Shanghai Changning Central Hospital

Shanghai, China

Shanghai Changning Central Hospital

Shanghai, China
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Su S.-H.,Tongji University | Xu W.,Shanghai Changning Central Hospital | Hai J.,Tongji University | Yu F.,Tongji University | And 3 more authors.
Journal of Clinical Neuroscience | Year: 2014

Detected unruptured intracranial aneurysms (UIA) are becoming more common with the increased utilization of CT angiography, MR angiography and digital subtraction angiography. A proportion of patients with UIA remain untreated. We investigated to assess cognitive function, depression, anxiety and quality of life (QoL) in Chinese patients with untreated UIA. Thirty one Chinese patients with untreated UIA and 25 healthy controls were identified and matched for variables including age, sex, and living area. Cognitive function was evaluated with the Montreal Cognitive Assessment (MoCA). Depression, anxiety and QoL were screened with the Self-Rating Depression Scale, Self-Rating Anxiety Scale, and Short Form-36, respectively. Non-parametric tests were used for comparisons between groups. No patient had cognitive dysfunction at 1 month or 1 year after detection of UIA. However, a significant decrease of overall MoCA subscores was found in 30 (97%) of 31 patients 5 years after UIA discovery, suggestive of mild cognitive impairment. A significant decrease in depression and anxiety was found in patients over time. QoL in patients was reduced most prominently in psychosocial function and social activities 1 year after detection of UIA, but these improved to within normal limits at the end of the follow-up period. For Chinese patients with untreated UIA, depression, anxiety and reduced QoL may be short-term complications. Mild cognitive impairment may be a long-term complication. © 2014 Elsevier Ltd. All rights reserved.


Su S.-H.,Tongji University | Xu W.,Shanghai Changning Central Hospital | Li M.,Shanghai JiaoTong University | Zhang L.,Shanghai JiaoTong University | And 3 more authors.
Brain, Behavior, and Immunity | Year: 2014

The pathogenesis of persistent unfavourable outcomes following mild traumatic brain injury (mTBI) are not fully understood. Low-grade systemic inflammation might contribute to the development of persistent unfavourable outcomes in patients with mTBI. We used plasma high-sensitivity C-reactive protein (CRP) levels as the biomarker of systemic inflammation to investigate whether elevated CRP levels were associated with persistent adverse outcomes in these patients. A total of 213 consecutive patients with mTBI were identified in our study. Plasma high-sensitivity CRP levels were measured at baseline, 1. month, 2. months and 3. months after initial traumatic brain injury. The study endpoints included persistent postconcussion syndrome (PCS), persistent psychological problems (depression and anxiety), persistent physiological problems (frequent headache, nausea, insomnia, dizziness and fatigue) and persistent cognitive impairment, which were screened by International Classification of Diseases (ICD-10), diagnostic and statistical manual of mental disorders (DSM-IV), Beck anxiety inventory (BAI), Beck depression inventory (BDI) and montreal cognitive assessment (MoCA) 3. months post-injury. The associations between baseline CRP levels and persistent unfavourable outcomes were estimated from multiple regression models adjusting for various confounding covariates. Elevated baseline CRP levels were associated with a significant increase in the incidence of persistent PCS (odds ratio [OR], 2.719; 95% confidence interval [CI], 1.609-4.594; p= 0.000), persistent psychological problems (OR, 1.535; 95% CI, 1.063-2.216; p= 0.022), and persistent cognitive impairment (OR, 1.687; 95% CI, 1.135-2.507; p= 0.010). However, elevated CRP levels were not associated with persistent physiological problems (OR, 1.330; 95% CI, 0.905-1.956; p= 0.146). Furthermore, three adjusted models did not essentially affect the OR of elevated CRP levels for these persistent unfavourable outcomes. Among patients with mTBI, baseline elevated CRP levels may be an independent predictor of persistent persistent PCS, psychological problems and cognitive impairment. © 2014 Elsevier Inc.


Li G.-M.,Shanghai JiaoTong University | Wang Y.-G.,Shanghai Changning Central Hospital | Pan Q.,Shanghai JiaoTong University | Wang J.,Shanghai JiaoTong University | And 2 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2014

Sorafenib is the first drug currently approved to treat advanced hepatocellular carcinoma (HCC). However, very low response rate and acquired drug resistance makes rare patients benefit from sorafenib therapy, therefore it is urgent to find biomarkers for sorafenib sensitivity. Histone modifications, including histone methylation, have been demonstrated to influence the initiation and progression of HCC. It is of great interest to elicit the possibility whether histone methylation plays a role in regulation of sorafenib sensitivity. In present work, a high throughput RNAi screening with 176 shRNA pools against 88 histone methyltransferases (HMTs) and histone demethyltransferases genes was applied to HepG2 cells. Silencing of 3 genes (ASH1L, C17ORF49 and SETD4) was validated to specifically promote HepG2 cells sensitivity to sorafenib. Western blotting results showed that those 3 HMT genes knockdown alone or sorafenib treatments alone both induce AKT/ERK activation. However, combination treatment with sorafenib and silencing of C17ORF49 or SETD4 downregulated AKT phosphorylation and hence induced HCC cells death. Our work may provide potential biomarkers for sorafenib sensitivity and therapeutic combination for sorafenib treatment in HCC patients.


Shi J.,Tongji University | Zhang M.,Shanghai Changning Central Hospital | Zhang L.,First Peoples Hospital of Yunnan Province | Wang P.,First Peoples Hospital of Yunnan Province | And 2 more authors.
Microbial Biotechnology | Year: 2014

Xylose fermentation is necessary for the bioconversion of lignocellulose to ethanol as fuel, but wild-type Saccharomyces cerevisiae strains cannot fully metabolize xylose. Several efforts have been made to obtain microbial strains with enhanced xylose fermentation. However, xylose fermentation remains a serious challenge because of the complexity of lignocellulosic biomass hydrolysates. Genome shuffling has been widely used for the rapid improvement of industrially important microbial strains. After two rounds of genome shuffling, a genetically stable, high-ethanol-producing strain was obtained. Designated as TJ2-3, this strain could ferment xylose and produce 1.5 times more ethanol than wild-type Pichiastipitis after fermentation for 96h. The acridine orange and propidium iodide uptake assays showed that the maintenance of yeast cell membrane integrity is important for ethanol fermentation. This study highlights the importance of genome shuffling in P.stipitis as an effective method for enhancing the productivity of industrial strains. Designated as TJ2-3, this strain could ferment xylose and produce 1.5 times more ethanol than wild-type P. stipitis after fermentation for 96 h. The acridine orange and propidium iodide uptake assays showed that the maintenance of yeast cell membrane integrity is important for ethanol fermentation. This study highlights the importance of genome shuffling in P. stipitis as an effective method for enhancing the productivity of industrial strains. © 2013 The Authors.


Su S.-H.,Tongji University | Xu W.,Shanghai Changning Central Hospital | Hai J.,Tongji University | Wu Y.-F.,Tongji University | Yu F.,Tongji University
Scientific Reports | Year: 2014

Aneurysmal subarachnoid hemorrhage (aSAH)-induced cerebral vasospasm and delayed ischemic neurological deficit (DIND) are the major causes of morbidity and mortality in patients with aSAH. The effects of statins-use for patients with aSAH remain controversial. Here,a total of 249 patients from six randomized controlled trials(RCTs) were subjected to meta-analysis. No significant decrease was found in the incidence of vasospasm(RR, 0.80; 95% CI, 0.54-1.17), with substantial heterogeneity (I2 = 49%, P = 0.08), which was verified by the further sensitivity analysis and subgroup meta-analysis. Furthermore, no significant difference was presented in the incidence of poor neurological outcome(RR, 0.94; 95% CI, 0.77-1.16), and potential side effects(RR, 2.49; 95% CI, 0.75-8.33). Nevertheless, significant difference was reported in the occurrence of DIND(RR, 0.58; 95% CI, 0.37-0.92) and mortality(RR, 0.30; 95% CI, 0.14-0.64). At present, although statins-use in the patients with aSAH should not be considered standard care at present, statins-use may have the potential effects in the prevention of mortality in patients with aSAH.


Chen Q.-Q.,Nantong University | Chen Q.-Q.,Shanghai Changning Central Hospital | Zhang W.,Nantong University | Chen X.-F.,Nantong University | And 3 more authors.
Canadian Journal of Physiology and Pharmacology | Year: 2012

Most cardiac diseases are associated with fibrosis. Calcineurin (CaN) is regulated by Ca2+/calmodulin (CaM). The CaN-NFAT (nuclear factor of activated T cell) pathway is involved in the process of cardiac diseases, such as cardiac hypertrophy, but its effect on myocardial fibrosis remains unclear. The present study investigates whether the CaN-NFAT pathway is involved in cardiac fibroblast (CF) proliferation induced by electrical field stimulation (EFS), which recently became a popular treatment for heart failure and cardiac tissue engineering. CF proliferation was evaluated by a cell survival assay (MTT)and cell counts. Myocardial fibrosis was assessed by collagen I and collagen III protein expression. Green fluorescent protein (GFP)-tagged NFAT was used to detect NFAT nuclear translocation. CF proliferation, myocardial fibrosis, CaN activity, and NFAT nuclear translocation were enhanced by EFS. More importantly, these effects were abolished by CaN inhibitors, dominant negative CaN (DN-CaN), and CaN gene silenced with siRNA. Furthermore, buffering intracellular Ca2+ with BAPTA-AM and blocking Ca2+ influx with nifedipine suppressed EFS-induced increase in intracellular Ca2+ and CF proliferation. These results suggested that the CaN-NFAT pathway mediates CF proliferation, and that the CaN-NFAT pathway might be a possible therapeutic target for EFS-induced myocardial fibrosis and cardiac tissue engineering.


Ni Z.,Shanghai University of Traditional Chinese Medicine | Tao K.,Shanghai Changning Central Hospital | Chen G.,Shanghai University of Traditional Chinese Medicine | Chen Q.,Shanghai University of Traditional Chinese Medicine | And 4 more authors.
PLoS ONE | Year: 2012

CLPTM1L is believed to be associated with lung cancer. However, there is little information regarding its expression and function. Here using immunohistochemistry, we found that CLPTM1L expression was markedly increased in lung cancer tissues relative to normal tissues, especially in lung adenocarcinoma. CLPTM1L expression was not found to be associated with stages, smoking status, lymph node metastasis, or T lymphocyte infiltration but with differentiation stage. We found CLPTM1L to be enriched in the mitochondrial compared with plasma membrane protein extracts. CLPTM1L-EGFP transfection showed that the molecule product was expressed in cytoplasm and indicated the mitochondrial localization stained with mitochondrial marker MitoTracker. CLPTM1L transferred lung cancer cell line 95-D showed no growth inhibition or cell apoptosis, but it did show inhibited sensitivity to cis-diamminedichloroplatinum(II) (cisplatin, CDDP). Knockdown of CLPTM1L by RNAi did not interfere with cell proliferation but it did increase cell sensitivity to CDDP and activation of caspase-9 and caspase-3/7. These data indicate CLPTM1L is a mitochondria protein and that it may be associated with anti-apoptotic mechanism which affects drug-resistance in turn. © 2012 Ni et al.


Shi M.,Shanghai Changning Central Hospital | Wei J.,Shanghai Changning Central Hospital | Dong J.,Shanghai Changning Central Hospital | Meng W.,Shanghai Changning Central Hospital | And 4 more authors.
Molecular Medicine Reports | Year: 2015

Intrahepatic T helper (Th)17 cytokine and serum interleukin (IL)-17 levels in patients with hepatitis B are positively correlated with the progression of liver cirrhosis (LC). IL-35 can significantly inhibit the differentiation of Th17 cells and the synthesis of IL-17. The present study aimed to investigate the function and expression of IL-17 and IL-35 in the blood of patients with hepatitis B.related LC. The levels of IL-17 and IL-35 in the peripheral blood of 30 patients with chronic hepatitis B (CHB), 79 with LC, 14 with chronic severe hepatitis B (CSHB), and 20 normal controls were detected by ELISA. Quantitative polymerase chain reaction was used to evaluate Epstein-Barr virus-induced gene 3 (EBI3), forkhead box (FOX)P3 and IL-17 mRNA expression levels in peripheral blood mononuclear cells (PBMCs). Western blotting was used to determine protein expression. The liver function of patients and normal controls was measured. EBI3, IL-17 and FOXP3 mRNA expression levels in PBMCs from patients with LC, CHB and CSHB were higher than those in cells from the controls. IL-17 mRNA levels differed significantly according to the Child.Pugh classification and exhibited an upward trend over time in contrast to a downward trend for EBI3 and FOXP3 mRNA. The changes in protein expression in the peripheral blood were consistent with the changes in mRNA expression. Serum IL-17 levels were positively correlated with total bilirubin (TBIL), alanine aminotransferase (ALT) and Child.Pugh grade, and were negatively correlated with albumin. These observed differences were significant. Serum IL-35 levels were negatively correlated with albumin, but not with Child.Pugh grade, ALT and TBIL. IL-17 and IL-35 may be critically involved in the pathogenesis of hepatitis B.related LC.


Wei J.,Shanghai Changning Central Hospital | Shi M.,Shanghai Changning Central Hospital | Wu W.-Q.,Shanghai Changning Central Hospital | Xu H.,Shanghai Changning Central Hospital | And 4 more authors.
World Journal of Gastroenterology | Year: 2011

AIM: To investigate the anti-fibrosis effect of IκB kinase-beta inhibitor (IKK2 inhibitor IMD0354) in liver fibrosis. METHODS: Twenty male C57BL6 mice were divided into four groups. Five high-fat fed mice were injected with lipopolysaccharide (LPS, 10 mg/kg) intraperitoneally and five high-fat fed mice were without LPS injection to build models of liver injury, and the intervention group (five mice) was injected intraperitoneally with IKK2 inhibitor (IMD 30 mg/kg for 14 d), while the remaining five mice received a normal diet as controls. Hepatic function, pathological evaluation and liver interleukin-6 (IL-6) expression were examined. Western blotting and real-time polymerase chain reaction were used to detect the expressions of nuclear factor-κB (NF-κB), alpha-smooth muscle actin (α-SMA), tumor growth factor-beta1 (TGF-β1), tumor necrosis factor-alpha (TNF-α), type I and type III collagen proteins and mRNA. RESULTS: A mouse model of liver injury was successfully established, and IMD decreased nuclear translocation of NF-κB p65 in liver cells. In the IMD-treated group, the levels of alanine aminotransferase (103 ± 9.77 μ/L vs 62.4 ± 7.90 μ/L, P < 0.05) and aminotransferase (295.8 ± 38.56 μ/L vs 212 ± 25.10 μ/L, P < 0.05) were significantly decreased when compared with the model groups. The histological changes were significantly ameliorated. After treatment, the expressions of IL-6 (681 ± 45.96 vs 77 ± 7.79, P < 0.05), TGF-β1 (Western blotting 5.65% ± 0.017% vs 2.73% ± 0.005%, P < 0.05), TNF-α (11.58% ± 0.0063% vs 8.86% ± 0.0050%, P < 0.05), type I collagen (4.49% ± 0.014% vs 1.90% ± 0.0006%, P < 0.05) and type III collagen (3.46% ± 0.008% vs 2.29% ± 0.0035%, P < 0.05) as well as α-SMA (6.19 ± 0.0036 μ/L vs 2.16 ± 0.0023 μ/L, P < 0.05) protein and mRNA were downregulated in the IMD group compared to the fibrosis control groups (P < 0.05). CONCLUSION: IKK2 inhibitor IMD markedly improved non-alcoholic fatty liver disease in mice by lowering NF-κB activation, which could become a remedial target for liver fibrosis. © 2011 Baishideng.


Wang Y.-G.,Shanghai Changning Central Hospital | Fang W.-L.,Shanghai Changning Central Hospital | Wei J.,Shanghai Changning Central Hospital | Wang T.,Shanghai Changning Central Hospital | And 3 more authors.
Journal of the Chinese Medical Association | Year: 2013

Background: Increasing evidence suggests that innate immunity is involved in the development of nonalcoholic fatty liver disease. Nod-like receptors (NLRs) have recently been identified as key mediators of inflammatory and immune responses. The aim of this article is to explore the correlation of nucleotide-binding oligomerization domain (NOD)-like receptor (NLR)X1 and NLRP3 with nonalcoholic steatohepatitis (NASH) in mice. Methods: In our study, a high-fat diet, lipopolysaccharides (LPSs), and normal diet were given to C57BL mice to establish high fat (HF), HF+LPS, and control groups. Thereafter, serum alanine and aspartate aminotransferase (ALT and AST) levels were measured, and NASH severity was histologically examined. We measured tumor necrosis factor (TNF)-α levels by enzyme-linked immunosorbent assay, protein expression by Western blotting, and mRNA expression by real-time fluorescent quantitative reverse transcription-polymerase chain reaction. Results: Levels of ALT and AST were higher in HF+LPS mice than in HF mice (<0.05). NLRX1 mRNA and protein expression was lower in HF and HF+LPS mice than in control mice (<0.05). NLRP3 mRNA expression was higher in HF and HF+LPS mice than in control mice (<0.05). The mRNA and protein expression of TNF receptor-associated factor (TRAF)6, interleukin-1β, caspase-1, and apoptosis-associated speck-like protein were significantly higher in HF+LPS mice than in control and HF mice; furthermore, mRNA expression was higher in HF mice than in control mice (<0.05), but protein expression was similar. Conclusion: NLRX1 and NLRP3 inflammasomes may be important in NASH development. © 2013.

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