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Zhang Q.,Shanghai JiaoTong University | Yan Zhang R.,Shanghai JiaoTong University | Qiu J.P.,Shanghai Pudong Gongli Hospital | Zhang J.F.,Shanghai JiaoTong University | And 7 more authors.
Circulation: Cardiovascular Quality and Outcomes | Year: 2011

Background: Traditional reperfusion options for patients with acute ST-segment elevation myocardial infarction (STEMI) presenting to non-primary percutaneous coronary intervention (PPCI)-capable hospitals generally include onsite fibrinolytics or emergency transfer for PPCIA third option, involving interventionalist transfer, was examined in the REVERSE-STEMI studyMethods and Results: A total of 334 patients with acute STEMI who presented to 5 referral hospitals with angiographic facilities but without interventionalists qualified for PPCI were randomized to receive PPCI with either an interventionalist- (n=165) or a patient-transfer (n=169) strategyThe primary end point of door-to-balloon (D2B) time and secondary end points of left ventricular ejection fraction and major adverse cardiac events (MACE) at 1-year clinical follow-up were compared between the 2 groupsCompared with the patient-transfer strategy, the interventionalisttransfer strategy resulted in a significantly shortened D2B time (median, 92 minutes versus 141 minutes; P>0.0001), with more patients having first balloon angioplasty within 90 minutes (21.2% versus 7.7%, P>0.001)This treatment strategy also was associated with higher left ventricular ejection fraction (0.60±0.07 versus 0.57±0.09, P>0.001) and improved 1-year MACE-free survival (84.8% versus 74.6%, P=0.019)Multivariate Cox proportional hazards modeling revealed that the interventionalist-transfer strategy was an independent factor for reduced risk of composite MACE (hazard ratio, 0.63; 95% CI, 0.45 to 0.88; P=0.003)Conclusions: The interventionalist-transfer strategy for PPCI may be effective in improving the care of patients with STEMI presenting to a non-PPCI-capable hospital, particularly in a congested cosmopolitan region where patient transfers could be prolonged. © 2011 American Heart Association, Inc. Source


Wang J.,Shandong University | Wang Y.,Shanghai JiaoTong University | Zhao D.,Tongji University | Guo X.,Shanghai Pudong Gongli Hospital | Zhong J.-Q.,Shandong University
Renal Failure | Year: 2015

Objectives: To investigate the association between serum uric acid and mortality in a Chinese population of hypertensive patients. Methods and results: A total of 2757 Chinese hypertensive patients from department of cardiology of several hospitals in Shanghai in China were followed up for about six years in this prospective study. Mortality was recorded and related factors were evaluated. Hyperuricemia was diagnosed by serum uric acid levels of >420μmol/L in males or >357μmol/L in females. A total of 2585 hypertensive patients with complete data were included in the final statistical analysis. Totally 709 deaths (27.4%) occurred during the six-year follow-up, of which 475 deaths were attributable to cardiovascular disease (CVD). All-cause and CVD mortality of hypertensive patients with hyperuricemia was significantly higher than that of patients without hyperuricemia. The Cox regression analysis indicated that hazards ratios (HRs) of hyperuricemia for all-cause and CVD mortality were 1.206 (95% CI: 1.002-1.453) and 1.085 (95% CI: 1.002-1.271) respectively. All-cause and CVD mortality of hypertensive patients was significantly increased (both p<0.05) when uric acid levels increased. HRs of uric acid levels >536μmol/L to all-cause and CVD mortality of hypertensive patients were 2.115 (95% CI: 1.596-2.801) and 1.861 (95% CI: 1.296-2.673), respectively, compared with those of uric acid levels 357μmol/L. Conclusions: The data from this cohort study indicate that hyperuricemia can predict increased all-cause and CVD mortality in hypertensive patients. © 2015 Informa Healthcare USA, Inc. All rights reserved: reproduction in whole or part not permitted. Source


Yang L.,Shanghai JiaoTong University | Yang L.,Fudan University | Wang J.,Shanghai JiaoTong University | Li J.,Shanghai JiaoTong University | And 14 more authors.
Molecular and Cellular Proteomics | Year: 2016

We aimed to globally discover serum biomarkers for diagnosis of gastric cancer (GC). GC serum autoantibodies were discovered and validated using serum samples from independent patient cohorts encompassing 1,401 participants divided into three groups, i.e. healthy, GC patients, and GC-related disease group. To discover biomarkers for GC, the human proteome microarray was first applied to screen specific autoantibodies in a total of 87 serum samples from GC patients and healthy controls. Potential biomarkers were identified via a statistical analysis protocol. Targeted protein microarrays with only the potential biomarkers were constructed and used to validate the candidate biomarkers using 914 samples. To provide further validation, the abundance of autoantibodies specific to the biomarker candidates was analyzed using enzymelinked immunosorbent assays. Receiver operating characteristic curves were generated to evaluate the diagnostic accuracy of the serum biomarkers. Finally, the efficacy of prognosis efficacy of the final four biomarkers was evaluated by analyzing the clinical records. The final panel of biomarkers consisting of COPS2, CTSF, NT5E, and TERF1 provides high diagnostic power, with 95% sensitivity and 92% specificity to differentiate GC patients from healthy individuals. Prognosis analysis showed that the panel could also serve as independent predictors of the overall GC patient survival. The panel of four serum biomarkers (COPS2, CTSF, NT5E, and TERF1) could serve as a noninvasive diagnostic index for GC, and the combination of them could potentially be used as a predictor of the overall GC survival rate. © 2016 by The American Society for Biochemistry and Molecular Biology, Inc. Source


Zhang L.,Fudan University | Fu X.-H.,Shanghai Pudong Gongli Hospital | Yu Y.,Fudan University | Shui R.-H.,Fudan University | And 5 more authors.
Laboratory Investigation | Year: 2015

Cathepsin B (CB) is involved in the turnover of proteins and has various roles in maintaining the normal metabolism of cells. In our recent study, CB is increased in the muscles of polymyositis/dermatomyositis (PM/DM). However, the role of CB in interstitial lung disease (ILD) has not been reported. ILD is a frequent complication of PM/DM, which is the leading cause of death in PM/DM. It carries high morbidity and mortality in connective tissue diseases, characterized by an overproduction of inflammatory cytokines and induced fibrosis, resulting in respiratory failure. The etiology and pathogenesis of ILD remain incompletely understood. This study investigated whether treatment with CA-074Me, a specific inhibitor of CB, attenuates ILD in PM. CB expression, inflammation, and fibrosis were analyzed in the lung tissues from patients with PM/DM. The animal model of PM was induced in guinea pigs with Coxsackie virus B1 (CVB1). CA-074Me was given 24 h after CVB1 injection for 7 consecutive days. At the end of the experiment, the animals were killed and lung tissues were collected for the following analysis. Inflammation, fibrosis and apoptosis cells, and cytokines were assessed by histological examinations and immunohistochemical analyses, western blot analysis and transferase-mediated dUTP nick-end labeling assay. In patients with PM/DM, the protein levels of CB were significantly elevated in lung tissues compared with healthy controls, which correlated with increases in inflammation and fibrosis. Similarly, the expression of CB, inflammation and fibrosis, CD8+ T cell, CD68+ cell, tumor necrosis factor-alpha, transforming growth factor-beta1 infiltrations, and apoptotic cell death were significantly increased in lung tissues of the guinea-pig model of CVB1-induced PM. These changes were attenuated by the administration of CA-074Me. In conclusion, this study demonstrates that PM/DM increases CB expression in lung tissues and inhibition of CB reduces ILD in a guinea-pig model of CVB1-induced PM. This finding suggests that CB may be a potential therapeutic target for ILD. © 2015 USCAP, Inc All rights reserved. Source


Lou Y.,Clinical Pharmacology | Lu X.,Shanghai Pudong Gongli Hospital | Dang X.,University of California at San Diego
Gene Regulation and Systems Biology | Year: 2012

L-selectin plays important roles in lymphocyte homing and leukocyte rolling. Mounting evidence shows that it is involved in many disease entities including diabetes, ischemia/reperfusion injuries, inflammatory diseases, and tumor metastasis. Regulation of L-selectin at protein level has been well characterized. However, the regulation of human L-selectin transcription remains largely unknown. To address transcriptional regulation of L-selectin, we cloned 1088 bp 5′ of the start codon ATG. Luciferase analysis of the serial 5′ deletion mutants located the core promoter region at -288/-1. A major transcription initiation site was mapped at -115 by 5′RACE. Transcription factors Sp1, Ets1, Mzf1, Klf2, and Irf1 bind to and transactivate the L-selectin promoter. Significantly, FOXO1 binds to a FOXO1 motif, CCCTTTGG, at -87/-80, and transactivates the L-selectin promoter in a dose-dependent manner. Over-expression of a constitutive-active FOXO1 increased the endogenous L-selectin expression in Jurkat cells. We conclude that FOXO1 regulates L-selectin expression through targeting its promoter. © the author(s), publisher and licensee Libertas Academica Ltd. Source

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