BACKGROUND: There are some cytokines like interleukin-6, tumor necrosis factor-alpha as well as neurohormones such as norepinerphrine in serum of patients with congestive heart failure. However, whether they influence the occurrence and development of congestive heart failure is uncertain.OBJECTIVE: To explore the changes and significance of interleukin-6,tumor necrosis factor-alpha and norepinerphrine in order to provide basis for assessing the severity of heart failure and its prognosis.DESIGN: A case control study.SETTING: Department of Cardiology, Shidong Hospital of Shanghai City.INTERVENTIONS: A total of 58 patients with congestive heart failure admitted to Department of Cardiology, Shidong Hospital of Shanghai City from January 2000 to October 2001 were chosen as patient group with 33 males and 25 females. According to NYHA heart function classification,there were 12 cases of level Ⅱ, 32 cases with level Ⅲ and 14 cases of level Ⅳ. Thirty healthy volunteers who took physical examination during the same time were chosen as control group with 18 males and 12 females.ELISA was used to assay the levels of interleukin-6, tumor necrosis factoralpha and norepinerphrine in serum while two-dimension echocardiography was used to test the left ventricular ejection fraction in order to observe the relationship between cytokines and heart function.RESULTS: ① The levels of interleukin-6 [(367.6±78.6), (569.7±117.3)ng/L], tumor necrosis factor-alpha [(395.3±82.4), (583.1±124.8) ng/L] and norepinerphrine [(396.5±85.3),(675.9±136.2) ng/L] in patients with level Ⅰ-Ⅱ, Ⅳ heart function was remarkably higher than those of patients with level Ⅱ heart function and people in control group[(221.5±58.4), (170.2±42.7)ng/L; (205.4±59.2), (180.3±43.8) ng/L; (227.4±65.6),(163.8±41.5) ng/L] (P ＜ 0.05). Compared patients of level Ⅱ heart function with people in the control group, there was no difference on the above indicators (P ＞ 0.05).②There was highly negative correlation between interleukin-6, tumor necrosis factor-alpha, norepinerphrine and left ventricular ejection fraction (r=-0.63, P＜ 0.01; r=-0.54, P＜ 0.05;r=-0.58,P ＜ 0.01). The more severe the heart failure, the higher the levels of interleukin-6, tumor necrosis factor-alpha and norepinerphrine. There was obviously positive correlation between tumor necrosis factor-alpha and norepinerphrine as well as between interleukin-6 and norepinerphrine (r=0.57,P ＜ 0.01;r=0.51,P ＜ 0.05). The more severe the heart failure, the higher the level of interleukin-6 and tumor necrosis factor-alpha and that there was positive correlation between them (r=0.39, P ＜ 0.05).CONCLUSION: The tumor necrosis factor-alpha and interleukin-6 levels in patients with congestive heart failure all increased, especially in patients with moderate or severe congestive heart failure, and represented negative correlation with left ventricular ejection fraction. It suggests that the levels of interleukin-6, tumor necrosis factor-alpha in serum can be used as indicators to assess the severity and prognosis of congestive heart failure and provide assessment basis for quantitative evaluation of rehabilitation interventions.

Objec ive: o inves iga e he effec s of differen dose of bisoprolol on neurohormonal ac ivi y,cy okines,cardiac func ion,cardiac dea h in chronic sys olic hear failure pa ien s Me hods: One hundred and wen y chronic hear failure pa ien s were randomly divided in o large dose group (average 8 5? 1 2 mg) and small dose group (average 3 5?1 2 mg) he changes of norepinephrine (NE) ,angio ensionⅡ (AngⅡ) ,aldos erone (Ald) ,endo helin (E ) ,in erleukin 6 BF (IL 6) , umour necrosis fac or ? ( NF ?) Q ,plasm rennin ac ivi y (PRA) ,cardiona rin (ANP) ,brain na riure ic pep ide (BNP) ,cardiac func ion,cardiac dea h were observed Resul s:Af er rea men , he hear ra e were decreased in wo groups, p

MicroRNAs (miRNAs) are a family of endogenous, small (approximately 22 nucleotides in length), noncoding, functional RNAs. With the development of molecular biology, the research of miRNA bio-logical function has attracted significant interest, as abnormal miRNA expression is identified to contribute to serious human diseases such as cancers. Traditional methods for miRNA detection do not meet current demands. In particular, nanomaterial-based methods, nucleic acid amplification-based methods such as rolling circle amplification (RCA), loop-mediated isothermal amplification (LAMP), strand-displacement amplification (SDA) and some enzyme-free amplifications have been employed widely for the highly sensitive detection of miRNA. MiRNA functional research and clinical diagnostics have been accelerated by these new techniques. Herein, we summarize and discuss the recent progress in the development of miRNA detection methods and new applications. This review will provide guidelines for the development of follow-up miRNA detection methods with high sensitivity and spec-ificity, and applicability to disease diagnosis and therapy.

Objective:To build mice ulcerative colitis(UC)model by dextran sodium sulfate salt(DSS),and to explore effect and molecular mechanism of oridonin(Ori)on alleviating UC by mediating Sirt1 signaling pathway,as well as to find new drugs for UC treatment.Methods:Sixty BALB/c mice were randomly divided into normal group(NC),model group(DSS),DSS+mesalazine sustained-release granule group(AC),DSS+low-dose Ori group(Ori-L),DSS+medium-dose Ori group(Ori-M)and DSS+high-dose Ori group(Ori-H),with 10 mice in each group.Except NC group,mice in other groups were given 3%DSS aqueous solution free for 7 days.After successful modeling,Ori-L group,Ori-M group and Ori-H group were intragastric with 50,100 and 150 mg/kg Ori suspension,respectively.NC group and DSS group drank distilled water free,AC group was intragastric with mesalazine sustained-release granules 100 mg/kg,lasted for 10 days.Weight changes of mice were recorded and disease active index(DAI)score was performed.After treatment,serum levels of IL-1β and tumor necrosis factor-α(TNF-α)were detected by ELISA.Whole colon tissues were extracted,length was measured,and HE staining was performed.Real-time fluorescence quantitative PCR and Western blot were used to detect expressions of Sirt1,NF-κB and p53 in colon tissues of each group.Results:After successful modeling,compared with NC group,the other 5 groups of mice showed weight loss,DAI score increased and colon length shortened,Sirt1 expression was signi-ficantly inhibited,while expressions of NF-κB and p53 were significantly increased,accompanied by obvious inflammatory pathologi-cal features.Compared with DSS group,Ori-L,Ori-M,and Ori-H groups and AC group had less weight loss during experiment,and DAI scores showed lower disease activity and relatively less colon length shortening,Sirt1 expression was less inhibited,expressions of NF-κB and p53 were also relatively small.Results of AC group could prove that Ori has therapeutic effect on UC.Conclusion:Ori can improve UC in mice,whose effect may be related to regulation of Sirt1 signal.

BACKGROUNDTo get early laboratory study of type specific antigenicity of herpes simplex virus II.

METHODSPCR and prokaryotic expression technique.

RESULTSHerpes simplex virus II type specific gene fragment was expressed in E.coli and the products can be used as specific antigen for the detection of anti\HSV in the recovery sera.

CONCLUSIONSCloning and express of HSVII type specific antigen found the basis for developing specific diagnosis methods and vaccine of HSV.

Antigens, Viral ; immunology ; Cloning, Molecular ; Gene Expression ; Herpesvirus 2, Human ; genetics ; Humans ; Immunoglobulin G ; blood ; Polymerase Chain Reaction ; Recombinant Proteins ; immunology

Pancreatitis is one of the most common inflammatory diseases of the pancreas caused by autodigestion induced by excessive premature protease activation. However, recognition of novel pathophysiological mechanisms remains a still challenge. Both genetic and environmental factors contribute to the pathogenesis of pancreatitis, and the gut microbiota is a potential source of an environmental effect. In recent years, several new frontiers in gut microbiota and genetic risk assessment research have emerged and improved the understanding of the disease. These investigations showed that the disease progression of pancreatitis could be regulated by the gut microbiome, either through a translocation influence or in a host immune response manner. Meanwhile, the onset of the disease is also associated with the heritage of a pathogenic mutation, and the disease progression could be modified by genetic risk factors. In this review, we focused on the recent advances in the role of gut microbiota in the pathogenesis of pancreatitis, and the genetic susceptibility in pancreatitis.

Vaccination is a main measure for protecting chickens against Marek's disease,while it is not able to suppress the infection,proliferation,transmission,and virulence enhancement on Marek's disease virus.Inhibiting the proliferation of Marek's disease virus in chicken is therefore an im-portant option for enhancing defense effectiveness.In this study,a compound,DUBs-IN-1,was found to inhibit the activity of MDV049,a protease encoded by Marek's disease virus,via screening a protease inhibitor library using MDV049 as target and ubiquitin probe.Molecular docking re-vealed that DUBs-IN-1 can interact with the residues which formed the catalytic pocket of MDV049,blocking the interaction between Ub substrate and the catalytic center of MDV049,then suppress the activity of MDV049 with competitive inhibition.Using the CPE model,it was found that DUBs-IN-1 at the concentration of 0.35 and 0.70 μmol/L significantly inhibited the CPE in-duced by Marek's disease virus in CEF cells.Quantitative analysis revealed that DUBs-IN-1 inhibi-ted the proliferation of Marek's disease virus in CEF cells(P＜0.01).Furthermore,it was found that the administration of 80 and 150 pg/(kg·d)of DUBs-IN-1 in chicken infected by Marek's disease virus significantly inhibited the proliferation of MDV in T cells(P＜0.01).In summary,this study demonstrated that the compound DUBs-IN-1 is able to inhibit the proliferation of Marek's disease virus in chicken cells,laying a theoretical and practical foundation for further de-velopment of the drugs against Marek's disease virus.

OBJECTIVE： To establish the method for PCR identification of bullwhip， and to identify the authenticity of bullwhip at the molecular level. METHODS： DNA samples of bullwhip and its counterfeits （donkey whip， pig whip， sheep whip） were extracted and their integrity， purity and concentration were detected. Using GenBank related information， using mitochondrial cytochrome b （Cyt b） gene of bullwhip as target gene， Primer-BLAST online software was used to design specific primer. PCR amplification was performed for whips of different species， and electrophoretic analysis was conducted for the product. PCR products of bullwhip samples were cloned and confirmed by DNA sequencing. The specificity and repeatability of the established PCR method were verified. RESULTS： DNA purity of the bullwhip and its counterfeits was high， and there was no protein or RNA pollution. 1.5％ agarose gel electrophoresis showed that there were obvious target gene bands of bullwhip samples at 200-300 bp， while no corresponding bands appeared in other counterfeit products. The results of DNA sequencing showed that the nucleotide sequence of the gene fragment of bullwhip was 100％ similar to that of the bullwhip in GeneBank. Results of methodological validation showed that established method was specific and reproducible. CONCLUSIONS： The established PCR identification method based on Cyt b gene in the study is simple， rapid， accurate， specific and reproducible， and can meet the requirements of analysis and identification of bullwhip and its counterfeits.