Objective To investigate the efficacy of intravenous antioxidants therapy in treating moderately severe acute pancreatitis (MSAP) and severe acute pancreatitis (SAP).Methods Pubmed,Embase,Cochrane library and CNKI databases for all randomized control trials published before March 18st,2016 manually was searched by computer.Data on AP associated mortality and length of stay (LOS) were collected.The quality of the trials included was assessed by the Cochrane systematic review method.Results Fifteen trials with data of 620 patients were eligible for final inclusion.Among the 15 trials,detailed randomization for grouping was clearly described in 5 studies and obvious bias was observed in 1 study.Three studies had obvious biases considering whether outcome assessment was blinded,outcome data was incomplete and outcome report was selective.No other apparent bias was found.Statistical analysis showed that compared with control group,intravenous antioxidants administration did not significantly reduce mortality (12.1 vs 9.7,RD=-0.02,95％ CI-0.08～-0.03,P=0.44;RR=0.83.95％ CI0.51～ 1.34,P=0.44),but could shorten LOS (MD=-2.02;95％ CI-4.00～-0.05;P=0.04).Conclusions Intravenous antioxidants could greatly shorten LOS of patients with MSAP and SAP.

AIM: To determine the relationship between the mutation of the RII gene and RER status in the tumorigenesis of sporadic colorectal cancer. METHODS: We screened RER status and mutation of the RII gene from 50 sporadic colorectal cancers (19 in the proximal colon, 31 in the distal colorectum). RESULTS: RER was found in 13 cases (8 in the proximal colon, 5 in the distal colorectum), and 5 of them showed mutations of the RII gene. All 5 cancers carrying a TGF-? RII gene mutation showed RER+, but there wasn't any mutation of RII gene in RER(-) cases. Four of 5 RII mutation were located at the cecum. CONCLUSION: These data indicate that the TGF-? RII gene is a major target of microsatellite instability and mutation of the RII gene play an important role in carcinogenesis of sporadic colorectal cancer with microsatellite instability, especially at the cecum. [

The idea of establishing Shanghai Academy of Medical Sciences was brought forward　in the background of great external changes.It was to meet the demand for resolving all kinds of　conflicts about researches arised from the long time operation of Medical Institutes in Shanghai.This　article mainly discusses about the necessity and plans for establishing Shanghai Academy of Medical　Sciences.

Medical research institutions in Shanghai have been developing in at a slow pace because of problems such as out of date institution structures, unreasonable resource allocation and distribution,shortage of research resources, insufficient creativity, and unfocused effort and investment. Hence reform is the only way out. This research discussed the possible strategies for development and proposed some suggestions on the institution categorization, structure change, allocation of resource and overall arrangement.

One hundred and ten patients with primary hepatocellular carcinoma underwent hepatectomy from 2005 to 2010.Different methods of hepatic exclusion were applied in the surgery,including 54 patients with total hepatic vascular exclusion,22 with half hepatic vascular exclusion and 34 with regional hepatic vascular exclusion.The recovery of postoperative liver function was retrospectively analyzed.The results showed that the postoperative liver function of regional hepatic vascular exclusion [ALT(311 ± 80) U/L,total bilirubin (TB) (22.2 ± 8.3) μmoL/L at 1 st day and ALT (58 ± 17) U/L,TB (11.3 ± 3.1)μmol/L at 7th day] was better than that of total hepatic vascular exclusion [ALT(874 ±299)U/L,TB (42.9± 19.1) μmol/L at 1st day (P＜0.05) and ALT (108-±52)U/L,TB (14.6±9.2) μmol/L at 7th day] (P ＜ 0.05,＞ 0.05),indicating that regional hepatic vascular exclusion can effectively reduce hepatic injury during the operation and promote recovery of liver function after operation.

The latest definition of sepsis (Sepsis-3) is the life-threatening organ dysfunction due to overreaction of immune system caused by infection. The situation can develop into multiple organ dysfunction syndromes (MODS). In the pathological process of pathogen invasion, a large number of inflammatory factors directly damage organ function, while dysfunction of coagulation system is also involved in this process. With the overreaction of inflammation, disseminated intravascular coagulation (DIC) occurred, which further exacerbated organ damage. As excessive inflammation and coagulation disorders are mutually reinforced, the clearance of pathogenic microorganisms and the control of inflammatory reactions cannot effectively improve the sepsis caused by MODS. As a clinically readily available anticoagulant, heparin is widely used in a variety of severe situations caused by DIC, thromboembolic disease and some invasive procedure for anticoagulant treatment. In recent years, domestic and foreign studies have found that heparin has a certain anti-inflammatory effect, which can reduce the incidence of DIC, improve sepsis patients with microcirculation and MODS, reduce 28-day mortality. However, there is controversy in its effectiveness and safety. Therefore, the application of heparin in the treatment of sepsis need to be further defined and discussed.

Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN).AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.