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Institution

XinHua Hospital

HealthcareShanghai, China
About: XinHua Hospital is a healthcare organization based out in Shanghai, China. It is known for research contribution in the topics: Medicine & Biology. The organization has 908 authors who have published 596 publications receiving 11785 citations.
Topics: Medicine, Biology, Internal medicine, Cancer, Gene


Papers
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Journal ArticleDOI
TL;DR: In this article, the authors assessed NAFLD knowledge and associated factors among physicians of different specialties globally and found that despite rapidly increasing nonalcoholic fatty liver disease (NAFLD) prevalence, providers' knowledge may be limited.

30 citations

Journal ArticleDOI
TL;DR: It was revealed that selenium decreased the EMT events of peritoneal mesothelial cells via inhibition of PI3k/AKT pathways, enabling a better understanding of the mechanism of peritonal fibrosis and explore a new idea for the prevention and treatment.
Abstract: Peritoneal fibrosis resulting from long-term clinical peritoneal dialysis has been the main reason of dropout from peritoneal dialysis. Peritonitis as a common complication of peritoneal dialysis treatment may lead to the occurrences of peritoneal fibrosis. We cultured peritoneal mesothelial cells with lipopolysaccharides (LPS) in order to stimulate the environment of peritonitis and investigate whether lipopolysaccharides could induce epithelial-to-mesenchymal transition (EMT). Oxidative stress could stimulate fibrogenesis while selenium has antioxidant properties. So, this study also explored whether selenium supplementation affects lipopolysaccharide-induced EMT and fibrosis. We found that lipopolysaccharides could activate EMT changes such as the loss of E-cadherin and the increase of α-smooth muscle actin (α-SMA), collagen I, vimentin, and fibronectin (FN), while selenium inhibits EMT by modulating reactive oxygen species (ROS) generation and ROS/MMP-9 signaling pathways in peritoneal mesothelial cells. Moreover, it was revealed that selenium decreased the EMT events of peritoneal mesothelial cells via inhibition of PI3k/AKT pathways. In conclusion, these findings enable a better understanding of the mechanism of peritoneal fibrosis and explore a new idea for the prevention and treatment.

30 citations

Journal ArticleDOI
TL;DR: It is reported that TMEM16F, a Ca2+-activated phospholipid scramblase (CaPLSase), plays an essential role in placental trophoblast fusion by translocating PS to cell surface independent of apoptosis, providing insight into understanding cell-cell fusion mechanism of other cell types and on mitigating pregnancy complications such as miscarriage, intrauterine growth restriction, and preeclampsia.
Abstract: Cell-cell fusion or syncytialization is fundamental to the reproduction, development, and homeostasis of multicellular organisms. In addition to various cell type-specific fusogenic proteins, cell surface externalization of phosphatidylserine (PS), a universal eat-me signal in apoptotic cells, has been observed in different cell fusion events. Nevertheless, the molecular underpinnings of PS externalization and cellular mechanisms of PS-facilitated cell-cell fusion are unclear. Here, we report that TMEM16F, a Ca2+-activated phospholipid scramblase (CaPLSase), plays an essential role in placental trophoblast fusion by translocating PS to cell surface independent of apoptosis. The placentas from the TMEM16F knockout mice exhibit deficiency in trophoblast syncytialization and placental development, which lead to perinatal lethality. We thus identified a new biological function of TMEM16F CaPLSase in trophoblast fusion and placental development. Our findings provide insight into understanding cell-cell fusion mechanism of other cell types and on mitigating pregnancy complications such as miscarriage, intrauterine growth restriction, and preeclampsia.

29 citations

Journal ArticleDOI
31 Jan 2014-PLOS ONE
TL;DR: Significantly more episodes of MDD occur among those with lower educational attainment (rather than longer episodes of disease), consistent with the hypothesis that the lower socioeconomic position increases the likelihood of developing MDD.
Abstract: Background The prevalence of major depressive disorder (MDD) is higher in those with low levels of educational attainment, the unemployed and those with low social status. However the extent to which these factors cause MDD is unclear. Most of the available data comes from studies in developed countries, and these findings may not extrapolate to developing countries. Examining the relationship between MDD and socio economic status in China is likely to add to the debate because of the radical economic and social changes occurring in China over the last 30 years. Principal findings We report results from 3,639 Chinese women with recurrent MDD and 3,800 controls. Highly significant odds ratios (ORs) were observed between MDD and full time employment (OR = 0.36, 95% CI = 0.25–0.46, logP = 78), social status (OR = 0.83, 95% CI = 0.77–0.87, logP = 13.3) and education attainment (OR = 0.90, 95% CI = 0.86–0.90, logP = 6.8). We found a monotonic relationship between increasing age and increasing levels of educational attainment. Those with only primary school education have significantly more episodes of MDD (mean 6.5, P-value = 0.009) and have a clinically more severe disorder, while those with higher educational attainment are likely to manifest more comorbid anxiety disorders. Conclusions In China lower socioeconomic position is associated with increased rates of MDD, as it is elsewhere in the world. Significantly more episodes of MDD occur among those with lower educational attainment (rather than longer episodes of disease), consistent with the hypothesis that the lower socioeconomic position increases the likelihood of developing MDD. The phenomenology of MDD varies according to the degree of educational attainment: higher educational attainment not only appears to protect against MDD but alters its presentation, to a more anxious phenotype.

29 citations

Journal ArticleDOI
Yuan-wen Chen1, Ding-guo Li1, Jian-xin Wu1, Ying-Wei Chen1, Han-ming Lu1 
TL;DR: Results suggest that tetrandrine at lower concentrations has a significant inhibiting effect on culture-activation and TGF-beta(1)-stimulated activation of rat HSCs, and that it may be due to an up-regulation of Smad 7 which in turn blocks T GF- beta(1) expression and its downstream signaling.

29 citations


Authors

Showing all 969 results

NameH-indexPapersCitations
Qian Wang108214865557
Lin Li104202761709
Tao Chen8682027714
Bo Li8389128722
Jun Zhang6342419149
Tingting Tang5625610045
Wei Yao532419033
Yingbin Liu381794538
Lei-Sheng Jiang36843558
Zhenan Zhu351183588
Li-Yang Dai34693174
Maolan Li321273084
Xiang-Yang Wang302133316
Yuhong Chen301493038
Qiang Wu29754203
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202330
202252
202126
202037
201914
201814