Objective: To study the dynamic expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-3 p17 after ischemia/reperfusion (IR) in rates. Methods: Thirty male Wistar rats were divided into sham-operated, ischemia 1.5 hours and reperfusion for 6, 12, 24, 48 and 72 hours (n = 5 in each group). A model of reperfusion after 1.5 hours of focal cerebral ischemia was established with the suture method. The expression of XIAP and caspase-3p17 in brains were observed respectively by immunohistochemical method. Results: A small amount of XIAP-positive cells were observed in the non-ischemic side in the sham-operated and IR groups, but no caspase-3 p17 positive cells were observed. The XI-APpositive cells expression began to increase (P = 0. 00) at 6-hour reperfusion, it reached to the peak at 12 hours and began to decrease at 24 hours, and then it gradually returned to normal at 48 hours (P = 0.549) as compared with the sham-operated group; a small amount of caspase-3 p17 positive cells were observed at 6-hour reperfusion, they reached the peak at 24 hours and remained for 72 hours, and they were significantly more than those at 6 hours after reperfusion (P = 0.004). Conclusion: Focal cerebral ischemia may induce the expression of apoptosis-inhibiting gene XIAP and apoptosis-promoting gene caspase-3 p17 to increase transiently, and the peak time of the former expression is earlier than that of the latter.

Infected pancreatic necrosis (IPN) is a serious complication which may cause organ failure and death in patients with acute pancreatitis. Surgical debridement is an important therapeutic approach for IPN. With the development of evidence-based medicine, more and more high-level evidences emerge for surgical debridement of pancreatic necrosis tissue, and the traditional treatment strategy has also changed. In the era of minimally invasive surgery, whether 'delayed surgery' should still be executed and how to achieve 'delayed surgery' are the research hotspots in the treatment of IPN. Research evidences reveal that the 'step-up' strategy is not the best strategy for all IPN patients, and alternatives should be explored. In addition, the indications, advantages and disadvantages of open surgery, surgical minimally invasive surgery and endoscopic surgical debridement of pancreatic necrosis tissue have been widely discussed in recent years, and no consensus has yet been reached. At present, the personalized, multidisciplinary, and minimally invasive treatment of IPN is still the mainstream development direction. The authors investigate the timing and strategy of surgical treatment for IPN in order to provide theoretical basis for clinical practice.

Adult ; Brucellosis ; Humans ; Male ; Middle Aged ; Occupational Diseases

AIM: To investigate the repair mechanism associated with cholesterol synthesis regulated by silent information regulator 1 (SIRT1) in rat model of optic nerve damage.METHODS: Preparation of optic nerve damage in 70 rats was randomly divided into normal group (10 rats), resveratrol treatment group ( experimental group 30 rats) and PBS buffer control group ( 30 rats ) . The experimental group and control group was further divided into 3 subgroups ( each group 10 rats ) , respectively. After 7, 14, 21d injected resveratrol or PBS, optic nerve injury were observed, then the rats were sacrificed. Retina was segregated; the surviving retinal ganglion cell ( RGCs ) was counted. Dissection of optic nerve, cholesterol content of them were tested; RT-PCR was used to detect mRNA expression of SIRT1, SREBP2 and HMGCR; Western blot assay was used to test the protein expression levels of SIRT1, cholesterol regulatory element binding protein 2 (SREBP2) and HMGCR.
RESULTS:The numbers of RGCs and cholesterol levels of rat model with optic nerve injury decreased significantly (P<0. 01). The mRNA and protein expression levels of SIRT1, SREBP2 and HMGCR were all decreased in a time-dependent manner (P<0. 05). Three components of the three time points, with time injuries were aggravated, and the extent of damage was significantly reduced in the treatment group compared with the control group. But in resveratrol treatment group, the cholesterol levels and mRNA or protein expression of SIRT1, SREBP2, HMGCR in optic nerve were significantly restored in a time-dependent ( P<0.05 ) . The number of surviving RGCs restored significantly in resveratrol treatment group (P<0. 01) in a time-dependent manner.
CONCLUSION:Up-regulating the expression of SIRT1, SREBP2 and down- regulating HMGCR by resveratrol could repair the injury of optic nerve through promoting the synthesis of cholesterol in neurons and retinal ganglion cells in the repair process. SIRT1 may be as a promising new target for treatment on optic nerve damage.

AIM:To study the effect of integrin β1 on multidrug resistance in gastric cancer and its possible mechanisms .METHODS:The expression of integrin β1 at mRNA and protein levels in the SGC-7901 cells and SGC-7901/DDP cells was determined by qPCR and Western blot .The expression of integrin β1 in the SGC-7901/DDP cells was silenced by antisense oligodeoxynucleotide .The cell viability was detected by the CCK-8 assay, the cell apoptosis were ana-lyzed by flow cytometry, and the protein levels of integrin β1, Bcl-2/Bax, cleaved caspase-3/caspase-3, cytochrome C ( Cyt-C) and p-AKT/AKT were determined by Western blot .RESULTS:The expression of integrin β1 at both mRNA and protein levels was significantly upregulated in SGC-7901/DDP cells.The expression of integrin β1 was increased in SGC-7901 cells treated with chemotherapeutic agents such as cisplatin , paclitaxel and 5-fluorouracil .Knockdown of integrin β1 induced apoptosis of SGC-7901/DDP cells with an increased sensitivity to the chemotherapeutic agents .Meanwhile , knock-down of integrin β1 downregulated the protein levels of Bcl-2/Bax, p-AKTSer473 and p-AKTThr308 , while promoted the release of Cyt-C and upregulated the protein level of cleaved caspase-3.CONCLUSION:Knockdown of integrin β1 increases the sensitivity of SGC-7901/DDP cells to the chemotherapeutic agents , and promotes the cell apoptosis via mitochondrial apop-tosis pathway .The mechanism may be related to the attenuation of AKT pathway by inhibiting phosphorylations of AKT at Ser473 and Thr308.

Objective To analyze the methylation status and protein expression of Ras association domain family- 1A (RASSF1A) in endometriosis (EMS). Methods The ectopic and corresponding eutopic endometrium tissues were collected from 45 women with EMS and normal endometrium tissues of 20 women without EMS. The methylation status of RASSF1A was examined by methylation specific PCR (MSP). Immunohistochemistry was performed to measure the level of RASSF1A in endometrium tissues. Results The RASSF1A protein expression rate in ectopic endometrium, eutopic endometrium, and normal endometrium was 37.78%(17/45), 60.00%(27/45) and 85.00%(17/20), and there was significant difference (χ2 = 13.136, P = 0.001). The frequency of aberrant methylation of RASSF1A was 55.56%(25/45), 33.33%(15/45) and 0 in ectopic endometrium , eutopic endometrium, and normal endometrium, and there was significant difference (χ2 =18.770, P = 0.000). The frequency of aberrant methylation of RASSF1A had no significant differnce throughout the menstrual cycle in ectopic endometrium and eutopic endometrium: 66.67%(14/21) vs. 45.83%(11/24), 38.10%(8/21) vs. 29.17%(7/24), P>0.05. In ectopic endometrium, the frequency of aberrant methylation of RASSF1A inⅢ-Ⅲstage was significantly higher than that in Ⅰ-Ⅱstage (χ2=5.940, P=0.015). In ectopic endometrium and eutopic endometrium, the RASSF1A protein expression had negative correlation with aberrant methylation of RASSF1A (r =- 0.594、- 0.577, P<0.01). Conclusions Epigenetic inactivation of RASSF1A through aberrant promoter methylation may be strongly correlated with the formation and progression of EMS, and assessment of RASSF1A methylation status in eutopic endometrium may be a potentially useful biomarker to enhance the early detection of EMS.

Objective To investigate the prevalence rates of healthcare-associated infection (HAI)and antimicrobial use in a hospital in 2011-2013,and provide scientific basis for prevention and control of HAI.Methods HAI prevalence rates and antimicrobial use in a hospital in 2011-2013 were investigated by combination of bedside visiting and medical records reviewing.Results A total of 3 011 patients were investigated during three years,the prevalence rates were 3.49%, 2.87% and 3.98% respectively,difference of prevalence rates during three years were not significantly different (χ2 =2.105,P =0.356).Among HAI sites,lower respiratory tract ranked first,the major pathogens were gram-negative bacil-li,constituent ratios of different pathogens were not significantly different among three years(χ2 =1.003,P =0.972);anti-microbial usage rates and specimen detection rates among 3 years were both significantly different(χ2 =12.569,P <0.01;χ2=6.758,P <0.01,respectively),antimicrobial usage rate was highest in 2011(63.40%),and specimen detection rate was highest in 2012(62.14%).Conclusion Point prevalence rate in this hospital is at average national level,antimicrobial usage rate decreased, the consciousness of pathogenic detection gradually enhanced,clinical application management of antimicrobial agents still needs to be strengthened continuously.

Objective To investigate the inhibitory effect of DHA and its mechanism of apoptosis induced by DHA on human gastric cancer cell SGC-7901.Methods The survival rate of tumor cells was evaluated by MTT assay,cell morphology of apoptotic cell was observed with Hoechest 33258 staining.The contents of MDA and GSH were measured respectively by TBA and DTNB assay.Flow cytometry was used to detect the rate of apoptotic cell and intracellular variation of ROS level.Results After being treated with different concentrations of DHA,the survival rate of tumor cells was decreased in a dose-dependent manner and apoptosis was induced.The morphological characterizes of apoptotic cells were chromatin condensation and formation of apoptotic bodies.Intracellular MDA content was increased in the treated cells compared with control group,whereas GSH was decreased.After treated with 80 ?mol?L-1 DHA 5 h,flow cytometic analysis showed ROS peak and NAC could block the generation of ROS.Conclusion DHA can inhibit the growth of human gastric cancer cell SGC-7901 via inducing apoptosis.The increase of lipid peroxidation production and ROS may play an important role in apoptosis of the cells.

Objective: To evaluate the relationship between air pollutants and mortality of residents in Huairou District, Beijing, providing a basis for the formulation of air pollution control measures. Methods : The data of daily deaths, meteorological factors and air pollutants in Huairou District from 2014 to 2018 were collected from Beijing Disease Prevention Monitoring Information Integration and Analysis System, Huairou Meteorological Bureau and Environmental Monitoring Station. The generalized additive models were used to analyze the relationship between the average daily concentration of air pollutants and the daily deaths. Results: The medians of daily average concentrations of SO2, NO2, CO, O3, PM10 and PM2.5 were 5.00 μg/m3, 24.00 μg/m3, 0.71 mg/m3, 77.27 μg/m3, 64.25 μg/m3 and 44.13 μg/m3, respectively. Except for O3, the daily average concentrations of SO2, NO2, CO, PM10 and PM2.5 showed decreasing trends from 2014 to 2018. An increase of 10 μg/m3 of NO2 resulted in an elevation of 1.69% ( 95%CI: 0.31%-3.08% ) , 3.31% ( 95%CI: 1.24%-5.42% ) and 3.31% ( 95%CI: 0.51%-6.19% ) for non-accidental death in the whole population, females and people under 65 years old, respectively, with a delay of 2 days (lag2). For every 10 μg/m3 increase in the daily average concentrations of CO and PM2.5, the risk of non-accidental death among people under 65 years old at lag2 increased by 0.08% ( 95%CI: 0.01%-0.14% ) and 0.88% ( 95%CI: 0.12%-1.64% ) , respectively. For every 10 μg/m3 increase in daily average concentration of O3, there was 0.69% ( 95%CI: 0.02%-1.36% ) increase in daily male non-accidental death risk at lag4. The results of the multi-pollutant model showed that after adjusting the effects of the other two air pollutants, NO2, CO and PM2.5 had no statistically significant effects on the daily non-accidental deaths of people under 65 years old at lag2 ( P>0.05 ) . Conclusion The ambient NO2, CO, O3 and PM2.5 pollution increase daily non-accidental deaths, which shows a lag effect．

Objective To study the relationship between long-term high-salt water and the morbidity mechanism of chronic atrophic gastritis (CAG), The expression of HSP60 and ras protein were detected in the gastric mucosa of CAG rates induced by high-salt water.Methods The atrophic gastritis rat model was made by high-salt-hot water perfusion and the ultrastructure of gastric mucosa was observed by Laser Scanning ConfocaI Microscopy. Results There was no expression in gastric mucosa in normal group. The expression of HSP60 and ras was observed in the cell plasm of rats at 12 weeks. The higher expression was observed in the rats at 24, 32 and 65 weeks. Using laser scanning confocaI microscopy and immunofluorescence technique had observed coexistence of HSP60 and ras.Conclusion Long time high-salt-hot water can induce CAG and increasing the expression of HSP60 and ras. HSP60 and ras play an important role in the formation of atrophic gastritis.