Objective To evaluate the inhibitory effects of NF-κB inhibitor pyrrolidine dithiocar-bamate (PDTC) on NF-kappa B activity and the serum inflammatory mediators in hypertensive-ventricular hypertrophy-congestive heart fail?ure rats. Methods The rat model of hypertension-cardiac hypertrophy-heart failure was made from 42 male Dahl salt sen?sitive rats. Rats were randomly divided into seven groups including group A (normal diet group), group B (high salt diet group), group C (NF-κB inhibition in early stage), group D (NF-κB inhibition in hypertensive stage), group E (NF-κB inhibi?tion in cardiac hypertrophy stage of week 12) and group G (NF-κB inhibition in heart failure stage). There were six rats for each group. Rats were administrated 8%high salt diet and injected PDTC 100 mg/(kg·d)intraperitoneally according to the prescribed time. Changes of blood pressure, left ventricular end diastolic interventricular septal thickness (IVSD), left ven?tricular end diastolic posterior wall thickness (LVPWD), left ventricular end diastolic diameter (LVEDD), systolic left ventric?ular end diastolic diameter (LVESD), left ventricular ejection fraction (LVEF), heart, lung weight/ body weight ratio, NF-kappa B activity, tumor necrosis factor (TNF)-α, interleukin (IL)-6, monocyte chemotactic protein (MCP)-1 and C-reactive protein (CRP) were observed in different treatment time points of PDCT. Results Levels of NF-κB and proinflammatory cy?tokines were reduced after early administration of PDTC, and the cardiac function was also decreased. The longer the treat?ment time, the greater the protective effect on heart. PDTC can effectively control blood pressure, and block left ventricular hypertrophy and left ventricular failure in a certain extent. The effects of PDTC were limited after persistent hypertension, and myocardial hypertrophy formation accompanied by heart failure. Conclusion PDTC plays a role in prevention and treatment of hypertension, left ventricular hypertrophy and congestive heart failure in model rats. Early application of PDTC could obviously maintain the normal cardiac function in rats with heart disease.

Objective To study the expression of LI-cadherin in gastric cancer, gastric stromal tumor, chronic gastritis and intestinal metaplasia. Methods Two hundred and forty four specimens were collected, including normal epithelia (n=28), chronic superficial gastritis (n=30), chronic atrophic gastritis(n=42), intestinal metaplasia (n=58), gastric adenocarcinoma (n=46), paracancerous gastric tissues (n=30), gastric stromal tumor (n=10). The expression of LI-cadherin was detected by S-P immunohischemistry with purified goat polyclonal antibody. Results The expression of LI-cadherin in normal epithelia and chronic gastritis are all negative, the positive rates of LI-cadherin expression in intestinal metaplasia and gastric adenocarcinoma is 83% (48/58) and 65% (30/46) respectively. By Laurien classification, the positive rate of LI-cadherin expression in intestinal type was higher(78% ) than those in the diffuse type (35%) (P<0.05). LI-cadherin was in positive correlation with lymph node metastasis and staging. Paracancerous tissues and gastric stromal tumor did not express LI-cadherin. Conclusions The abnormal expression of LI-cadherin was correlated with intestinal metaplasia and gastric adenocarcinoma. GCs with high LI-cadherin index have more lymph node metastasis. High expression rate of LI-cadherin in gastric cancer tissues may predict poor prognosis.

Objective To analyse the risk factors of vulnerable plaque biomarker and to construct an early warning system. Methods Ninety patients with suspected acute coronary syndrome (ACS) hospitalized during December 2012 and December 2013 were selected. The coronary artery lesions were divided into type I, II and III plaque groups by the morphology of atherosclerotic plaque. Serum SAA, PLGF, sCD40L and Npt were measured. The results of SAA, PLGF, sCD40L and Npt were compared. Logistic regression model was fitted to explore the main influencing factors of the vulnerable plaque. Results SAA, PLGF, sCD40L, and Npt were main influencing factors of the vulnerable plaques, and the ORs were 1.61, 1.88, 1.96 and 1.79 respectively. Conclusion The detection of SAA, PLGF, sCD40L and Npt biochemical markers in patients with chest pain is important for predicting the vulnerable plaque and guiding clinical treatment.

Objective:To assess the clinical utility of a fluorescence in situ hybridization(FISH) assay as a non-invasive method for diagnosing and monitoring urothelial carcinoma(UC) in the upper urinary tract(UUT).Methods:Urine specimens from 63 consecutive patients with UUT-UC and 69 controls with benign disease were analyzed by means of cytology and FISH.For FISH analysis,labeled probes specific for chromosomes 3,7,and 17 and for the p16(9p21) gene were used to assess chromosomal abnormalities indicative of malignancy.Sensitivity and specificity of both techniques were determined and compared.The frequency of chromosomal aberrations of malignant cells from UUT-UC was also determined.Results:Of 63 patients with UUT-UC,FISH affords an overall sensitivity of 84.1%(53/63),the figure being 71.4%(20/28)for PTa and PT1 tumors,94.3%(33/35) for PT2-4 tumors.The sensitivities of urine cytology were 35.7%(10/28)for PTa and PT1 tumor,45.7%(16/35)for PT2-4 tumors,with an overall sensitivity of 41.3%(26/63).The sensitivities of the two methods for the low grade tumors were 80%(20/25)and 44%(11/25),and for high grade tumors were 86.8%(33/38)and 39.5%(15/38),respectively.Specificities for FISH and urine cytology were 91.3%(63/69)and 94.2%(65/69)respectively.Conclusion:According to the results,the sensitivity of FISH for the detection of UUT-UC is superior to that of urine cytology and the specificities of FISH and urine cytology are not significantly different.FISH can promote the diagnosis of UUT-UC,especially for the low stage and low grade cases,it may be a new promising non-invasive method for the diagnosis of UUT-UC.

Background: Insulin regulates glucose homeostasis and has important effects on metabolism, cell growth, and differentiation. Depending on the cell type and physiological context, insulin signal has specific pathways and biological outcomes in different tissues and cells. For studying the signal pathway of insulin on glycolipid metabolism in porcine embryonic fibroblast (PEF), we used high-throughput sequencing to monitor gene expression patterns regulated by insulin. Objectives: The goal of our research was to see how insulin affected glucose and lipid metabolism in PEFs. Methods: We cultured the PEFs with the addition of insulin and sampled them at 0, 48, and 72 h for RNA-Seq analysis in triplicate for each time point. Results: At 48 and 72 h, 801 and 1,176 genes were differentially expressed, respectively. Of these, 272 up-regulated genes and 264 down-regulated genes were common to both time points. Gene Ontology analysis was used to annotate the functions of the differentially expressed genes (DEGs), the biological processes related to lipid metabolism and cell cycle were dominant. And the DEGs were significantly enriched in interleukin-17 signaling pathway, phosphatidylinositol-3-kinase-protein kinase B signaling pathway, pyruvate metabolism, and others pathways related to lipid metabolism by Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Conclusions These results elucidate the transcriptomic response to insulin in PEF. The genes and pathways involved in the transcriptome mechanisms provide useful information for further research into the complicated molecular processes of insulin in PEF.

Objective To explore the correlation between exon region polymorphism of PPP1R3A gene and schizophrenia in Uygur Chinese population. Methods PPP1R3A gene exon region DNA amplification was performed using multiple PCR targeted capture next-generation sequencing method in 528 patients with schizophrenia and 576 healthy controls of Uyghur descent, Illumina HiSeq X Ten was used for sequencing, the symptoms of schizophrenia were assessed by positive and negative symptoms scale (PANSS). Results The allelic and genotypic distributions in rs1800000 of PPP1R3A gene between patients with schizophrenia and healthy controls had significant difference (P＜0.05), rs1799999 in genotype frequency between the female case and control groups showed significant difference (P＜0.05). Furthermore, the allelic distributions of rs8192686 between male cases and controls had significant difference (P＜0.05). Conclusion PPP1R3A gene rs1800000 may be associated with the development of schizophrenia in Uygur Chinese population; rs1799999 may be a risk factor for susceptibility of female Uygur Chinese schizophrenia; The C allele at rs8192686 may be associated with male Uygur Chinese schizophrenia.

Studies have suggested that the nucleus accumbens (NAc) is implicated in the pathophysiology of major depression; however, the regulatory strategy that targets the NAc to achieve an exclusive and outstanding anti-depression benefit has not been elucidated. Here, we identified a specific reduction of cyclic adenosine monophosphate (cAMP) in the subset of dopamine D1 receptor medium spiny neurons (D1-MSNs) in the NAc that promoted stress susceptibility, while the stimulation of cAMP production in NAc D1-MSNs efficiently rescued depression-like behaviors. Ketamine treatment enhanced cAMP both in D1-MSNs and dopamine D2 receptor medium spiny neurons (D2-MSNs) of depressed mice, however, the rapid antidepressant effect of ketamine solely depended on elevating cAMP in NAc D1-MSNs. We discovered that a higher dose of crocin markedly increased cAMP in the NAc and consistently relieved depression 24 h after oral administration, but not a lower dose. The fast onset property of crocin was verified through multicenter studies. Moreover, crocin specifically targeted at D1-MSN cAMP signaling in the NAc to relieve depression and had no effect on D2-MSN. These findings characterize a new strategy to achieve an exclusive and outstanding anti-depression benefit by elevating cAMP in D1-MSNs in the NAc, and provide a potential rapid antidepressant drug candidate, crocin.