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Automatic de-identification of electronic medical records using token-level and character-level conditional random fields
CRP regulates the expression and activity of tissue factor as well as tissue factor pathway inhibitor via NF‐κB and ERK 1/2 MAPK pathway
Local activation of cardiac stem cells for post-myocardial infarction cardiac repair
- Zhuzhi Wen, Zun Mai, Jingfeng Wang
- Biology, MedicineJournal of cellular and molecular medicine
- 29 October 2012
Current knowledge opening up the possibilities of cardiac repair through CSCs activation in situ in the setting of MI is reviewed, suggesting several strategies, such as growth factors, mircoRNAs and drugs, may be implemented to potentiate endogenous CSCS to repair infarcted heart without cell transplantation.
Hydrogen sulfide suppresses endoplasmic reticulum stress-induced endothelial-to-mesenchymal transition through Src pathway.
An automatic system to identify heart disease risk factors in clinical texts over time
Dyssynchronous pacing triggers endothelial-mesenchymal transition through heterogeneity of mechanical stretch in a canine model.
- Jing-ting Mai, Qingsong Hu, Jingfeng Wang
- Biology, MedicineCirculation journal : official journal of the…
- 25 December 2014
RVP-induced DHF could aggravate fibrosis due to regional heterogeneity of mechanical stress, and it was better in the BiVP group where mechanical stress-induced EndMT might play a pivotal role through the integrin β1 pathway.
C-reactive protein can upregulate VEGF expression to promote ADSC-induced angiogenesis by activating HIF-1α via CD64/PI3k/Akt and MAPK/ERK signaling pathways
It is found that CRP did not affect ADSC apoptosis, cell cycle, or proliferation but did increase their migration by activating the PI3K/Akt pathway, and CRP can upregulate vascular endothelial growth factor-A (VEGF-A) expression by activating hypoxia inducible factor-1 α (HIF-1α) in ADSCs.
Tumor necrosis factor-alpha G-308A gene polymorphism and coronary heart disease susceptibility: an updated meta-analysis.
C-reactive protein promotes vascular endothelial dysfunction partly via activating adipose tissue inflammation in hyperlipidemic rabbits.