To realize dynamic and standardized periodical quality control of medical equipment. A set of auto reminder module for medical equipment quality control was established by using the user-defined flow of medical equipment operation maintenance system, and the continuous improvement was realized for medical equipment quality control in some hospital. Dynamic medical equipment quality control was formed from the static one, so that the efficiency of medical equipment quality control was enhanced greatly. References were provided for other hospitals in dynamic and informatzied medical equipment quality control and testing.

It is possible for microbial infection (including parasitic infection) to disrupt the balance of autoimmune tolerance,result in the dysfunction of immune system,and make the organism encountered with the attack of the autoimmune disease.As one of the common places between foreign antigens and autoantigens,molecular mimicry is believed to play a vital role in the pathogenesis of autoimmune diseases.However,a large number of studies suggest that rather than inducing various symptoms of autoimmune diseases,many infection of microorganisms covered with mimic peptide of the autoantigen may even protect the infected organism from the disease at the level of antibodies or T cells when the analogous antigen invaded again.The present paper reviews the possible prognosis after microbial infection based on molecular mimicry.

Tumor necrosis factor-α (TNF-α) is a key molecule of the inflammatory response, and plays a significant role in regulating cell survival and death.Many studies demonstrate that TNF-α may be implicated in the pathogenesis of various inflammatory conditions.Inhibiting the activity of TNF-α can dramatically improve the manifestations of many diseases.This review introduced the structural and functional characters of TNF-α and its receptors, and then summarized the regulating mechanisms TNF-α on cell survival、apoptosis and necroptosis.Besides, combining with the newly achievements of clinical and fundamental researches, this review analyzed the connections between TNF-α and common disorders in ophthalmology, such as the inflammation of retina and cornea, choroidal neovascularization, and summarized the clinical application and efficacy of infliximab, TNF-α monoclonal antibody.This review may provide references for the treatment of inflammatory diseases in ophthalmology and scientific researches in the future.

Objective To establish the apoptosis model in mouse cone cell line 661W cells and to investigate the viability of 661W cells in the conditions of different levels of autophagy.Methods Different concentrations of anti-Fas antibody were added to establish the apoptosis model of 661W cells,the expression of caspase-3 was detected by Western blot and the appropriate concentration of anti-Fas antibody was screened.Different concentrations of the autophagy inhibitor 3-methyladenine (3-MA) or autophagy inducer rapamycin were added to inhibit or induce autophagy,the expression of microtubule-associated protein 1 light chain 3 (LC-3) Ⅱ/LC-3 Ⅰ were detected by Western blot and the appropriate concentrations were also screened.The cultured cells were divided into 6 groups:control group,simple 3-MA group,simple rapamycin group,model group,model + 3-MA group and model + rapamycin group.Western blot was adopted to detect the expression of caspase-3,caspase-8,autophagy related genes 5 (Atg-5) and LC-3 Ⅱ/LC-3 Ⅰ at 0 hour,3,6,12,24 and 48 hours after induction.Flowcytometer was adopted to detect the apoptosis rate of 661W cells.Results The apoptosis model of 661W cells was successfully established,and the appropriate concentration of anti-Fas antibody was 2.0 μg/ml.After stimulated by the anti-Fas antibody,the expression of caspase-3 and caspase-8 of 661W cells increased from the time point of 6 hours,peaked at 12 hours,and sustained to 48 hours.However,the expression of Atg-5 and LC-3 Ⅱ/LC-3 Ⅰ raised from the time point of 3 hours,peaked at 24 hours,and decreased to the basic level at 48 hours.In addition,the appropriate concentrations of 3-MA and rapamycin were 20 nmol/L and 2.0 nmol/L,respectively.There was no statistical difference among the control group,simple 3-MA group and simple rapamycin group on the expression of caspase-3 and caspase-8 and the apoptosis rate of 661W cells at different time points (all at P＞0.05).The expressions of Atg-5 and LC-3 Ⅱ/LC-3 Ⅰ in the simple rapamycin group were significantly higher than those in the control group at different time points (all at P＜0.05).The expressions of caspase-3 and caspase-8 and the apoptosis rate in the model + 3-MA group were significantlly higher than those in the model group at 3,6,12,24 and 48 hours after induction,while the expressions of Atg-5 and LC-3 Ⅱ/LC-3 Ⅰ were obviously lower than those in the model group at 3,6,12 and 24 hours after induction (all at P＜0.05).The expressions of caspase-3 and caspase-8 and the apoptosis rate at 6,12,24 and 48 hours after induction in the model+rapamycin group were significantly lower than those in the model group,while the expressions of Atg-5 and LC-3 Ⅱ/LC-3 Ⅰ at the time points of 3,6,12 and 24 hours after induction were obviously higher than those in the model group (all at P ＜ 0.05).Conclusions Under the condition of anti Fas antibody inducing apoptosis,enhancing autophagy can reduce the apoptosis rate of cells,inhibiting autophagy can increase the apoptosis rate.Autophagy may play a protective role in 661W cells.

Objective:To explore the incidence rates, clinical features, risk factors and its impacts on survival of central nervous system complications (CNSC) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).Methods:From June 2011 to October 2018, 237 consecutive patients undergoing allo-HSCT were retrospectively analyzed.Results:The incidence of CNSC was 10.5%(25/237) and the median time 82(-4 - 810) days post-transplantation. The most common instances of CNSC were drug-associated encephalopathy (n=6), CNS infection (n=5), unexplained convulsions (n=4), metabolic encephalopathy (n=3), immune-related encephalopathy (n=3), primary central relapse (n=3) and cerebrovasculopathy (n=1). The most common clinical symptom was epileptic seizure (n=11). CsA-related encephalopathy was manifested mainly as posterior reversible encephalopathy syndrome on brain MRI. Metabolic encephalopathy is mostly demyelination. Most hippocampal lesions were caused by immune-related encephalopathy or CNS infection. Analysis of risk factors indicated that umbilical cord blood transplantation, HLA incompatible transplantation and delayed platelet implantation were high risk factors for post-transplantation occurrence of CNSC. Survival analysis suggested that non-relapse mortality rate (42.9%, 9/21) in group with CNSC of malignant hemoblastosis was higher than that in group without CNSC (15.3%, 27/176) and inter-group difference was statistically significant ( χ2=9.511, P=0.005). The 1/3-year OS rates in group with CNSC were lower than those in group without CNSC (56.6% vs 77.8%; 37.1% vs 65.7%). And the difference was statistically significant ( P=0.022). Conclusions:With a complex etiology, CNSC is one of serious complications after allo-HSCT and it significantly reduces the overall survival rate of patients. Umbilical cord blood transplantation, HLA incompatible transplantation and delayed platelet implantation are high-risk groups for CNSC.

: Objective: To investigate the effects of ezrin enhancer knockout on ezrin gene expression, cell proliferation and migration of human esophageal carcinoma Eca-109 cells. : Methods: The CRISPR/Cas9 recombinant plasmids targeting upstream/downstream of human ezrin enhancer were co-transfected into human esophageal carcinoma Eca-109 cells, and the cell line Eca-C2 with ezrin enhancer knockout was screened by purinomycin. Then the expression levels of ezrin mRNAand protein in Eca-C2 cells were detected by Real-time quantitative PCR (qPCR) and Western blotting, respectively; The expression levels of MAPK-pathway-related proteins were detected by protein array technology; and the effects of ezrin enhancer knockout on the proliferation and migration of Eca-C2 cells were analyzed by WST-1 method and wound-healing assay, respectively. : Results:The human esophageal carcinoma cell line Eca-C2 with stable ezrin enhancer knockout was established successfully. Compared with control cells, the mRNA and protein expressions of ezrin in Eca-C2 cells were significantly reduced (all P<0.05).Among the 17 detected MAPK pathway related proteins in Eca-C2 cells, 9 proteins (AKT, CREB, GSK3b, MKK6, mTOR, P38, P53, P70S6K and RSK1) were down-regulated, and the cell proliferation and migration were significantly inhibited (all P<0.05). Conclusion: ezrin enhancer knockout can significantly inhibit the cell proliferation and migration of human esophageal carcinoma Eca-109 cells.