54 results match your criteria: "Zhengzhou University School of Medicine[Affiliation]"
Hepatobiliary Pancreat Dis Int
June 2011
Department of General Surgery, First Affiliated Hospital, Zhengzhou University School of Medicine, Zhengzhou 450052, China.
Background: The development of collaterals in Budd-Chiari syndrome has been described and these collaterals play an important role in the presentation of this disease. These collaterals are diagnostic and their use in management strategy has never been evaluated. This study aimed to investigate the indications, feasibility and necessity of invasive treatment for patients with Budd-Chiari syndrome and to determine whether such a strategy is necessary for optimal management.
View Article and Find Full Text PDFCancer Lett
August 2011
Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, No. 197, Ruijin Er Road, Shanghai 200025, China. Electronic address:
Angiotensin-converting enzyme 2 (ACE2) is a novel component of the renin-angiotensin system that could counterbalance the growth-promoting function of angiotensin-converting enzyme (ACE). Our previous results have shown that ACE2 is lowly expressed in pancreas, and widely down-regulated in pancreatic cancer tissues and cells. In the present study, we investigated the effect of restoration of ACE2 expression on the growth of pancreatic cancer.
View Article and Find Full Text PDFImmunol Invest
January 2009
Department of Gastroenterology, Zhengzhou University School of Medicine, Zhengzhou, China.
Skewed Th2 polarization and tissue mastocytosis are the main features of allergy; but how the antigen-specific Th2 polarization initiated remains unclear. The present study shows that cholera toxin (CT) activates mouse bone marrow mast cells (BMMC) to release interleukin (IL)-4. The activation process involved in Toll-like receptor 4, nucleotide oligomerisation domain 1, activate signal transducer and activator of transcription 6 (STAT6), and IL-4.
View Article and Find Full Text PDFAm J Clin Pathol
August 2005
Department of Pathology, Zhengzhou University School of Medicine, Henan, China.
Overexpression of decoy receptor (DcR) 3 protein, a recently discovered member of the tumor necrosis factor receptor superfamily, was examined in 40 esophagogastrectomy specimens containing areas of Barrett esophagus (n = 27), low-grade dysplasia (n = 27), high-grade dysplasia or carcinoma in situ (n = 22), and esophageal adenocarcinoma (EAC; n = 28) with immunohistochemical analysis. The results revealed significantly more overexpression of DcR3 in high-grade dysplasia or carcinoma in situ and EAC than in benign esophageal mucosa (both P < .0001), Barrett esophagus (both P < .
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