequences are flanked by TA target site duplications and have terminal inverted repeats (TIRs) similar to TIRs of DNA transposons. The sequences of five other families of repeats, MER41, MER48, MER50, MER51, and RMER3, resemble long terminal repeats of retroviruses. A potential involvement of some of the reported MER repeats in the regulation of transcription and genetic rearrangements is suggested. Age estimations place the origin of most MER repeats at the time of decline in MIR (Mammalian-wide Interspersed Repeats) retroposition and before the origin of the Alu familyMER41 repeat sequences contain inducible STAT1 binding sitesThe sequences of five families of repeats, MER41, MER48, MER50, MER51, and RMER3, resemble long terminal repeats of retroviruses. Age estimations place the origin of most MER repeats at the time of decline in MIR (Mammalian-wide Interspersed Repeats) retroposition and before the origin of the Alu family. MER41 repeat sequences contain inducible STAT1 binding sites. The observation of the binding of activated STAT1 protein to a specific repetitive element bolsters similar reports concerning p53 and other TFs, and strengthens the notion of an involvement of repeats in gene regulation.We report eleven new families of MEdium Reiteration frequency (MER) interspersed repeats in the genomes of Primates, Rodentia, and Lagomorpha. Two families of the human repeats, MER 46 and MER 47, represent non-autonomous DNA transposons. These sequences are flanked by TA target site duplications and have terminal inverted repeats (TIRs) similar to TIRs of DNA transposons. The sequences of five other families of repeats, MER41, MER48, MER50, MER51, and RMER3, resemble long terminal repeats of retroviruses. A potential involvement of some of the reported MER repeats in the regulation of transcription and genetic rearrangements is suggested. Age estimations place the origin of most MER repeats at the time of decline in MIR (Mammalian-wide Interspersed Repeats) retroposition and before the origin of the Alu family MER41 repeat sequences contain inducible STAT1 binding sites |
http://www.ncbi.nlm.nih.gov/pubmed/23034909,http://www.ncbi.nlm.nih.gov/pubmed/22418054,http://www.ncbi.nlm.nih.gov/pubmed/22905075,http://www.ncbi.nlm.nih.gov/pubmed/22623966,http://www.ncbi.nlm.nih.gov/pubmed/21693087,http://www.ncbi.nlm.nih.gov/pubmed/21191476,http://www.ncbi.nlm.nih.gov/pubmed/22218274,http://www.ncbi.nlm.nih.gov/pubmed/19289479,http://www.ncbi.nlm.nih.gov/pubmed/22039473,http://www.ncbi.nlm.nih.gov/pubmed/22563263 | How functional connectivity of the default mode network changes in patients with disorders of consciousness? | Functional connectivity in the default mode network (DMN) is reduced in patients with different disorders of consciousness, and correlates with the level of consciousness.
Specifically, functional connectivity in the default mode network was shown to be absent in brain death patients, extremely low in vegetative state patients and slightly decreased in minimally conscious state patients when compared to healthy subjects. Therefore, functional connectivity in the default mode network was suggested to be valuable in differentiating patients with different disorders of consciousness. Clinically, functional connectivity in the default mode network was also shown to be an indicator of the extent of cortical disruption and predict reversible impairments in consciousness. |
http://www.ncbi.nlm.nih.gov/pubmed/24198383,http://www.ncbi.nlm.nih.gov/pubmed/23188110,http://www.ncbi.nlm.nih.gov/pubmed/25519961,http://www.ncbi.nlm.nih.gov/pubmed/24284555,http://www.ncbi.nlm.nih.gov/pubmed/24424123 | Have C12orf65 mutations been associated with axonal neuropathy and optic atrophy? | Novel C12orf65 mutations in patients with axonal neuropathy and optic atrophyThe association of neuropathy and optic atrophy (also known as Charcot-Marie-Tooth [CMT] disease type 6) has been described with autosomal dominant, recessive and X-linked modes of inheritance. Mutations in Mitofusin 2 have been found to cause dominant forms of CMT6. Phosphoribosylpyrophosphate synthetase-I mutations cause X-linked CMT6, whereas a protein-truncating mutation in the C12orf65 gene, which codes for a protein involved in mitochondrial translation, was found to be the cause of an autosomal recessive form of the disease, with childhood onset neuropathy and optic atrophy. |
http://www.ncbi.nlm.nih.gov/pubmed/22136378,http://www.ncbi.nlm.nih.gov/pubmed/20709662,http://www.ncbi.nlm.nih.gov/pubmed/21947824,http://www.ncbi.nlm.nih.gov/pubmed/19406729,http://www.ncbi.nlm.nih.gov/pubmed/12478903,http://www.ncbi.nlm.nih.gov/pubmed/23692856,http://www.ncbi.nlm.nih.gov/pubmed/20660832,http://www.ncbi.nlm.nih.gov/pubmed/23233612,http://www.ncbi.nlm.nih.gov/pubmed/16702182,http://www.ncbi.nlm.nih.gov/pubmed/21656329,http://www.ncbi.nlm.nih.gov/pubmed/17971487 | List drugs included in the DHAP-R chemotherapy regiment. | Dexamethasone (a steroid hormone), cytarabine (ara-C), cisplatin (platinum agent) and rituximab are included in the DHAP-R chemotherapy protocol. |
http://www.ncbi.nlm.nih.gov/pubmed/2168257,http://www.ncbi.nlm.nih.gov/pubmed/8162148,http://www.ncbi.nlm.nih.gov/pubmed/3020860,http://www.ncbi.nlm.nih.gov/pubmed/8336812,http://www.ncbi.nlm.nih.gov/pubmed/3776472,http://www.ncbi.nlm.nih.gov/pubmed/8712177,http://www.ncbi.nlm.nih.gov/pubmed/8629394,http://www.ncbi.nlm.nih.gov/pubmed/19373908,http://www.ncbi.nlm.nih.gov/pubmed/1492779,http://www.ncbi.nlm.nih.gov/pubmed/3736772,http://www.ncbi.nlm.nih.gov/pubmed/6699695,http://www.ncbi.nlm.nih.gov/pubmed/7015802,http://www.ncbi.nlm.nih.gov/pubmed/10396741,http://www.ncbi.nlm.nih.gov/pubmed/1630573,http://www.ncbi.nlm.nih.gov/pubmed/7487408,http://www.ncbi.nlm.nih.gov/pubmed/8727067 | Are psammoma bodies characteristic to meningiomas? | Yes, psammoma bodies are commonly seen and are characteristic to meningiomas. However, they can be also present in other types of tumors or non-neoplastic tissues. |
http://www.ncbi.nlm.nih.gov/pubmed/8505927,http://www.ncbi.nlm.nih.gov/pubmed/16526254,http://www.ncbi.nlm.nih.gov/pubmed/24481713,http://www.ncbi.nlm.nih.gov/pubmed/24114606,http://www.ncbi.nlm.nih.gov/pubmed/21822385,http://www.ncbi.nlm.nih.gov/pubmed/18653248 | Which are the most common symptoms in Lambert-Eaton Myasthenic Syndrome? | Lambert-Eaton myasthenic syndrome is a neuromuscular junction disorder characterized by proximal limb muscle weakness, fatigability, decreased deep-tendon reflexes, and autonomic symptoms. There are 2 forms of Lambert-Eaton myasthenic syndrome: one most frequently associated with small-cell lung cancer (P-Lambert-Eaton myasthenic syndrome) and the other that is a pure autoimmune form (NP-Lambert-Eaton myasthenic syndrome)Lambert-Eaton myasthenic syndrome is a neuromuscular junction disorder characterized by proximal limb muscle weakness, fatigability, decreased deep-tendon reflexes, and autonomic symptoms, that may include dry mouth, constipation, blurred vision, impaired sweating, and orthostatic hypotension. There are 2 forms of Lambert-Eaton myasthenic syndrome: one most frequently associated with small-cell lung cancer, and the other that is a pure autoimmune form. |
http://www.ncbi.nlm.nih.gov/pubmed/21057511,http://www.ncbi.nlm.nih.gov/pubmed/25043180,http://www.ncbi.nlm.nih.gov/pubmed/21178113,http://www.ncbi.nlm.nih.gov/pubmed/24667705,http://www.ncbi.nlm.nih.gov/pubmed/25341033,http://www.ncbi.nlm.nih.gov/pubmed/24376002,http://www.ncbi.nlm.nih.gov/pubmed/23816851,http://www.ncbi.nlm.nih.gov/pubmed/26056317,http://www.ncbi.nlm.nih.gov/pubmed/25418070,http://www.ncbi.nlm.nih.gov/pubmed/23637985 | What is the pyroptotic pathway? | Pyroptosis is an inflammasome-mediated programmed cell death pathway. |
http://www.ncbi.nlm.nih.gov/pubmed/20976394,http://www.ncbi.nlm.nih.gov/pubmed/9526919,http://www.ncbi.nlm.nih.gov/pubmed/14598129,http://www.ncbi.nlm.nih.gov/pubmed/23937262 | Which types of bacterial microflora are associated with the progression of peri-implantitis? | Bacteria such as A. actinomycetemcomitans, P. gingivalis, T. forsythensis, T. denticola, P. intermedia and F. nucleatum are associated with the progression of peri-implantitis. |
http://www.ncbi.nlm.nih.gov/pubmed/19605561,http://www.ncbi.nlm.nih.gov/pubmed/11239395,http://www.ncbi.nlm.nih.gov/pubmed/22442711,http://www.ncbi.nlm.nih.gov/pubmed/12590136,http://www.ncbi.nlm.nih.gov/pubmed/22817748,http://www.ncbi.nlm.nih.gov/pubmed/23337855,http://www.ncbi.nlm.nih.gov/pubmed/15769875,http://www.ncbi.nlm.nih.gov/pubmed/21743004,http://www.ncbi.nlm.nih.gov/pubmed/20628353,http://www.ncbi.nlm.nih.gov/pubmed/12844354,http://www.ncbi.nlm.nih.gov/pubmed/11747467,http://www.ncbi.nlm.nih.gov/pubmed/21245038,http://www.ncbi.nlm.nih.gov/pubmed/23388391,http://www.ncbi.nlm.nih.gov/pubmed/19955262,http://www.ncbi.nlm.nih.gov/pubmed/17766253,http://www.ncbi.nlm.nih.gov/pubmed/11889047,http://www.ncbi.nlm.nih.gov/pubmed/14618157,http://www.ncbi.nlm.nih.gov/pubmed/23274303,http://www.ncbi.nlm.nih.gov/pubmed/15044470,http://www.ncbi.nlm.nih.gov/pubmed/19276069,http://www.ncbi.nlm.nih.gov/pubmed/22073225,http://www.ncbi.nlm.nih.gov/pubmed/21965533 | What are the known families of deadenylases? | All known deadenylases belong to either the DEDD or the exonuclease–endonuclease–phosphatase (EEP) superfamily. Members of DEDD include the POP2, CAF1Z, PARN and PAN2 families. Members of EEP include the CCR4, Nocturnin, ANGEL and 2'-PDE families. |
http://www.ncbi.nlm.nih.gov/pubmed/7591257,http://www.ncbi.nlm.nih.gov/pubmed/17009618,http://www.ncbi.nlm.nih.gov/pubmed/2162733,http://www.ncbi.nlm.nih.gov/pubmed/1333942,http://www.ncbi.nlm.nih.gov/pubmed/3004699,http://www.ncbi.nlm.nih.gov/pubmed/7571088,http://www.ncbi.nlm.nih.gov/pubmed/9213191,http://www.ncbi.nlm.nih.gov/pubmed/23674776 | Which translocation is harbored in the Askin tumor cells? | The Askin tumor is a primitive malignant small-cell tumor of the chest wall mostly seen among children and adolescents. It is closely related to Ewing's sarcoma of the same location, with both tumors harboring reciprocal translocation t(11;22) (q24;q12). |
http://www.ncbi.nlm.nih.gov/pubmed/14702298,http://www.ncbi.nlm.nih.gov/pubmed/21911592,http://www.ncbi.nlm.nih.gov/pubmed/19651859,http://www.ncbi.nlm.nih.gov/pubmed/9199422,http://www.ncbi.nlm.nih.gov/pubmed/9106214,http://www.ncbi.nlm.nih.gov/pubmed/18676674,http://www.ncbi.nlm.nih.gov/pubmed/22636778,http://www.ncbi.nlm.nih.gov/pubmed/9234759,http://www.ncbi.nlm.nih.gov/pubmed/17302796,http://www.ncbi.nlm.nih.gov/pubmed/20863885,http://www.ncbi.nlm.nih.gov/pubmed/10361306,http://www.ncbi.nlm.nih.gov/pubmed/9119194,http://www.ncbi.nlm.nih.gov/pubmed/8577251,http://www.ncbi.nlm.nih.gov/pubmed/21923765,http://www.ncbi.nlm.nih.gov/pubmed/24661624,http://www.ncbi.nlm.nih.gov/pubmed/17302798 | What is the function of the AtxA pleiotropic regulator? | AtxA is the gene encoding the trans-activator of anthrax toxin synthesis and is essential for virulence of B. anthracis. It is located on the resident 185-kb plasmid pXO1 and its activation is stimulated by bicarbonate. AtxA controls the expression of more than a hundred genes belonging to all genetic elements, the chromosome and both virulence plasmids, including those encoding the major virulence factors. AtxA can activate or repress gene expression. In atxA+ strains, toxin gene expression is increased 5- to 20-fold in cells grown in 5% CO2 relative to cells grown in air. Dual promoters control expression of AtxA. Transcription of the atxA gene occurs from two independent promoters, P1 and P2, whose transcription start sites are separated by 650 bp.Comparison of the resulting protein patterns indicated that synthesis of non-toxin proteins is influenced by growth in elevated CO2 and the toxin gene regulator, atxA. The AtxA virulence regulator of Bacillus anthracis is required for toxin and capsule gene expression. DNA sequence analysis of transposon insertion sites in 17 mutants carrying CO2- and atxA-regulated fusions revealed 10 mutants carrying independent insertions on the 185-kb toxin plasmid pXO1 which did not map to the toxin genes. We purified histidine-tagged AtxA [AtxA(His)] from Escherichia coli and used anti-AtxA(His) serum to detect AtxA in protein preparations from B. anthracis cells.The atxA gene product activates transcription of the anthrax toxin genes and is essential for virulence. |
http://www.ncbi.nlm.nih.gov/pubmed/23698027,http://www.ncbi.nlm.nih.gov/pubmed/23910705,http://www.ncbi.nlm.nih.gov/pubmed/24114579,http://www.ncbi.nlm.nih.gov/pubmed/24001705,http://www.ncbi.nlm.nih.gov/pubmed/23577724,http://www.ncbi.nlm.nih.gov/pubmed/23813702,http://www.ncbi.nlm.nih.gov/pubmed/23571811,http://www.ncbi.nlm.nih.gov/pubmed/24178972,http://www.ncbi.nlm.nih.gov/pubmed/24262510,http://www.ncbi.nlm.nih.gov/pubmed/23797027,http://www.ncbi.nlm.nih.gov/pubmed/23574755,http://www.ncbi.nlm.nih.gov/pubmed/23701892,http://www.ncbi.nlm.nih.gov/pubmed/24300829,http://www.ncbi.nlm.nih.gov/pubmed/23669156,http://www.ncbi.nlm.nih.gov/pubmed/23866593,http://www.ncbi.nlm.nih.gov/pubmed/23744636,http://www.ncbi.nlm.nih.gov/pubmed/24321840 | Is cystatin C or cystatin 3 used as a biomarker of kidney function? | Yes, cystatin C (CysC) is a novel biomarker of renal function. |
http://www.ncbi.nlm.nih.gov/pubmed/19297348 | Which R/bioconductor package utilizes the Hilbert curve in order to visualize genomic data? | The so-called Hilbert curve visualization can complement genome browsers and help to get further insights into the structure of one's data. An open-source application, called HilbertVis, has been developed for R/bioconductor that allows the user to produce and interactively explore such plots. |
http://www.ncbi.nlm.nih.gov/pubmed/23765643,http://www.ncbi.nlm.nih.gov/pubmed/25044397,http://www.ncbi.nlm.nih.gov/pubmed/23712453,http://www.ncbi.nlm.nih.gov/pubmed/24603453,http://www.ncbi.nlm.nih.gov/pubmed/25543032,http://www.ncbi.nlm.nih.gov/pubmed/23553438,http://www.ncbi.nlm.nih.gov/pubmed/21076134,http://www.ncbi.nlm.nih.gov/pubmed/25138112,http://www.ncbi.nlm.nih.gov/pubmed/24482806,http://www.ncbi.nlm.nih.gov/pubmed/21749753,http://www.ncbi.nlm.nih.gov/pubmed/23299662,http://www.ncbi.nlm.nih.gov/pubmed/22863603,http://www.ncbi.nlm.nih.gov/pubmed/24783433,http://www.ncbi.nlm.nih.gov/pubmed/26252102,http://www.ncbi.nlm.nih.gov/pubmed/17186566,http://www.ncbi.nlm.nih.gov/pubmed/10655451,http://www.ncbi.nlm.nih.gov/pubmed/24352524,http://www.ncbi.nlm.nih.gov/pubmed/25449088,http://www.ncbi.nlm.nih.gov/pubmed/21574485,http://www.ncbi.nlm.nih.gov/pubmed/24990604,http://www.ncbi.nlm.nih.gov/pubmed/24312358,http://www.ncbi.nlm.nih.gov/pubmed/23526649,http://www.ncbi.nlm.nih.gov/pubmed/26080919,http://www.ncbi.nlm.nih.gov/pubmed/25478006,http://www.ncbi.nlm.nih.gov/pubmed/24667696,http://www.ncbi.nlm.nih.gov/pubmed/22500971,http://www.ncbi.nlm.nih.gov/pubmed/21749752,http://www.ncbi.nlm.nih.gov/pubmed/23089167,http://www.ncbi.nlm.nih.gov/pubmed/26237478,http://www.ncbi.nlm.nih.gov/pubmed/23470070,http://www.ncbi.nlm.nih.gov/pubmed/25238658 | Can fetal aneuploidy be detected with non-invasive prenatal testing? | Yes, the non-invasive preanatal test of cell-free fetal DNA is being used for fetal aneuploidy screening. |
http://www.ncbi.nlm.nih.gov/pubmed/23950696 | Which packages are used for performing overlap analysis of genomic regions in R/bioconductor? | IRanges, GenomicRanges, and GenomicFeatures provide scalable data structures for representing annotated ranges on the genome, with special support for transcript structures, read alignments and coverage vectors. Computational facilities include efficient algorithms for overlap and nearest neighbor detection, coverage calculation and other range operations. This infrastructure directly supports more than 80 other Bioconductor packages, including those for sequence analysis, differential expression analysis and visualization.At the core of the infrastructure are three packages: IRanges, GenomicRanges, and GenomicFeatures. These packages provide scalable data structures for representing annotated ranges on the genome, with special support for transcript structures, read alignments and coverage vectors. Computational facilities include efficient algorithms for overlap and nearest neighbor detection, coverage calculation and other range operations. This infrastructure directly supports more than 80 other Bioconductor packages, including those for sequence analysis, differential expression analysis and visualization. |
http://www.ncbi.nlm.nih.gov/pubmed/3374500,http://www.ncbi.nlm.nih.gov/pubmed/18345024,http://www.ncbi.nlm.nih.gov/pubmed/6855804,http://www.ncbi.nlm.nih.gov/pubmed/18426576,http://www.ncbi.nlm.nih.gov/pubmed/10632100,http://www.ncbi.nlm.nih.gov/pubmed/19019313,http://www.ncbi.nlm.nih.gov/pubmed/18254068 | Is dichlorphenamide effective for periodic paralysis? | Yes, dichlorphenamide is effective for periodic paralysis. Dichlorphenamide--a carbonic anhydrase inhibitor--has been shown in a controlled trial to prevent attacks for many patients with both hypokalemic and hypokalemic periodic paralysis. |
http://www.ncbi.nlm.nih.gov/pubmed/18754895,http://www.ncbi.nlm.nih.gov/pubmed/17644917,http://www.ncbi.nlm.nih.gov/pubmed/21778677,http://www.ncbi.nlm.nih.gov/pubmed/19714338,http://www.ncbi.nlm.nih.gov/pubmed/16238072,http://www.ncbi.nlm.nih.gov/pubmed/21193992,http://www.ncbi.nlm.nih.gov/pubmed/20593981,http://www.ncbi.nlm.nih.gov/pubmed/21961548,http://www.ncbi.nlm.nih.gov/pubmed/15835100,http://www.ncbi.nlm.nih.gov/pubmed/18459898,http://www.ncbi.nlm.nih.gov/pubmed/16426953,http://www.ncbi.nlm.nih.gov/pubmed/15835099 | What is evaluated with the Hydrocephalus Outcome Questionnaire? | The Hydrocephalus Outcome Questionnaire (HOQ) is a simple, reliable, and valid measure of health status in children with hydrocephalus. |
http://www.ncbi.nlm.nih.gov/pubmed/7139628,http://www.ncbi.nlm.nih.gov/pubmed/15191928,http://www.ncbi.nlm.nih.gov/pubmed/24260161,http://www.ncbi.nlm.nih.gov/pubmed/15801484,http://www.ncbi.nlm.nih.gov/pubmed/12125967,http://www.ncbi.nlm.nih.gov/pubmed/8470663,http://www.ncbi.nlm.nih.gov/pubmed/12115571,http://www.ncbi.nlm.nih.gov/pubmed/8850274,http://www.ncbi.nlm.nih.gov/pubmed/11452935,http://www.ncbi.nlm.nih.gov/pubmed/10620527 | What is known about maternal smoking and brain tumor risk? | Findings regarding association of maternal smoking and brain tumor risk are mixed. It was shown that children of women who smoked during pregnancy had an increased incidence of brain tumors (hazard ratio = 1.24; 95% confidence interval: 1.01-1.53). The increase in risk was similar for benign and malignant tumors, and was most apparent for astrocytoma. However, other authors did not find association between maternal smoking and brain tumor risk. |
http://www.ncbi.nlm.nih.gov/pubmed/21890891,http://www.ncbi.nlm.nih.gov/pubmed/18006063,http://www.ncbi.nlm.nih.gov/pubmed/25069872,http://www.ncbi.nlm.nih.gov/pubmed/19535802,http://www.ncbi.nlm.nih.gov/pubmed/23142462,http://www.ncbi.nlm.nih.gov/pubmed/24336142,http://www.ncbi.nlm.nih.gov/pubmed/19939495,http://www.ncbi.nlm.nih.gov/pubmed/18261799,http://www.ncbi.nlm.nih.gov/pubmed/25178935 | Which pathway is activated by ficolin-3? | Ficolin-3 activates lectin complement pathway. |
http://www.ncbi.nlm.nih.gov/pubmed/26028407,http://www.ncbi.nlm.nih.gov/pubmed/25965365,http://www.ncbi.nlm.nih.gov/pubmed/24685885,http://www.ncbi.nlm.nih.gov/pubmed/25704439,http://www.ncbi.nlm.nih.gov/pubmed/25897158,http://www.ncbi.nlm.nih.gov/pubmed/24402925,http://www.ncbi.nlm.nih.gov/pubmed/25496336 | Is nivolumab used for treatment of Non–Small-Cell Lung Cancer? | Yes, nivolumab used for treatment of Non–Small-Cell Lung Cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/22345495,http://www.ncbi.nlm.nih.gov/pubmed/20340162,http://www.ncbi.nlm.nih.gov/pubmed/23485197,http://www.ncbi.nlm.nih.gov/pubmed/20927383,http://www.ncbi.nlm.nih.gov/pubmed/22499768,http://www.ncbi.nlm.nih.gov/pubmed/21822884,http://www.ncbi.nlm.nih.gov/pubmed/22499769,http://www.ncbi.nlm.nih.gov/pubmed/22369663,http://www.ncbi.nlm.nih.gov/pubmed/22906719,http://www.ncbi.nlm.nih.gov/pubmed/17372656 | Global quantitative phosphoproteomic analyses are emerging. List the preferred technologies for the enrichment for phosphorylated peptides? | There are many different approaches to enrich for phosphorylated peptides: titanium dioxide, IMAC, simple derivatization through phosphoramidate chemistry and antibodies. |
http://www.ncbi.nlm.nih.gov/pubmed/21347206,http://www.ncbi.nlm.nih.gov/pubmed/19365074,http://www.ncbi.nlm.nih.gov/pubmed/20139424,http://www.ncbi.nlm.nih.gov/pubmed/23401853,http://www.ncbi.nlm.nih.gov/pubmed/22876190,http://www.ncbi.nlm.nih.gov/pubmed/24722509,http://www.ncbi.nlm.nih.gov/pubmed/24600005 | Which histone modifications are correlated with transcription elongation? | This is accompanied by reductions in the level of H3K36 trimethylation, a posttranslational histone modification associated with efficient transcriptional elongation, and the number of full-length transcripts from these genes. The 3' ZNF exons contain H3K36me3, a mark of transcriptional elongation. |
http://www.ncbi.nlm.nih.gov/pubmed/17293442 | Does thyroid hormone receptor beta1 affect insulin secretion? | No |
http://www.ncbi.nlm.nih.gov/pubmed/22472876,http://www.ncbi.nlm.nih.gov/pubmed/25461954,http://www.ncbi.nlm.nih.gov/pubmed/24373612 | List disorders that have been associated to the polymorphism rs2535629. | schizophrenia and major depressive disorder. |
http://www.ncbi.nlm.nih.gov/pubmed/25891173,http://www.ncbi.nlm.nih.gov/pubmed/25324906,http://www.ncbi.nlm.nih.gov/pubmed/24685885,http://www.ncbi.nlm.nih.gov/pubmed/25605845,http://www.ncbi.nlm.nih.gov/pubmed/25034862,http://www.ncbi.nlm.nih.gov/pubmed/25828465,http://www.ncbi.nlm.nih.gov/pubmed/25960664,http://www.ncbi.nlm.nih.gov/pubmed/26028255 | What is targeted by monoclonal antibody Pembrolizumab? | Pembrolizumab inhibits the programmed cell death 1 (PD-1) immune checkpoint and has antitumor activity in patients with advanced melanoma. Pembrolizumab is approved by the US Food and Drug Administration for the treatment of advanced melanoma, and additional regulatory approvals are expected across the oncologic spectrum for a variety of other agents that target these pathways. |
http://www.ncbi.nlm.nih.gov/pubmed/23327985,http://www.ncbi.nlm.nih.gov/pubmed/23422670,http://www.ncbi.nlm.nih.gov/pubmed/22023572,http://www.ncbi.nlm.nih.gov/pubmed/23271586,http://www.ncbi.nlm.nih.gov/pubmed/12941181,http://www.ncbi.nlm.nih.gov/pubmed/9560368,http://www.ncbi.nlm.nih.gov/pubmed/19287383,http://www.ncbi.nlm.nih.gov/pubmed/23821616,http://www.ncbi.nlm.nih.gov/pubmed/22114361,http://www.ncbi.nlm.nih.gov/pubmed/22046001,http://www.ncbi.nlm.nih.gov/pubmed/24598232,http://www.ncbi.nlm.nih.gov/pubmed/21666225 | Does replication timing affect the rate of somatic mutations? | Mutation rate, as reflected in recent evolutionary divergence and human nucleotide diversity, is markedly increased in later-replicating regions of the human genome. All classes of substitutions are affected, suggesting a generalized mechanism involving replication time-dependent DNA damage. DNA repair systems, in general, are less efficient in late replicating heterochromatic regions compared to early replicating euchromatic regions of the genome. In yeast the mutation rate increases with the replication timing by more than 30% between the earliest and the latest replicating regions. Limited evidence from one chromosome arm in Drosophila melanogaster suggests the opposite pattern, with regions overlapping early-firing origins showing increased levels of diversity and divergence. In humans DNA replication patterns help shape the mutational landscapes of normal and cancer genomes.Recent studies revealed a long suspected replication-timing effect on mutation rate, but the mechanisms that regulate the increase in mutation rate as the genome is replicated remain unclear. The mutations were distributed randomly throughout the genome, independent of replication timing. Here, we show that the mutation rate increases with the replication timing by more than 30% between the earliest and the latest replicating regions. Interestingly, 5% of the single base pair substitutions might represent double-slippage events that occurred at the junction of immediately adjacent repeats, resulting in a shift in the repeat boundary.Here we observe that mutation rate, as reflected in recent evolutionary divergence and human nucleotide diversity, is markedly increased in later-replicating regions of the human genome |
http://www.ncbi.nlm.nih.gov/pubmed/18698431,http://www.ncbi.nlm.nih.gov/pubmed/19744324,http://www.ncbi.nlm.nih.gov/pubmed/22943432,http://www.ncbi.nlm.nih.gov/pubmed/16260744,http://www.ncbi.nlm.nih.gov/pubmed/19487332,http://www.ncbi.nlm.nih.gov/pubmed/14710190 | Which metazaon species or taxa are known to lack selenoproteins | Some insect genomes have lost the capacity of synthesizing selenoproteins. Several insect species without selenoproteins have been identified. |
http://www.ncbi.nlm.nih.gov/pubmed/22551571 | What is the mode of inheritance of Facioscapulohumeral muscular
dystrophy (FSHD)? | The mode of inheritance of Facioscapulohumeral muscular dystrophy is autosomal dominant. |
http://www.ncbi.nlm.nih.gov/pubmed/23740944,http://www.ncbi.nlm.nih.gov/pubmed/17690884,http://www.ncbi.nlm.nih.gov/pubmed/24829218,http://www.ncbi.nlm.nih.gov/pubmed/24828250,http://www.ncbi.nlm.nih.gov/pubmed/12813035,http://www.ncbi.nlm.nih.gov/pubmed/18574154,http://www.ncbi.nlm.nih.gov/pubmed/24279792,http://www.ncbi.nlm.nih.gov/pubmed/22870324,http://www.ncbi.nlm.nih.gov/pubmed/23712977,http://www.ncbi.nlm.nih.gov/pubmed/20921147,http://www.ncbi.nlm.nih.gov/pubmed/19074813,http://www.ncbi.nlm.nih.gov/pubmed/21715553,http://www.ncbi.nlm.nih.gov/pubmed/19074871,http://www.ncbi.nlm.nih.gov/pubmed/24534531,http://www.ncbi.nlm.nih.gov/pubmed/21330608,http://www.ncbi.nlm.nih.gov/pubmed/25253572,http://www.ncbi.nlm.nih.gov/pubmed/25732381,http://www.ncbi.nlm.nih.gov/pubmed/21677137,http://www.ncbi.nlm.nih.gov/pubmed/21469090,http://www.ncbi.nlm.nih.gov/pubmed/23162548,http://www.ncbi.nlm.nih.gov/pubmed/24041848,http://www.ncbi.nlm.nih.gov/pubmed/23848281,http://www.ncbi.nlm.nih.gov/pubmed/23259058 | Is NOD1 activated in inflammation? | Nod proteins fight off bacterial infections by stimulating proinflammatory signaling and cytokine networks and by inducing antimicrobial effectors, such as nitric oxide and antimicrobial peptides. NOD1 engagement generates an inflammatory response via activation of NFκB and MAPK pathways and several inflammatory disorders, such as Crohn's disease and asthma, are linked to genetic changes in either Nod1 or Nod2. Nod1 is also critically implicated in shaping adaptive immune responses towards bacterial-derived constituents. Together, Nod1 and Nod2 represent central players in the control of immune responses to bacterial infections and inflammation. Mice deficient for both Nod1 and Nod2 had attenuated inflammatory pathology, reduced levels of inflammatory cytokines, and increased colonization of the mucosal tissueNod1/2 DKO mice show increased susceptibility for intestinal permeability while vascular permeability was not affected. The present study analyzed Nod1 and Nod2 double deficient (Nod1/2 DKO) mice under physiological and inflammatory conditions. The increased intestinal permeability is associated with enhanced inflammatory cytokine production and epithelial cell proliferation in Nod1-deficient mice as compared with wild-type mice. However, the influence of Rip2 was strictly dependent on infection conditions that favored expression of the Salmonella pathogenicity island 2 (SPI-2) type III secretion system (TTSS), as Rip2 was dispensable for inflammation when mice were infected with bacteria grown under conditions that promoted expression of the SPI-1 TTSS.Nod1 and Nod2 control bacterial infections and inflammation |
http://www.ncbi.nlm.nih.gov/pubmed/23701010,http://www.ncbi.nlm.nih.gov/pubmed/20590842,http://www.ncbi.nlm.nih.gov/pubmed/22505457,http://www.ncbi.nlm.nih.gov/pubmed/20013286,http://www.ncbi.nlm.nih.gov/pubmed/24081567,http://www.ncbi.nlm.nih.gov/pubmed/23960723,http://www.ncbi.nlm.nih.gov/pubmed/24298040,http://www.ncbi.nlm.nih.gov/pubmed/17168521,http://www.ncbi.nlm.nih.gov/pubmed/22560840,http://www.ncbi.nlm.nih.gov/pubmed/20399192,http://www.ncbi.nlm.nih.gov/pubmed/19830834,http://www.ncbi.nlm.nih.gov/pubmed/18787103,http://www.ncbi.nlm.nih.gov/pubmed/23856045,http://www.ncbi.nlm.nih.gov/pubmed/18576335,http://www.ncbi.nlm.nih.gov/pubmed/23828821,http://www.ncbi.nlm.nih.gov/pubmed/23030787,http://www.ncbi.nlm.nih.gov/pubmed/15704193,http://www.ncbi.nlm.nih.gov/pubmed/23022892,http://www.ncbi.nlm.nih.gov/pubmed/21136610,http://www.ncbi.nlm.nih.gov/pubmed/23118341,http://www.ncbi.nlm.nih.gov/pubmed/23576281,http://www.ncbi.nlm.nih.gov/pubmed/16856138,http://www.ncbi.nlm.nih.gov/pubmed/16730216 | List diseases where protein citrullination plays an important role. | Rheumatoid arthritis, multiple sclerosis, prion diseases, cancer and Alzheimer's disease are examples of diseases where protein citrullination involvement has been demonstrated. |
http://www.ncbi.nlm.nih.gov/pubmed/21699851,http://www.ncbi.nlm.nih.gov/pubmed/14646469,http://www.ncbi.nlm.nih.gov/pubmed/11048776,http://www.ncbi.nlm.nih.gov/pubmed/11208236,http://www.ncbi.nlm.nih.gov/pubmed/11334832,http://www.ncbi.nlm.nih.gov/pubmed/17957272,http://www.ncbi.nlm.nih.gov/pubmed/22869311,http://www.ncbi.nlm.nih.gov/pubmed/22816548,http://www.ncbi.nlm.nih.gov/pubmed/17229310,http://www.ncbi.nlm.nih.gov/pubmed/23107651,http://www.ncbi.nlm.nih.gov/pubmed/15331287,http://www.ncbi.nlm.nih.gov/pubmed/10392228,http://www.ncbi.nlm.nih.gov/pubmed/9930916,http://www.ncbi.nlm.nih.gov/pubmed/10894918,http://www.ncbi.nlm.nih.gov/pubmed/22027166,http://www.ncbi.nlm.nih.gov/pubmed/15744544,http://www.ncbi.nlm.nih.gov/pubmed/6496438,http://www.ncbi.nlm.nih.gov/pubmed/9703576,http://www.ncbi.nlm.nih.gov/pubmed/20086611,http://www.ncbi.nlm.nih.gov/pubmed/11879111,http://www.ncbi.nlm.nih.gov/pubmed/18691236,http://www.ncbi.nlm.nih.gov/pubmed/10338239,http://www.ncbi.nlm.nih.gov/pubmed/11555799,http://www.ncbi.nlm.nih.gov/pubmed/10498299,http://www.ncbi.nlm.nih.gov/pubmed/19749607 | What is commotio cordis? | Commotio cordis is a term used to describe cases of blunt thoracic impact causing sudden death without structural damage of the heart |
http://www.ncbi.nlm.nih.gov/pubmed/26451147,http://www.ncbi.nlm.nih.gov/pubmed/24909484,http://www.ncbi.nlm.nih.gov/pubmed/16903509,http://www.ncbi.nlm.nih.gov/pubmed/12523816,http://www.ncbi.nlm.nih.gov/pubmed/20339456,http://www.ncbi.nlm.nih.gov/pubmed/19728949,http://www.ncbi.nlm.nih.gov/pubmed/24556565,http://www.ncbi.nlm.nih.gov/pubmed/22707338,http://www.ncbi.nlm.nih.gov/pubmed/23993722,http://www.ncbi.nlm.nih.gov/pubmed/12898406,http://www.ncbi.nlm.nih.gov/pubmed/24157356 | What is the cause of Phthiriasis Palpebrarum? | Phthiriasis palpebrarum is a rare eyelid infestation caused by phthirus pubis. |
http://www.ncbi.nlm.nih.gov/pubmed/12480542,http://www.ncbi.nlm.nih.gov/pubmed/25451386,http://www.ncbi.nlm.nih.gov/pubmed/17030629,http://www.ncbi.nlm.nih.gov/pubmed/11504710,http://www.ncbi.nlm.nih.gov/pubmed/20807542,http://www.ncbi.nlm.nih.gov/pubmed/22952658,http://www.ncbi.nlm.nih.gov/pubmed/19403607,http://www.ncbi.nlm.nih.gov/pubmed/17526652,http://www.ncbi.nlm.nih.gov/pubmed/22040806,http://www.ncbi.nlm.nih.gov/pubmed/10531621,http://www.ncbi.nlm.nih.gov/pubmed/11741309 | Does the histidine-rich Ca-binding protein (HRC) interact with triadin? | Yes. HRC may play a key role in the regulation of SR Ca cycling through its direct interactions with SERCA2 and triadin, mediating a fine cross talk between SR Ca uptake and release in the heart. A direct binding of HRC (histidine-rich Ca(2+)-binding protein) to triadin, the main transmembrane protein of the junctional sarcoplasmic reticulum (SR) of skeletal muscle, seems well supported.Histidine-rich calcium binding protein (HRC) is located in the lumen of sarcoplasmic reticulum (SR) and binds to triadin (TRN), a protein associated with the ryanodine receptor and thought to be involved in calcium release. |
http://www.ncbi.nlm.nih.gov/pubmed/24057217,http://www.ncbi.nlm.nih.gov/pubmed/19951682,http://www.ncbi.nlm.nih.gov/pubmed/20944598,http://www.ncbi.nlm.nih.gov/pubmed/19151715,http://www.ncbi.nlm.nih.gov/pubmed/23887935,http://www.ncbi.nlm.nih.gov/pubmed/19881528,http://www.ncbi.nlm.nih.gov/pubmed/20720541,http://www.ncbi.nlm.nih.gov/pubmed/23157493,http://www.ncbi.nlm.nih.gov/pubmed/22479372 | How are CpG island shores defined? | CpG island "shores" are defined as genomic regions up to 2kb distant to known CpG islands. Differential DNA methylation correlates with gene expression more strongly at CpG island shores than CpG islands. |
http://www.ncbi.nlm.nih.gov/pubmed/21299874,http://www.ncbi.nlm.nih.gov/pubmed/19398856,http://www.ncbi.nlm.nih.gov/pubmed/18705917,http://www.ncbi.nlm.nih.gov/pubmed/21125466,http://www.ncbi.nlm.nih.gov/pubmed/22170177,http://www.ncbi.nlm.nih.gov/pubmed/16463831,http://www.ncbi.nlm.nih.gov/pubmed/15790946,http://www.ncbi.nlm.nih.gov/pubmed/19658274,http://www.ncbi.nlm.nih.gov/pubmed/16759446,http://www.ncbi.nlm.nih.gov/pubmed/16628069,http://www.ncbi.nlm.nih.gov/pubmed/21748496,http://www.ncbi.nlm.nih.gov/pubmed/23931043,http://www.ncbi.nlm.nih.gov/pubmed/12632115,http://www.ncbi.nlm.nih.gov/pubmed/16164489,http://www.ncbi.nlm.nih.gov/pubmed/22633825,http://www.ncbi.nlm.nih.gov/pubmed/24619389,http://www.ncbi.nlm.nih.gov/pubmed/11883835,http://www.ncbi.nlm.nih.gov/pubmed/22890635,http://www.ncbi.nlm.nih.gov/pubmed/20538692,http://www.ncbi.nlm.nih.gov/pubmed/17121134,http://www.ncbi.nlm.nih.gov/pubmed/20228677,http://www.ncbi.nlm.nih.gov/pubmed/19828484,http://www.ncbi.nlm.nih.gov/pubmed/16159090,http://www.ncbi.nlm.nih.gov/pubmed/23002400,http://www.ncbi.nlm.nih.gov/pubmed/17536487,http://www.ncbi.nlm.nih.gov/pubmed/19370322,http://www.ncbi.nlm.nih.gov/pubmed/15753761,http://www.ncbi.nlm.nih.gov/pubmed/21608279,http://www.ncbi.nlm.nih.gov/pubmed/17636626,http://www.ncbi.nlm.nih.gov/pubmed/19812935,http://www.ncbi.nlm.nih.gov/pubmed/25201463,http://www.ncbi.nlm.nih.gov/pubmed/16427437,http://www.ncbi.nlm.nih.gov/pubmed/22966500,http://www.ncbi.nlm.nih.gov/pubmed/20378868,http://www.ncbi.nlm.nih.gov/pubmed/20334471,http://www.ncbi.nlm.nih.gov/pubmed/18054611,http://www.ncbi.nlm.nih.gov/pubmed/22059101,http://www.ncbi.nlm.nih.gov/pubmed/11426093,http://www.ncbi.nlm.nih.gov/pubmed/21489317,http://www.ncbi.nlm.nih.gov/pubmed/19700328,http://www.ncbi.nlm.nih.gov/pubmed/16463861,http://www.ncbi.nlm.nih.gov/pubmed/16723884 | Does magnesium sulfate improve outcomes of subarachnoid hemorrhage patients? | No. Although initial studies have provided with encouraging findings regarding administration of magnesium sulphate in aneurysmal subarachnoid haemorrhage patients, but subsequent larger studies have reported that intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended. |
http://www.ncbi.nlm.nih.gov/pubmed/18937352,http://www.ncbi.nlm.nih.gov/pubmed/21880664,http://www.ncbi.nlm.nih.gov/pubmed/16096717,http://www.ncbi.nlm.nih.gov/pubmed/21789513,http://www.ncbi.nlm.nih.gov/pubmed/12574890,http://www.ncbi.nlm.nih.gov/pubmed/11691526,http://www.ncbi.nlm.nih.gov/pubmed/15851108,http://www.ncbi.nlm.nih.gov/pubmed/10902626,http://www.ncbi.nlm.nih.gov/pubmed/17924338,http://www.ncbi.nlm.nih.gov/pubmed/22315228 | Which gene is mutated in a subtype of arrhythmogenic right ventricular cardiomyopathy known as Naxos disease? | Identification of a deletion in plakoglobin in arrhythmogenic right ventricular cardiomyopathy with palmoplantar keratoderma and woolly hair (Naxos disease).Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disorder associated with arrhythmias and sudden death. A recessive mutation in the gene encoding plakoglobin has been shown to cause Naxos disease, a cardiocutaneous syndrome characterized by ARVC and abnormalities of hair and skin.Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disorder associated with arrhythmias and sudden death. A recessive mutation in the gene encoding plakoglobin has been shown to cause Naxos disease, a cardiocutaneous syndrome characterized by ARVC and abnormalities of hair and skin. A homozygous loss-of-function mutation of the Plakoglobin (Jup) gene, which encodes a major component of the desmosome and the adherens junction, had been identified in Naxos patients, although the underlying mechanism remained elusive.A homozygous loss-of-function mutation of the Plakoglobin (Jup) gene, had been identified in Naxos Disease patients, a subset of ARVC, which is characterized by cutaneous disorder. |
http://www.ncbi.nlm.nih.gov/pubmed/23564113,http://www.ncbi.nlm.nih.gov/pubmed/23710445,http://www.ncbi.nlm.nih.gov/pubmed/22977573,http://www.ncbi.nlm.nih.gov/pubmed/17115943,http://www.ncbi.nlm.nih.gov/pubmed/17115906,http://www.ncbi.nlm.nih.gov/pubmed/24163818,http://www.ncbi.nlm.nih.gov/pubmed/19590930,http://www.ncbi.nlm.nih.gov/pubmed/24066191,http://www.ncbi.nlm.nih.gov/pubmed/22982593,http://www.ncbi.nlm.nih.gov/pubmed/22251821,http://www.ncbi.nlm.nih.gov/pubmed/20398468,http://www.ncbi.nlm.nih.gov/pubmed/21677777,http://www.ncbi.nlm.nih.gov/pubmed/21732763,http://www.ncbi.nlm.nih.gov/pubmed/19768539 | What is the role of edaravone in traumatic brain injury? | Edaravone, a free radical scavenger, has been shown to have neuroprotective effects after traumatic brain injury. In animal models, edaravone has been shown to reduce neuronal damage by scavenging reactive oxygen species (ROS), maintain intact the autoregulation of the cerebral vasculature, decrease neuronal loss, reduce programmed cell death, the presence of inflammatory cytokines, cerebral edema, and blood-brain barrier (BBB) permeability. Edaravone also protects against neurological deficits and memory deficits following traumatic brain injury. |