Renji Hospital

About: Renji Hospital is a healthcare organization based out in Shanghai, China. It is known for research contribution in the topics: Medicine & Biology. The organization has 1112 authors who have published 714 publications receiving 15442 citations. The organization is also known as: Rénjì Yīyuàn.

Helicobacter pylori “test-and-treat” strategy is not suitable for the management of patients with uninvestigated dyspepsia in Shanghai

Abstract: Objective. The safety of Helicobacter pylori “test-and-treat” and “test-and-endoscopy” strategies for the management of young patients with uninvestigated dyspepsia has not been evaluated in Shanghai. Material and methods. A total of 14,101 consecutive patients with dyspepsia receiving endoscopy in our hospital from October 2002 to December 2003 were retrospectively studied. The detection rates of esophageal or gastroduodenal malignancies and alarm symptoms were investigated, and H. pylori status was assessed. Results. A total of 202 (1.4%) gastrointestinal (GI) malignancies were found, including 162 cases (1.15%) of gastric cancer, 4 of gastric lymphoma, 35 (0.25%) of esophageal cancer and 1 case of duodenal cancer. Among those patients with GI malignancies, 99 (49.0%) were infected with H. pylori and 108 (53.5%) presented with alarm symptoms. Eighteen patients (0.46%, 18/3952) under 45 years of age were diagnosed as having gastric cancer. Of these patients, 5 (27.8%) presented with alarm symptoms and 13...

Bactericidal and Morphological Effects of NE-2001, a Novel Synthetic Agent Directed against Helicobacter pylori

Abstract: The antibacterial activities of NE-2001 were tested against 24 clinical isolates of Helicobacter pylori and compared with those of amoxicillin, clarithromycin, metronidazole, and furazolidone. The MIC50 and MIC90 of this synthetic compound on the isolates were 8 and 16 μg/ml, respectively. This action was highly selective against Helicobacter pylori; there was a >4-fold difference between the concentration of NE-2001 required to inhibit the growth of Helicobacter pylori and that required to inhibit the growth of common aerobic and anaerobic bacteria. Exposure of Helicobacter pylori (ATCC43504) to NE-2001 at the MIC (4 μg/ml), or at a greater concentration, resulted in an extensive loss of viability. The phenomenon was also observed at pH levels between 3.0 and 7.0. When two clinical Helicobacter pylori strains were successively cultured at subinhibitory concentrations of NE-2001, no significant changes in the bactericidal effects were found. The morphological alterations of Helicobacter pylori cells (ATCC43504), exposed to NE-2001 at various concentrations for 6 h, were observed using transmission electron microcopy. The bacterium displayed features such as swelling, vacuole-like structures in the cytoplasm, and cell destruction following exposure to NE-2001. The efficacy of NE-2001 was maintained when evaluated in eight clinical isolates resistant to metronidazole and five isolates resistant to both metronidazole and clarithromycin (MIC ranging between 4 and 16 μg/ml). The above-described results suggest that NE-2001 may have the potential to be developed as a candidate agent for the treatment of Helicobacter pylori infection.

Neuroprotective properties of vitamin C on equipotent anesthetic concentrations of desflurane, isoflurane, or sevoflurane in high fat diet fed neonatal mice.

Abstract: Obesity has been reported to be one of the significant contributors to various chronic disease conditions. Childhood obesity has been on an alarming increase over recent years leading to various health complications. Millions of children undergo surgery each year as a part of medical care on various health grounds. In the present study, influence of vitamin C on the effect of obesity and over-weight under anaesthetic exposure was analysed. Separate groups of neonatal mice (C57BL/6) were fed on high-fat diet to induce obesity. The mice were administered with vitamin C at 30 and 60 mg/kg b.wt post natal day 1 (P1) to P21. P7 mice were exposed to equipotent doses of isoflurane or sevoflurane or desflurane. Neuroapoptosis was assessed by measuring activated caspase-3 and TUNEL assay. Plasma S100β levels were detected by ELISA. The mice were assessed for their general behaviour. Morris water maze test was performed to assess the spatial working memory. Anesthesia exposure caused severe neuroapoptosis and also raised the levels of plasma S100β. Neuroapotosis, working memory and learning impairments observed following anesthetics were comparatively more profound on high fat diet fed mice. Desflurane exposure resulted in higher apoptotic counts, learning and memory deficits than equipotent dose of isoflurane and sevoflurane. Vitamin C supplementation offered significant protection against anesthetic induced neurotoxicity and behavioural alterations. Vitamin C administration resulted in marked reduction in neurotoxicity induced by anesthesia and as well improved learning and memory of both normal and high fat diet fed mice.

Targeting mTORC2 component rictor inhibits cell proliferation and promotes apoptosis in gastric cancer.

Abstract: The mammalian target of rapamycin (mTOR) kinase acts downstream of phosphoinositide 3-kinase/Akt and plays an important role in tumor growth and progression of gastric cancer. It is well characterized that mTOR complex1 (mTORC1) controls cell metabolism and proliferation, whereas the contribution of mTOR complex2 (mTORC2) and its key component, Rictor, remains poorly understood. Therefore, we investigated clinical significance of Rictor expression by immunohistochemical analysis of 391 tissue samples from gastric cancer patients. In addition, the roles of Rictor in cell proliferation, apoptosis, migration and invasion in vitro were evaluated by RNA interference. The results showed that over expression of Rictor was associated with increased tumor size, depth of tumor invasion, lymph node metastasis and advanced TNM stage, together with poorer overall and relapse-free survival. Stable sh-RNA mediated down-regulation of Rictor significantly inhibited SGC7901 and MGC803 gastric cancer cells proliferation, migration and invasion. Furthermore, Rictor knockdown attenuated cell cycle progression and enhanced apoptosis, synergistic with treatment of mTORC1 inhibitor rapamycin owing to abrogating the feedback activation of Akt. Our findings identify Rictor as an important mediator of tumor progression and metastasis, providing the rationale for targeting both mTORC1 and mTORC2 as part of therapeutic strategy for gastric cancer.