Objective:To do research on prediction method of medical equipment sudden fault for the requirement of medical security at sea which is away from base.Methods: Sudden fault data of the medical equipment is a random variable which often manifest as the time of sudden fault happening. The possible distribution type of fault data is hypothesized according to the engineering experience. In order to ensure the sudden fault density function of medical equipment, parameter estimation and distribution fit test are carried out for the fault data.Results: The sudden fault prediction model of medical equipment is established to get the future sudden fault probability of medical equipment based on the distribution function of fault data.Conclusion: The results of case analysis validate the rationality of sudden fault prediction model.

AIM: To evaluate the effects of all-trans retinoic acid (atRA) on the proliferation in cultured mouse cerebral microvascular endothelial cells (bEnd.3) . METHODS: Cultured cells were divided into five groups randomly, one as control group, the other four groups were 10-9, 10-8, 10-7 and 10-6 mol/L group. Effects of atRA on proliferation in bEnd.3 cells were detected by flow cytometry and immunocytochemitry of PCNA and MTT at 24 h, 48 h and 72 h. The effects of atRA (10-6 mol/L group) on the expressions of angiogenic genes in bEnd.3 cells were studied using microarray. RESULTS: The results of MTT and flow cytometry showed that all- trans retinoic acid at concentration of 10-6 mol/L significantly inhibited the proliferation of bEnd.3 cells. Immunocytochemical staining showed the expression of PCNA was markedly decreased in bEnd.3 cells at 24 h after treatment with atRA. Microarray results demonstrated that there were 11 down - regulated angiogenic genes and 2 up - regulated angiogenic genes in 10-6mol/L atRA group. CONCLUSION: All - trans retinoic acid at concentration of 10-6mol/L may significantly inhibit the proliferation of bEnd.3 cells treated for 24 h ire vitro via down-regulation of angiogenic genes and PCNA expression.

Objective To explore the value of echocardiography in the diagnosis of anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) in children.Methods The echocardiographic images of 14 patients with ALCAPA confirmed by operation and 18 patients with endocardial fibroelastosis (EFE) diagnosed by clinical were compared and analyzed.Results Both ALCAPA and EFE exhibited obvious dilated left ventricle,decreased left ventricular systolic function,thick endocardium and mitral regurgitation of different degree.The former additionally showed dilated right coronary artery(RCA) with normal origin,left coronary artery(LCA) emerging from the root or wall of the pulmonary artery(PA),the retrograde flow into PA in LCA and abundant collateral vessels in myocardium.However the later exhibited normal diameter of LCA and RCA and no collateral vessels.Conclusions Color Doppler echocardiography not only demonstrates left ventricular systolic function,endocardium,mitrial regurgitation and collateral vessels in myocardium,but also shows the origination and courses of LCA clearly,which provide exact informations to diagnose ALCAPA.The echocardiography can be used as a powerful tool of ALCAPA diagnosis and preoperative assessment.

Microvascular endothelial cell (MVEC) is one of the target cells of TNFα (TNF effect). The dysfunction of MVEC induced by TNF plays an important role in some cardio-cerebral vascular diseases. ① Cell proliferation kinetic: Using flow cytometry, we found cell count ［(4.30±0.34)×107／L)］ in TNF group (4×105 U/L) was obviously less than that in control ［(5.23±0.50)×107／L, P＜0.01］. The cells of G1 phase were more than those of the control, while the cells of G2, S and M phase became less (P＜0.05). ② Coagulant and anticoagulant: 72 h after MVEC cultued in the media, the content of 6-keto-PGF1α (RIA) and activity of PAI decreased significantly in TNF (4×105 U/L) group (P＜0.01, vs control). The difference between TXB2 content and t-PA activity in groups was not significant (P＞0.05). ③ Adhesive molecule: The effect of low concentration TNF (＜4×105 U/L) on adhesion between cultured MVEC and leukocytes was not signficant, but when the concentration of TNF reached 8×105 U/L or more, 12 h after culture the adhesion rate between MVEC and neutrophil increased 30.8%±4.5%. If adding monoclonal antibody of ICAM-1/CD11 into media, the adhesion rate of leukocytes decreased significantly (from 31.2% to 63.4%). ④ NO: The level of nitrite in culture media (Griess reaction) was higher than that of control (P＜0.05) after pretreatment of TNF (2×106 U/L) for 6 h. Adding L-NMMA, Dexamethasone or Cycloheximide in media could block the increase of nitrite induced by TNF, while L-Arg could enhance it. The expression of iNOS mRNA of PMVEC increased significantly after treated with TNF (2×106 U/L) for 24 h (quantitative RT/PCR). Pretreatment with Dexamethasone or Cycloheximide could block the increase (P＜0.05). Meanwhile, the expression of eNOS mRNA decreased significantly compared with control, the decrease can be blocked by Cycloheximide but not by Dexamethasone. So that TNF can induce the expression of iNOS mRNA in PMVEC, but inhibited the expression of eNOS mRNA. NO production in PMVEC can be time-dependently induced by TNF. ⑤ Apoptosis: Adding high concentration TNF(＞1.2×106 U/L) in culture media for 12 h can induce apoptosis of PMVEC with electron microscopy, flow cytometry (PI/AnnexinV stain), TUNEL and DNA ladder eletrophoresis. Meanwhile, expression of apoptosis-associated gene Bcl-2 mRNA decreased and that of Fas mRNA increased (Northern blot). The expression of FADD, caspase 3 and caspase 8 enhanced too. So that signal of apoptosis induced by TNF may be transmitted following the cascade of Fas→FADD→caspase8→caspase3. In conclusion, it should be paid attention to metabolism inability and dysfunction induced by TNF which can not found easyily using light microscope. High concentration TNF can induce apoptosis of endothelial cells regulated by apoptosis-associated genes. The changes mentioned above are common pathway in pathogenesis of some diseases related to TNF.

To study on the phylogenetic characterization of the VP1 genes of coxsackievirus A16 (CVA16) causing hand-food-mouth disease (HFMD) isolated from Anhui province in 2014. A total of 413 throat swab specimens from HFMD patients were collected during January to November, 2014 for the isolation and identification of enteroviruses using real-time RT-PCR assays. The VP1 regions of CVA16 isolates were amplified using RT-PCR and sequenced. And the phylogenetic tree was constructed among the VP1 regions of those isolates, the different genotypes and sub-genotypes of CVA16 strains. A total of 97 enteroviruses were isolated from 413 samples, the positive rate was 23.49% (97/413), including seventeen CVA16, seventy six HEV71 and four other enteroviruses. The results of the phylogenetic tree showed that 17.CVA16 strains isolated from Anhui in 2014 clustered within B1b evolution branch of B1 genotype. The nucleotide and amino acid sequence identities were 95.30%-100% and 98.70%-100% among the isolates, respectively, but within B1b branch of 17 strains formed several small transmission chains. The nucleotide acid of 17 CVA16 isolates in Anhui province were closed to the strains isolated from Yunnan, Hunan, Guangdong, Tibet and Jiangsu, especially from Hunan in 2013 and from Shenzhen of Guangdong in 2014, the identity were 96.40%-99.70%. The CVA16 strains isolated from Anhui in 2014 were all belong to genetic subtype B1b of B1 genotype was dominant, and among those isolates, several small virus transmission chains had formed with co-circulating and evolution.
China ; Enterovirus A, Human ; classification ; genetics ; isolation & purification ; Enterovirus Infections ; virology ; Genotype ; Humans ; Molecular Sequence Data ; Phylogeny ; Viral Proteins ; genetics ; metabolism

Stimulator of interferon genes (STING) is an important protein of the innate immune response, and protects against viral infections. To search for an alternative splicing isoform of STING, we undertook rapid amplification of cDNA ends (RACE) and RT-PCR with RNA extracted from human embryonic kidney (HEK) 293 cells and primers designed according to the mRNA sequence of full-length STING(NM-198282. 82). The new sequence was compared using a bioinformatics method. Then, a newly discovered, alternative splicing isoform of STING, named "STING(sv)", and STING(wt) were subcloned into the eukaryotic expression vector pEGFP-C1 and pcDNA 3. 1. Whole-cell extracts were analyzed by western blotting and then probed with monoclonal antibody against enhanced green fluorescent protein (EGFP) after transfection of EGFP-STING(wt) and EGFP-STING(wt) plasmids in HEK293 cells. pcDNA-STING(wt) and pcDNA-STING(wt) were transfected in HEK293 cells, and the luciferase assay carried out. Compared with STING(wt), STING(sv) lacks exon 7 so that shift in the reading frame may produce a protein with a different C-terminal in amino acids 1-30. Western blotting confirmed an expected strong band at 58 x 10(3) kD. The functional luciferase assay showed that STING(sv) inhibited the activity of the interferon (IFN)-β promoter. STING(sv) can be expressed in multiple tissues and distinct cell lines. Our discovery of a new, alternative splicing isoform of STING provides new insights into the functional regulation of STING. STING(sv) could be a dominant negative inhibitor for the activity of the IFN-β promoter in the virus-infection pathway. Hence, STING(sv) could participate in the "fine tuning" of the virus-induced activation of IFN. Therefore, exploring the role of STING(sv) in the pathogenesis of human diseases could be very worthwhile.
Alternative Splicing ; Amino Acid Sequence ; HEK293 Cells ; Humans ; Interferon-beta ; genetics ; Membrane Proteins ; genetics ; metabolism ; Molecular Sequence Data ; Promoter Regions, Genetic ; Protein Isoforms ; genetics ; metabolism ; Sequence Alignment

Objective To study the function of cyclooxygenase 2(COX 2) and its specific inhibitor NS 398 on the cell growth and invasion ability of urothelial carcinoma cell line EJ. Methods The cox 2 cDNA was transfected into the urothelial carcinoma cell line EJ and a cell line EJ COX 2 which highly expressed cox 2 gene permanently was gained. The cell growth rate before and after transfection was observed. Then at various concentrations of NS 398, the invasion ability was detected by Boyden Chamber and expression levels of uPA by RT PCR and Western blot. Results The EJ COX 2 cell line grew more rapidly and had a stronger invasion ability than EJ and its uPA expression increased significantly. NS 398 could dose dependently inhibit the expressions of COX 2 and uPA and the invasiveness of EJ COX 2 cell. Conclusion COX 2 can stimulate the growth of urothelial cell line EJ and promote its invasion ability by stimulating the expression of uPA.

Objective To explore the roles of urokinase type PA (uPA) and uPA receptor (uPA R) in the course of repair after human embryo corneal alkali burn in vitro . Methods After the alkali burn model in vitro was established successfully, some techniques such as the observation of cell culture and morphology, ICC and image analysis were used. Results No significant difference was found between the cells from corneal limbus and central cornea and almost all of them expressed AE1/AE3. The expressions of uPA and uPA R increased to the maximum at about 24 h after alkali burn. uPA expression distributed mainly in the cytoplasm but uPA R expression distributed mainly in the cell membrane. Conclusion The corneal epithelial cells of comparatively high purity can be acquired by tissue culture. There probably exists difference in development and vitality between embryo and adult cornea. There might be commonness of the roles of uPA and uPA R in epithelial tissue.

Objective To study the echocardiographic characteristics and its diagnosis value on congenital supravalvular aortic stenosis (SVAS) in children. Methods Thirty-one patients with SVAS diagnosed by multiplane echocardiography were enrolled in the study. Their echocardiographic characteristics were compared with cardiac catheterization, operation, and gene detection results. Echocardiographic changes were mainly observed in aortic valve, supravalve, descending aortic arch, pulmonary artery valve, main pulmonary artery and its branches,and coronary artery. Results Of the 31 patients,26 had hourglass type SVAS,4 hypoplastic type,and 1 membranous type; 2 patients had extremely mild stenosis (defined as a Doppler gradient <25 mm Hg) ,20 mild (25～49 mm Hg) ,5 moderate (50～75 mm Hg) ,and 4 severe C>75 mm Hg) ones. Nineteen patients were diagnosed with Williams syndrome by gene detection. Three patients were associated with aortic valve stenosis including one missed at the initial diagnosis; 10(32.26%) patients with pulmonary stenosis, including pulmonary valve stenosis in 6, left and right pulmonary artery stenosis in 3 ,and branch stenosis in 1:6 patients with coronary stenosis. Conclusions The sternal border and five chamber apical views are the best to detect SVAS. Williams syndrome patients are prone to SVAS.Pulmonary stenosis echocardiography forms a great proportion of the SVAS patients. Routine examination is necessary for coronary stenosis in cases of SVAS.