metadata
tags:
- spacy
- token-classification
language:
- en
widget:
- text: >-
Blood glucose control is the primary strategy to prevent complications in
diabetes. At the onset of kidney disease, therapies that inhibit
components of the renin angiotensin system (RAS) are also indicated, but
these approaches are not wholly effective. Here, we show that once daily
administration of the novel glucose lowering agent, empagliflozin, an
SGLT2 inhibitor which targets the kidney to block glucose reabsorption,
has the potential to improve kidney disease in type 2 diabetes. In male
db/db mice, a 10-week treatment with empagliflozin attenuated the
diabetes-induced upregulation of profibrotic gene markers, fibronectin and
transforming-growth-factor-beta. Other molecular (collagen IV and
connective tissue growth factor) and histological (tubulointerstitial
total collagen and glomerular collagen IV accumulation) benefits were seen
upon dual therapy with metformin. Albuminuria, urinary markers of tubule
damage (kidney injury molecule-1, KIM-1 and neutrophil
gelatinase-associated lipocalin, NGAL), kidney growth, and
glomerulosclerosis, however, were not improved with empagliflozin or
metformin, and plasma and intra-renal renin activity was enhanced with
empagliflozin. In this model, blood glucose lowering with empagliflozin
attenuated some molecular and histological markers of fibrosis but, as per
treatment with metformin, did not provide complete renoprotection. Further
research to refine the treatment regimen in type 2 diabetes and
nephropathy is warranted.
- text: >-
Chronic kidney disease (CKD) is a global public health problem, and its
prevalence is gradually increasing, mainly due to an increase in the
number of patients with type 2 diabetes mellitus (T2DM) [1,2,3,4]. Human
multidrug and toxin extrusion member 2 (MATE2-K, SLC47A2) plays an
important role in the renal elimination of various clinical drugs
including the antidiabetic drug metformin. The goal of this study was to
characterize genetic variants of MATE2-K and determine their association
with the pharmacokinetics of metformin.
model-index:
- name: en_BiomedNER_EuropePMC
results:
- task:
name: NER
type: token-classification
metrics:
- name: NER Precision
type: precision
value: 0.871384947
- name: NER Recall
type: recall
value: 0.9057132188
- name: NER F Score
type: f_score
value: 0.8882175227
Bio literature Named Entity Recognition using microsoft/BiomedNLP-PubMedBERT-base-uncased-abstract-fulltext transformer model. The model recognises the following entities:
CD: Chemical/Drugs, DS: Diseases, GP: Gene/Protein and OG: Organism
