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Wu H.,Chinese PLA General Hospital | Jing Q.,Shenyang General Hospital of PLA | Wang J.,Chinese PLA General Hospital | Guo X.,Chinese PLA General Hospital
Journal of Critical Care | Year: 2011

Purpose: The aim of this study is to evaluate the preventive effect of proton pump inhibitors on gastrointestinal (GI) bleeding in patients with acute coronary syndromes (ACS) who are at high risk for GI bleeding. Materials and Methods: We enrolled 665 patients with ACS who had one or more of the following risk factors for GI bleeding: 75 years of age or older, history of peptic ulcer disease, history of GI bleeding, cardiogenic shock, and chronic renal dysfunction (serum creatinine, >2 mg/dL). Patients were randomly assigned to receive 40 mg of pantoprazole or placebo twice daily for 7 days, in addition to standard treatment of ACS. The primary end point was the occurrence of GI bleeding during hospitalization. Results: During a median time of hospitalization of 12 days, 12 (3.6%) of 332 patients in the placebo group had an occurrence of GI bleeding, as compared with 4 (1.2%) of the 333 patients in the pantoprazole group (P =.046, Fisher exact test). The log-rank test showed a significant difference between the 2 groups in the time to the occurrence of GI bleeding (P =.015). Major GI bleeding occurred in 5 (1.5%) patients in the placebo group but only in 1 (0.3%) in the pantoprazole group (P =.12). Pneumonia developed in 22 (6.6%) patients in the placebo group and 24 (7.2%) in the pantoprazole group (- 2 = 0.077, P =.88). The 30-day mortality was 10.2% (34/332) in the placebo group and 10.5% (35/333) in the pantoprazole group. Conclusions: In patients with ACS who are at high risk for GI hemorrhage, prophylactic treatment with pantoprazole could reduce the risk of GI bleeding with no significant effects on the incidence of hospital-acquired pneumonia and 30-day mortality. © 2011 Elsevier Inc.

Wu C.-Y.,PLA Fourth Military Medical University | Yan J.,Beijing Institute of Radiation Medicine | Yang Y.-F.,Beijing Institute of Radiation Medicine | Xiao F.-J.,Beijing Institute of Radiation Medicine | And 5 more authors.
Biochemical and Biophysical Research Communications | Year: 2011

KAI1, a metastasis-suppressor gene belonging to the tetraspanin family, is known to inhibit cancer metastasis without affecting the primary tumorigenicity by inhibiting the epidermal growth factor (EGF) signaling pathway. Recent studies have shown that hypoxic conditions of solid tumors induce high-level autophagy and KAI1 expression. However, the relationship between autophagy and KAI1 remains unclear. By using transmission electron microscopy, confocal microscopy, and Western blotting, we found that KAI1 can induce autophagy in a dose- and time-dependent manner in the human pancreatic cell line MiaPaCa-2. KAI1-induced autophagy was confirmed by the expression of autophagy-related proteins LC3 and Beclin 1. KAI1 induces autophagy through phosphorylation of extracellular signal-related kinases rather than that of AKT. KAI1-induced autophagy protects MiaPaCa-2 cells from apoptosis and proliferation inhibition partially through the downregulation of poly [adenosine diphosphate (ADP)-ribose] polymerase (PARP) cleavage and caspase-3 activation. © 2010 Elsevier Inc.

Li X.,Shenyang General Hospital of PLA | Yan J.,Chinese PLA General Hospital | Wang L.,Beijing Institute of Radiation Medicine | Xiao F.,Beijing Institute of Radiation Medicine | And 3 more authors.
Cancer Cell International | Year: 2013

Background: Beclin1 is a well-known key regulator of autophagy, which is also a haploinsufficient tumor suppressor. Current studies revealed that down-regulation or monoallelic deletions of Beclin1 were frequently found in various cancers. The purpose of this study was to investigate the effects of Beclin1 inhibition on autophagy and Gemcitabine-induced apoptosis of pancreatic cancer cells.Methods: Beclin1 expression was inhibited by siRNA transduction and gene expression was determined by Real-time PCR and Western blot. The effects of Beclin1 inhibition on autophagy and Gemcitabine-induced apoptosis of Miapaca2 cells were analyed through LC3 expression, cell viability, cell cycle and apoptosis by using Western blot.Results: We observed that Beclin1 silence promoted microtubule-associated protein 1 light chain 3-II (LC3-II) protein formation and increased punctate fluorescent signals in Miapaca2 cells transfected with green fluorescent protein (GFP)-tagged LC3. Beclin1 inhibition showed a greater suppressive effect on Gemcitabine-induced apoptosis of Miapaca2 cells.Conclusion: Our data suggested that Beclin1 silence not only up-adjusted autophagy process, but also played an important role in the regulation of apoptosis. Beclin1 inhibition could inhibit apoptosis signaling induced by Gemcitabine in Miapaca2 cells. © 2013 Li et al.; licensee BioMed Central Ltd.

Liu X.,PLA Fourth Military Medical University | Guo X.-Z.,Shenyang General Hospital of PLA | Zhang W.-W.,Shenyang General Hospital of PLA | Lu Z.-Z.,Beijing Institute of Radiation Medicine | And 3 more authors.
Hepatobiliary and Pancreatic Diseases International | Year: 2011

BACKGROUND: KAI1/CD82 has been reported to attenuate the process of metastases in a variety of tumors; however, its mechanism of action in invasion has not been fully elucidated. The present study aimed to investigate the importance of KAI1 in invasion and its correlation with activation of sphingosine kinase (SPK) in human pancreatic cancer PANC1 and Miapaca-2 cell lines. METHODS: The expression of KAI1 in PANC1 and Miapaca-2 cells, which was mediated by recombinant adenovirus (Ad-KAI1), was assessed by a flow cytometer and Western blotting. After successful infection was established, in vitro growth curve and invasive ability in Boyden Chamber assay were studied. The presence of KAI1 correlating with c-Met and SPK was detected by co-immunoprecipitation and [γ-32P] ATP incorporation. RESULTS: KAI1 genes had no significant effects on the curve representing cell growth. After infection with the KAI1 gene, decreased invasive ability in the Boyden Chamber assay was observed in PANC1 and Miapaca-2 cells that were induced by hepatocyte growth factor. Over-expression of KAI1 in the cells led to the deactivation of SPK and a decreased level of intracellular sphingosine-1-phosphate. No correlation was observed between c-Met and KAI1 during co-immunoprecipitation. CONCLUSION: The results of this study for the first time demonstrated a regulatory role for KAI1 in SPK activation, which leads to decreased invasive ability in disease progression of human pancreatic cancer. © 2011, Hepatobiliary Pancreat Dis Int.

Xu W.,251st Hospital of PLA | Qi X.,Shenyang General Hospital of PLA | Chen J.,Shenyang General Hospital of PLA | Su C.,PLA Fourth Military Medical University | Guo X.,Shenyang General Hospital of PLA
Gastroenterology Research and Practice | Year: 2015

Splanchnic vein thrombosis (SVT) may be negatively associated with the prognosis of pancreatitis. We performed a systematic review and meta-analysis of literatures to explore the prevalence of SVT in pancreatitis. All observational studies regarding the prevalence of SVT in pancreatitis were identified via PubMed and EMBASE databases. The prevalence of SVT was pooled in the total of patients with pancreatitis. And it was also pooled in the subgroup analyses according to the stage and causes of pancreatitis, location of SVT, and regions where the studies were performed. After the review of 714 studies, 44 studies fulfilled the inclusion criteria. Meta-analyses showed a pooled prevalence of SVT of 13.6% in pancreatitis. According to the stage of pancreatitis, the pooled prevalence of SVT was 16.6% and 11.6% in patients with acute and chronic pancreatitis, respectively. According to the causes of pancreatitis, the pooled prevalence of SVT was 12.2% and 14.6% in patients with hereditary and autoimmune pancreatitis. According to the location of SVT, the pooled prevalence of portal vein, splenic vein, and mesenteric vein thrombosis was 6.2%, 11.2%, and 2.7% in pancreatitis. The prevalence of SVT in pancreatitis was 16.9%, 11.5%, and 8.5% in Europe, America, and Asia, respectively. © 2015 Wenda Xu et al.

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