Acute pancreatitis (AP) is activated trypsin-induced pancreatic and its peripheral tissue inflammation caused by their own digestion.The activation in advance of trypsinogen and the inflammation cascade in pancreatic acinar cells are thought to be a key mechanism of the onset and development of AP.Autophagy pathway acting as Ⅱ type of programmed cell death occurs in the early pathological course of AP,blockade of which contributes to aggravating necrosis of acinar cells in AP.This article mainly discussed the recent advances in the understanding of autophagy researches and its function in the mechanism of AP.

OBJECTIVETo investigate in vivo survival of retinal ganglion cells (RGCs) after partial blockage of optic nerve (ON) axoplasmic flow by sub-retinal space or vitreous cavity injection of brain-derived neural factor (BDNF) produced by genetically modified neural progenitor cells (NPCs).

METHODSAdult Sprague-Dawley (SD) rat RGCs were labeled with granular blue (GB) applied to their main targets in the brain. Seven days later, the left ON was intra-obitally crushed with a 40 g power forceps to partially block ON axoplasmic flow. Animals were randomized to three groups. The left eye of each rat received a sham injection, NPCs injection or an injection of genetically modified neural progenitors producing BDNF (BDNF-NPCs). Seven, 15 and 30 days after ON crush, retinas were examined under a fluorescence microscope. By calculating and comparing the average RGCs densities and RGC apoptosis density, RGC survival was estimated and the neuro-protective effect of transplanted cells was evaluated.

RESULTSSeven, 15 and 30 days after crush, in the intra-vitreous injection group, mean RGC densities had decreased to 1885 +/- 68, 1562 +/- 20, 1380 +/- 7 and 1837 +/- 46, 1561 +/- 58, 1370 +/- 16, respectively with sham injection or neural progenitors injection. However, RGCs density in the groups treated with intra-vitreous injection of BDNF-NPC was 2101 +/- 15, 1809 +/- 19 and 1625 +/- 34. Similar results were found in groups after sub-retinal injection. Higher densities were observed in groups treated with BDNF-NPCs. There were statistically significant differences among groups through nonparametric tests followed by the Mann-Whitely test. RGC apoptosis density in BDNF-NPC at each follow-up time was less than in other groups.

CONCLUSIONSA continuous supply of neurotrophic factors by the injection of genetically modified neural progenitors presents a highly effective approach to counteract optic neuropathy and RGC degeneration after partial ON axoplasmic flow blockage.

Animals ; Apoptosis ; Axonal Transport ; Brain-Derived Neurotrophic Factor ; genetics ; Cell Survival ; Gene Transfer Techniques ; Genetic Therapy ; Glaucoma ; therapy ; Male ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells ; cytology ; Stem Cells ; physiology ; Vitreous Body ; metabolism

Objective To investigate the role and mechanism of inflammatory response of Kupffer cells induced by Chemerin in the progression of non-alcoholic fatty liver disease (NAFLD) in mice.Methods Wortmannin was used to treated on KCs which pre-treated with Chemerin in vitro for two hours,and treated on C57BL/6J mice which was fed with a high-fat die.Levels of cytokines in supernatant/serum were tested by enzyme-linked immunosorbent assays(ELISA);mRNA and protein levels of KCs' Chemokine-like receptor 1 (CMKLR) and nucleotide oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) in vivo and vitrowere detected by real time polymerase chain reaction(real time-PCR) and Western blot;changes of mouse weight were recorded;insulin resistance and glucose tolerance were detected;the severity of liver steatosis was evaluated by HE staining combined with NAS score.Results The levels of interleukin 1β (IL-1β) and IL-18 in the KCs and mice treated with wortmannin were significantly lower than the KCs treated with Chemerin only and mice fed with high fat diet only.The mRNA and protein levels of CMKLR1 and inflammasome 3 (NLRP3) were significantly lower in the KCs and mice treated with Wortmannin than the KCs treated with Chemerin only and mice fed with high fat diet only.In addition,changes in mouse weight,hepatic steatosis,liver function,insulin resistance and glucose tolerance were much milder in mice treated with Wortmannin than those mice fed with high fat diet.Conclusion Wortmannin alleviates liver steatosis and inflammation mediated by KCs via down-regulating the expression of CMKLR1 and NLRP3 in high fat diet fed mice.

Objective To compare the effects of different anesthesia techniques on early prognosis in patients undergoing hip joint replacement. Methods The demographic, preoperative and postoperative data of 478 patients, aged 18-95 yr, of American Society of Anesthesiologists physical statusⅠ-Ⅳ, who underwent elective unilateral hip joint replacement in Tongji Hospital from May 2014 to December 2016, were retrospectively analyzed. Patients were divided into general anesthesia group (group GA, n=197), peripheral nerve block group ( group PNB, n=147) and peripheral nerve block combined with general an-esthesia group ( group PNB+GA, n=134) . The amount of crystalloid solution and colloid solution infused, consumption of sufentanil and requirement for vasoactive agents were recorded during operation. The dura-tion of anesthetic recovery room stay, length of hospital stay before and after operation and total length of hospital stay were recorded. The development of complications within 48 h after operation, therapy after ad-mission to intensive care unit and in-hospital fatality were also recorded. Results Compared with group GA, the intraoperative consumption of sufentanil was significantly decreased in group PNB+GA, and the a-mount of crystalloid solution infused, urine output, consumption of sufentanil, requirement for vasoactive agents and incidence of postoperative hypoxemia, pulmonary infection and acute cerebral infarction were significantly decreased in group PNB+GA ( P<0. 05) . Compared with group PNB+GA, the consumption of sufentanil, requirement for vasoactive agents and incidence of postoperative hypoxemia, pulmonary infec-tion and acute cerebral infarction were significantly decreased in group PNB (P<0. 05). Conclusion Compared with general anesthesia or with peripheral nerve block-general anesthesia, peripheral nerve block is more helpful in improving early prognosis in patients undergoing hip joint replacement.

Objective:To investigate the effects of poly adenosine diphosphate ribose polymerase-1(PARP-1) inhibitor fluzoparib on proliferation, apoptosis and migration of pancreatic cancer PANC1 cells.Methods:PANC1 cells cultured in conventional culture medium were used as control group, and PANC1 cells cultured in the medium containing fluzoparib were used as fluzoparib group. The effects of fluzoparib with different concentrations on the proliferation of PANC1 cells were detected by CCK8 method, and the half inhibitory concentration (IC 50) of fluzoparib on PANC1 cells was calculated. The effect of fluzoparib on apoptosis and cell cycle of PANC1 cells was detected by flow cytometry, and the migration ability of PANC1 cells was detected by cell scratch test and Transwell chamber. Results:Compared with control group, with the increase of fluzoparib concentration and the prolongation of the action time, the cell proliferation activity of PANC1 in fluzoparib group was significantly decreased, and the differences were statistically significant (all P values <0.05). IC 50 of fluzoparib on PANC1 cells cultured for 24 h was 0.03 mmol/L. After 24 h culture, the IC 50 apoptosis rate of fluzoparib group was (32.19±2.48)%, and the apoptosis rate of control group was (21.99±6.30)%. The former was greatly higher than the latter, and the difference was statistically significant ( P<0.05). The proportion of cells in G 2/M phase was (16.28±0.62)% in the fluzoparib group and (11.64±0.88)% in the control group, and the difference between the two groups was statistically significant ( P<0.05). The migration rates of PANC1 cells in IC 50 fluzoparib group in 12 h and 24 h culture were (2.59±1.46)% and (19.76±7.84)%; and those in control group were (27.08±2.17)% and (45.92±3.61)%, respectively. The number of transmembrane cells was (348±19) cells/10 visual field in the fluzoparib group and (587±14) cells/10 visual field in the control group. The migration ability of PANC1 cells in fluzoparib group was significantly lower than that in control group ( P<0.05). Conclusions:Fluzoparib can inhibit the proliferation and migration of PANC1 cells and promote the apoptosis of PANC1 in vitro, which may be an effective drug for the treatment of pancreatic cancer.