Asians ; China ; Humans ; von Willebrand Diseases/therapy* ; von Willebrand Factor

ADAMTS13 Protein ; Asians ; China ; Humans ; Plasma Exchange ; Purpura, Thrombotic Thrombocytopenic/therapy*

We used retrovial vector LXSN to construct recombinant retroviral vector with mutant membrane bound TNF - ? gene. The vectors were introduced into packaging cell line, CRIP cells. The G418-resistant colonies were selected and the supernatants of the colonies were used to determine the virus titers. The titer of virus was 1? 104CFU/ml and the retroviral vectors were used to tranduced the human gastric cancer cell line, MGC-803 cells. The results of southern blot assay showed thai the targel gene had integrated into the genomic DNA of MGC-803T. MGC - 803Tcells were ablc to kill L929 cell line, but the parent cell line showed no cytotoxicily to the cells at all. There was no any variance in the morphological appearance and growlh rate in vilro of MGC-803N and MGC-803T cells. The results of inoculation in nude mice with these cells indicated that MGC-803T cells showed a considerable decrease in size of tumor. These results suggested that the retroviral vectors expressing mulant TNF -? gene were successfully construed. MGC - 803T cells showed cytotoxicily slrongly lo L929 cell line in vilro and lumorigenicity .

0.05).Conclusions HPC has protective effect on neonatal rats with cerebral hypoxia-ischemia,but it does not have obvious effect on NGB.

Objective To explore the association between Q-1 and T1 locus polymorphism in ADAM33 gene and chronic obstructive pulmonary disease in Han population in northern Guizhou by detecting Q-1 and T1 locus polymorphism in ADAM33 gene in patients with COPD in the distribution of frequency ,provide a theoretical basis for the prevention and treatment of COPD. Methods Polymerase chain reaction and DNA sequencing tech-nology,electrophoresis separation method were applied to detect Q-1 and T1 locus polymorphism in ADAM33 gene. Results The genotype distribution of Q-1 and T1 locus in the case group and the control group of ADAM33 gene were in accordance with the Hardy-Weinberg equilibrium law and ADAM33 gene Q-1,T1 locus were C and T alleles. There was no significant difference in genotype and allele frequency distribution between the case group with control group,and COPD complicated with chronic respiratory failure(COPD)and hypoxemia(P > 0.05). T1(83 bp,112 bp)at a high probability of two heterozygous in the same samples(18/19),and is located in the encoding region. Conclusion No association was found between Q-1,T1 locus polymorphism in ADAM33 gene and chronic obstructive pulmonary disease in Han population in northern Guizhou.

Connexin 43 ; genetics ; Connexins ; genetics ; Heart Defects, Congenital ; genetics ; Homeobox Protein Nkx-2.5 ; Homeodomain Proteins ; genetics ; Humans ; Infant ; Infant, Newborn ; Mutation ; genetics ; Myocardium ; metabolism ; Transcription Factors ; genetics

Objective To determine the relationship between subclinical hypothyroidism and asymptomatic myocardial ischemia in type 2 diabetes mellitus.Methods All of 399 asymptomatic subjects who underwent coronary CT angiography with type 2 diabetes mellitus but without thyroid disease were enrolled retrospectively.Totally patients were divided into subclinical hypothyroidism group (17 patients,type 2 diabetes mellitus with subclinical hypothyroidism) and euthyroid group(382 patients,type 2 diabetes mellitus with normal thyroid function).Results The incidence of subclinical hypothyroidism in type 2 diabetes mellitus was 4.3％(17/399).The ratio of male and smoking in subclinical hypothyroidism group was significantly lower than that in euthyroid group (3/17 vs.194/382,P =0.007;2/17 vs.136/382,P =0.043).The incidence of asymptomatic myocardial ischemia in subclinical hypothyroidism group was 5 cases and in euthyroid group was 130 cases,and there was no significant difference(P=0.694).The age,course of type 2 diabetes mellitus,level of glycosylated hemoglobin and low density lipoprotein cholesterol between two groups had no significant difference(P＞ 0.05).Conclusion Subclinical hypothyroidism is not an independent risk factor for asymptomatic myocardial ischemia in type 2 diabetes mellitus.

Objective To evaluate the methylation status of RASSF2A in epithelial ovarian cancer (EOC) tissues and plasma, and to explore the correlations in two kinds of samples with clinicopathological characteristics. Methods The frequency of methylation of the RASSF2A gene in tissues and corresponding plasma samples from 60 EOC patients, 20 patients with benign ovarian tumors and 10 patients with normal ovarian tissues were detected respectively. The methylation-specific PCR was used to determine the methylation status. Results The frequency of aberrant methylation of RASSF2A was 58.3% (35/60) in EOC tissues and 43.3%(26/60) in corresponding plasma samples respectively, however, such hypermethylation was not detected in the benign ovarian tumors and normal ovarian samples, and there was significant difference between them (P<0.05). Besides, RASSF2A methylation levels in serum of EOC patients correlated reasonably well with methylation status in tumor samples (r=0.739, P=0.000). No significant differences were observed between the promoter hypermethylated status of the RASSF2A and clinicopathological characteristics (P>0.05). Conclusions The promoter methylation of RASSF2A gene is an early and frequent epigenetic event in EOC. Detection of promoter hypermethylation in plasma specimens can help the early diagnosis of EOC.

Endothelial mesenchymal transition ( EndMT) , a biological process in which endothelial cells under specific environmental stimuli, gradually lose close connection and expression of specific markers, and obtain stromal cells or muscle fiber cell plienolypic expression and characteristics of movement and shrinkage. EndMT not only plays a crucial role in the development of heart and vascular, but lias been widely studied in the process of organ fibrosis such as heart, lung and kidney. It may be the key step in the prevention and treatment of myocardial fibrosis. We review the research progress of EndMT in myocardial fibrosis.

Objective To investigate the effect of indoor coal PM2.5 on the airway inflammation and the pathological morphology alterations of lung tissue in asthmatic rats induced by ovalbumin(OVA). Methods Forty six?week?old male SD rats were randomly divided into four groups(Control,OVA,PM2.5,PM2.5+OVA). Normal saline,OVA(15μg/mL)and(or)PM2.5(2.5 mg/mL)were given to rats in the four groups through intratracheal instillation for four times (two weeks one time),respectively. Twenty?four hours after the last intratracheal instillation ,bronchoalveolar irrigation lavage fluid (BALF) was collected for determinations of serum interleukin 4(IL?4),interferon gamma (IFN?γ). The lung tissue was collected for HE staining and electron microscopy detection. Results HE staining showed less inflammatory cell infiltration was observed in the control group;In PM2.5 group and OVA group,there was medium quantity of inflammatory cell infiltration,In PM2.5+OVA group, severe inflammatory cell infiltration was observed. Electron microscopy showed no abnormal lung tissue in the control group,but organelles were gradually destroyed,endothelial cell edama,alveolar interval with a large number of fibersin were observed in PM2.5 group. The exfoliated cells,local typeⅡ cells with visible damage were found in OVA group. A large number of fibers were existed among the lung tissues and organelles were destroyed,thickness of basement membrane was non?uniform,and blood air barrier structure was not clear in PM2.5 + OVA group. Compared with PM2.5+OVA group,concentration of IL?4 in PM2.5,OVA and the control group was siganificantly different(P < 0.05). A negative correlation between IL?4 and IFN?γ was observed (r =-0.358,P < 0.05). Conclusion Indoor coal PM2.5 exacerbates the airway inflammatory cell infiltration and airway remodeling in OVA?induced asthmatic rats.