Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Carbon Tetrachloride ; toxicity ; Chemical and Drug Induced Liver Injury ; drug therapy ; Female ; Liver ; drug effects ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mice ; Mice, Inbred ICR ; Silymarin ; administration & dosage ; pharmacology ; therapeutic use

OBJECTIVETo clarify the mechanism by which interleukin?22 (IL?22) promotes the proliferation of fibroblast?like synoviocytes (FLS) from patients with rheumatoid arthritis (RA).

METHODSFLS were isolated from the synovial tissues of patients with RA and identified by immunohistochemistry for vimentin/CD68. The cells were subcultured and incubated with different concentrations of IL?22 for 24, 48, or 72 h, and their proliferation was examined using MTT assay. After treatment of the cells with IL?22 and AG490, alone or in combination, the expressions of the total and phosphorylated proteins of STAT3, ERK1/2 and P38 were detected with Western blotting.

RESULTSIL?22 significantly increased the proliferation of FLS in a dose?dependent manner (P<0.05). The total protein of STAT3 in the cells showed no significant changes with extended time of IL?22 treatment (P=0.68), but the expression of phosphorylated STAT3 protein increased significantly (P<0.001). The total and phosphorylated proteins of ERK1/2 and P38 underwent no significant changes after IL?22 treatment (P>0.05). A combined treatment with 50 ng/mL IL?22 and 100 µmol/L AG490 resulted in a significant decrease in the proliferation of FLS as compared with IL?22 treatment alone (P<0.01).

CONCLUSIONIL?22 can dose?dependently promote the proliferation of FLS from patients with RA by inducing phosphorylation of STAT3 protein but not through ERK1/2 or P38 signal pathway.

Small ubiquitin-related modifiers (SUMOs) belong to an important class of ubiquitin like proteins. SUMOylation is a post-translational modification process that regulates the functional properties of many proteins, among which are several proteins implicated in neurodegenerative diseases. This study was aimed to investigate the changes of SUMO-1 expression and modification, and the relationship between SUMO-1 and Alzheimer's disease (AD) pathology in APP/PS1 transgenic AD mice. Using Western blot, co-immunoprecipitation and immunofluorescent staining methods, the SUMO-1 expression and modification and its relation to tau, amyloid precursor protein (APP) and β-amyloid protein (Aβ) in the 12-month-old APP/PS1 transgenic AD mice were analyzed. The results showed that: (1) Compared with the normal wild-type mice, the expression and modification of SUMO-1 increased in brain of AD mice, which was accompanied by an increase of ubiquitination; (2) In RIPA soluble protein fraction of cerebral cortex, co-immunoprecipitation analysis showed tau SUMOylated by SUMO-1 increased in AD mice, however, AT8 antibody labeled phosphorylated tau was less SUMOylated whereas PS422 antibody labeled phosphorylated tau was similar to control mice; (3) Double immunofluorescent staining showed that SUMO-1 could distributed in amyloid plaques, appearing that some of SUMO-1 diffused in centre of some plaques and some of SUMO-1 co-localized with AT8 labeled phosphorylated tau forming punctate aggregates around amyloid plaques which was concerned as dystrophic neurites, however, less Aβ, APP and PS422 labeled phosphorylated tau were found co-localized with SUMO-1. These results suggest that SUMO-1 expression and modification increase abnormally in transgenic AD mice, which may participate in modulation of the formation of senile plaques and dystrophic neurites.
Alzheimer Disease ; physiopathology ; Amyloid beta-Peptides ; metabolism ; Amyloid beta-Protein Precursor ; metabolism ; Animals ; Brain ; pathology ; Mice ; Mice, Transgenic ; Neurites ; pathology ; Phosphorylation ; Plaque, Amyloid ; physiopathology ; SUMO-1 Protein ; metabolism ; Sumoylation ; tau Proteins ; metabolism

Objective：To investigate the correct expression of dengue 2 virus 43 strain NS1 gene in transfected BHK-21 cell. Methods：The D2-43 DNA fragment coding for signal peptide plus NS1 protein was cloned between KpnⅠ site and EcoR Ⅰ site of expression plamid pcDNA3.1. The obtained recombinant vector pcDNA-NS1 was transfected into BHK-21 cells with electroporation technique. After selection by G418, resistant clones were screened by RT-PCR and Western blotting test. Results：The RT-PCR results of four in five randomly selected cell clones were positive. Western blotting test showed that NS1 gene could be expressed in BHK-21 cells. Conclusions：NS1 protein was capable of being expressed and appropriately processed in pcDNA-NS1 transfected BHK-21 cells. The present results suggest the feasibility of NS1-based DNA immunization.

Objective Evaluating the accuracy and safety as well as the equivalence compared with the control kit of RIDA(R) QUICK Norovirus detection kit(R-Biopharm,Germany).Methods Based on the results of commercially available IDEATM Norovirus detection kit (ELISA),the sensitivity and specificity and accuracy of RIDA (R) QUICK Norovirus detection kit (immunochromatographic assay ) were evaluated.Results The sensitivity and specificity of RIDA(R) QUICK Norovirus detection kit were 98.4％ and 92.4％,and the accuracy was 97.6％ compared with the control kit. Conclusion RIDA (R) QUICK Norovirus detection kit has good sensitivity and specificity for the detection of norovirus antigens.

OBJECTIVETo investigate the association of activated coagulation factor VII(F7a) and its gene Msp I polymorphism with coronary heart disease in elderly patients.

METHODSThis was a case-control study, and the method of candidate gene was adopted. F7 genotypes were identified with polymerase chain reaction amplified genomic deoxyribonulieic acid (DNA) and Msp I restriction fragment length polymorphism analysis, and the level of plasma F7a was detected with recombinant tissue factor method for 108 elderly patients with coronary heart disease and 120 sex- and age-matched healthy control subjects.

RESULTS(1) Plasma F7a levels was significantly higher in elderly patients with coronary heart disease than in healthy control subjects (2.88 +/- 0.62 vs 2.58 +/- 0.60 microg/L, P < 0.05), and was significantly higher in old myocardial infarction than in stable angina pectoris (3.12 +/- 0.62 vs 2.76 +/- 0.60, P < 0.05). F7a was shown to be a risk factor for coronary heart disease in elderly patients by Logistic regression analysis (OR=1.21 P < 0.05). (2) The allelic frequencies were in accordance with Hardy-Weinberg equilibrium. The results suggested that the distribution of genotype and allelic frequencies in the groups displayed no significant difference, and there was no difference between the subgroups of coronary heart disease in elderly patients, either (P > 0.05). (3) F7a level was significantly higher in RR genotype than in Q allele carriers (2.72 +/- 0.60 vs 1.98 +/- 0.59 microg/L, P < 0.05) and was associated with F7 gene polymorphism.

CONCLUSIONPlasma F7a level may be an independent risk factor of coronary heart disease in elderly patients, and it may be influenced by the Msp I polymorphism of F7 gene.

Aged ; Binding Sites ; genetics ; Case-Control Studies ; Coronary Disease ; blood ; genetics ; Deoxyribonuclease HpaII ; metabolism ; Factor VII ; genetics ; metabolism ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; genetics ; Genotype ; Humans ; Male ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length

OBJECTIVETo investigate the common TCM syndrome types of fatty liver by way of epidemic questionnaire, their occurrence ratio, and the correlation between various syndrome types and objective indexes.

METHODSA total of national wide 503 subjects with fatty liver were enrolled, the TCM syndromes, body mass index (BMI), abdominal perimeter/hip circumference, liver function, blood lipids, B ultrasonic examination and CT in them were observed and recorded.

RESULTSIn the 46 symptoms investigated in total, the first ten symptoms in order of appearing rate were lassitude, obese, oral dryness, vertigo, hypochondriac distending pain, soreness and pain in loin, spiritlessness, oral bitterness, aching and weakness in knee and abdominal distention. The mostly appeared tongue figures were pale and corpulent or pale dim tongue proper, white greasy or yellow greasy tongue coating, and the mostly appeared pulse figures were taut, taut-thin and taut slippery. Statistical cluster analysis showed that syndromes of fatty liver could be typed into 4 TCM types, the asthenia Pi-Shen with Gan-stagnation type, the asthenia Pi-Shen type, the asthenia Pi with phlegm-heat type and the unclassified type. Among them the asthenia Pi-Shen with Gan-stagnation type was the commonest one, which accounted to 62.32%.

CONCLUSIONThe mostly appeared syndrome type of fatty liver was asthenia Pi-Shen with Gan-stagnation type. The TCM pathogenesis of fatty liver was deficiency of origin, mainly deficiency of Shen, involving Pi, with excess superficiality, the turbid-phlegm and blood stasis.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; China ; epidemiology ; Diagnosis, Differential ; Fatty Liver ; diagnosis ; epidemiology ; etiology ; Female ; Humans ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Surveys and Questionnaires ; Yang Deficiency ; epidemiology ; Yin Deficiency ; epidemiology

OBJECTIVETo evaluate the effect of the length of covered stents in the portal and hepatic veins on long-term clinical efficacy of transjugular intrahepatic portosystemic shunt (TIPS).

METHODSWe retrospectively reviewed 53 cases receiving TIPSs between January, 2008 and December, 2011. All the shunts were created with Fluency stents (8 mm in diameter). Bare metal grafts of the same diameter were implanted to extend the length in the portal and hepatic veins as deemed necessary according to angiographic images. The primary patency, hepatic encephalopathy and patient survival were evaluated during the follow up. The length of the covered stents within the hepatic vein (X1) and in the portal vein (X2), and the total length of stents placed in the hepatic vein (X3) and the portal vein (X4) were measured and their effects on primary patency and the patients'outcomes were evaluated.

RESULTSThe procedures were completed successfully in all the patients and the mean portosystemic pressure decreased from 29.80∓4.83 mmHg to 19.00∓3.92 mmHg (t=13.44, P<0.01) after the procedure. The patients were followed up for a median of 64 months (3 to 89 months, 39 months on average). Hepatic encephalopathy occurred in 23% (12/53) of the patients after TIPS. Shunt dysfunction occurred in 16 cases, and the cumulative primary patency rates at 1 to 5 years were 83%, 75%, 63%, 62%, and 54%, respectively. The cumulative survival rates of the patients at 1 to 5 years were 79%, 72%, 72%, 69%, and 69%, respectively. Cox proportional regression analysis showed a significant association between the length of covered-stent in the hepatic vein and the primary patency (OR=0.42, P<0.01), and there was a significant association between the length of stent in the portal vein and the patient survival. No significant correlation was found between these parameters and hepatic encephalopathy.

CONCLUSIONIncreasing the length of the covered stent in the hepatic vein and decreasing the stent length in the portal vein can improve the primary patency and the patient survival receiving TIPS.

Angiography ; Hepatic Encephalopathy ; Hepatic Veins ; surgery ; Humans ; Portal Vein ; surgery ; Portasystemic Shunt, Transjugular Intrahepatic ; Retrospective Studies ; Stents ; Survival Rate ; Treatment Outcome

OBJECTIVETo investigate whether heart tissue-derived extracellular matrix (ECM) promotes the differentiation of cardiosphere-derived cells (CDCs) implanted in rat infracted myocardium to improve the cardiac structure and function.

METHODSRat CDCs were cultured by cardiac explant methods, and ECM was prepared by decelluariztion method. In a Wistar rat model of acute myocardial infarction established by ligating the left anterior descending branch, IMDM solution, ECM suspension, 10CDCs in IMDM solution, or 10CDCs in ECM suspension were injected into the infracted rat myocardium (6 rats in each group). The cardiac function of the rats was evaluated by cardiac ultrasonography, and the percentage of positive heart fibrosis area after infarction was determined with Masson staining. The differentiation of implanted CDCs in the infarcted myocardium was detected using immunofluorescence assay for the markers of cardiac muscle cells (α-SA), vascular endothelial cells (vWF) and smooth muscle cells (α-SMA).

RESULTSThree weeks after acute myocardial infarction, the rats with injection of CDCs in ECM showed the highest left ventricular ejection fraction (LVEF) and percentage of fraction shortening with the lowest percentage of positive heart fibrosis area; implantation of CDCs with ECM resulted in significantly higher rates of CDC differentiation into cardiac muscle cells, vascular endothelial cells and smooth muscle cell (P<0.05).

CONCLUSIONHeart-tissue derived ECM significantly promotes the differentiation of CDCs implanted in the infracted myocardium into cardiac muscle cells, vascular endothelial cells and smooth muscle cells to improve the cardiac structure and cardiac functions in rats.

Animals ; Cell Differentiation ; Cells, Cultured ; Disease Models, Animal ; Endothelial Cells ; cytology ; Extracellular Matrix ; transplantation ; Myocardial Infarction ; therapy ; Myocardium ; Myocytes, Cardiac ; transplantation ; Myocytes, Smooth Muscle ; cytology ; Rats ; Rats, Wistar

OBJECTIVETo study the linkage between K469E polymorphism of intercellular adhesion molecule 1(ICAM1) gene with ICAM1 plasma level and coronary heart disease (CHD) in Han population of China.

METHODSOne hundred and sixty-four controls without CHD and 160 patients with CHD were enrolled in our study. By nested PCR with allele-specific oligonucleotide primers, all patients and controls were genotyped for the ICAM1 polymorphism. And the ICAM1 plasma level was measured by ELISA.

RESULTSIn the patients with CHD, both K allele frequency and the plasma level of ICAM1 were higher than those in control (P<0.05). The individual with K allele had higher plasma level of ICAM1 than that without K allele (344.34+/-128.59 microg/L vs 303.54+/-108.74 microg/L, P=0.008). K allele enhanced the risk of CHD (P<0.01, OR=2.158, 95%CI: 1.250-3.727). There was the K allele cooperation with smoking in influencing the risk of CHD.

CONCLUSIONThere is the polymorphism of ICAM1 K469E gene in Han population of China, and the K allele may be a genetic factor influencing the risk of CHD.

China ; ethnology ; Coronary Disease ; blood ; genetics ; Gene Frequency ; Humans ; Intercellular Adhesion Molecule-1 ; blood ; genetics ; Polymorphism, Genetic ; Potassium ; antagonists & inhibitors