Adult ; Alkaline Phosphatase ; metabolism ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Cervix Uteri ; metabolism ; pathology ; surgery ; Choriocarcinoma ; metabolism ; pathology ; Chorionic Gonadotropin ; metabolism ; Diagnosis, Differential ; Female ; GPI-Linked Proteins ; metabolism ; Humans ; Hysterectomy ; Placental Lactogen ; metabolism ; Pregnancy ; Trophoblastic Tumor, Placental Site ; metabolism ; pathology ; surgery ; Uterine Cervical Neoplasms ; metabolism ; pathology ; surgery

AIM: To study the expression profile of QKI m RNA and protein in rat heart during pathological cardiac hypertrophy. ME THODS: A rat cardiac hypertrophy model was established using continuous norepinephrine (NE) perfusion. Real-time PCR and Western blotting were applied t o examine QKI mRNA and protein expression respectively in rat heart. RES ULTS: Both mRNA and protein of three QKI isoforms were detected in adult rat heart. QKI-5 mRNA and total QKI protein were remarkably decreased in NE-ind uced hypertrophic heart compared with those in control group (P

Objective To observe the effect of dexamethasone(Dex)on the proliferation and os- teogenic differentiation of human marrow stromal cells(MSCs)in vitro.Methods The primary human MSCs were isolated and cultured by Ficoll seperation culture in vitro.In subcultures,human MSCs were respectively treated with dexamethasone 10~(-9),10~(-8) and 10~(-7) mol/L.The proliferation of human MSCs was measured using MTF method;cytoplasmic alkaline phosphatase(ALP)activity was measured;the osteogenic marker osteopontin (OPN)mRNA were examined by reverse transcriptase polymerase chain reaction(RT-PCR).Results The op- tical density values in cultures treated with dexamethasone 10~(-8) and 10~(-7) mol/L for 8 days were significantly lower than those in the controls(P＜0.05).Treatment of cells with Dex for 12 days led to a significant increase in cytoplasmic ALP activity(P＜0.05)in a dose-dependent manner.Dex induced OPN mRNA.Conclusion Dex inhibits the proliferation of human MSCs and dexamethasone 10~(-7) mol/L leads to a strong decrease in cell number.Dex induces human MSCs differentiate to osteoblastic cells.

To explore the clinical features and common complications of fast resting heart rate (RHR) in hypertensionpatients. Methods: We retrospectively analyzed the entire rest electrocardiogram data of Qingdao study 2000 and Xinyang study2005 in community population elder than 18 years including hypertension patients and non-hypertension subjects. Clinical complications as diabetes, coronary artery disease, hyperlipidemia and stroke, laboratory findings, RHR in ECG, body mass index (BMI), waist to hip ratio and office blood pressure were collected in all participants. Results: A total of 18183 participants were enrolled including 61.6% male, the average age was (45.2±12.7) years including 6763 hypertension patients. Compared with normal BP subjects, hypertension patients had the faster RHR (73.5±11.6) times/min vs (70.6±9.6) times/min, P<0.001 and more hypertension patients combining fast RHR (14.5% vs 6.4%), P<0.001. In hypertension patients, compared with normal RHR patients, fast RHR patients had the elder age (53.9±12.2) years vs (51.8±11.2) years, lower BMI (25.8±3.6) kg/m2 vs (26.4±3.4) kg/m2 and higher ratio of grade 3 hypertension (68.2%vs 59.0%), all P<0.001; higher levels of fasting blood glucose (6.0±2.4) mmol/L vs (5.6±1.5) mmol/L and triglyceride (2.0±1.8) mmol/L vs (1.7±1.3) mmol/L, both P<0.001, higher LDL-C (3.2±0.9) mmol/L vs (3.1±0.8) mmol/L, P=0.001;more patients with diabetes (6.6% vs 3.9%), P=0.007 and stroke (11.1% vs 8.3%), P=0.005. Multivariate regression analysis indicated that with adjusted traditional risk factors, fast RHR was positively related to stroke occurrence in hypertension patients (OR=1.306, 95% CI 1.021-1.671). Conclusion: Fast RHR happened more in hypertension patients than in normal BP subjects; it had the increased risk for stroke occurrence in hypertension patients.

OBJECTIVETo explore the effects of arecoline on hepatic insulin resistance in type 2 diabetes rats and to elucidate its possible mechanism.

METHODSForty five Wistar rats were fed with high fructose diet for 12 weeks to induce type 2 diabetic rat model. rats were randomly divided into 5 groups (n = 8): control group, model group and model group were treated with different dose (0, 0.5, 1, 5 mg/kg) of arecoline. After 4 weeks, the fasting blood glucose, blood lipid and insulin level measured , mRNA expression of liver constitutive androstane receptor (CAR), pregnane X receptor (PXR), glucose-6-phosphatase (G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were detected by reverse transcription polymerase chain reaction (RT-PCR), the protein expression of p-AKT and glucose transporter4 (GLUT4) were detected by Western blot.

RESULTS1.5 mg/kg arecoline could significantly decrease the level of fasting blood glucose, blood lipid, blood insulin level and liver G6Pase, PEPCK, IL-6, TNF-alpha mRNA level in type 2 diabetes rats. 1.5 mg/kg arecoline also could significantly increase CAR, PXR mRNA level and p-AKT and GLUT4 protein expression.

CONCLUSIONArecoline improved hepatic insulin resistance in type 2 diabetes rats by increasing the mRNA levels of CAR and PXR leading to the creased glucose metabolism and inflammation related genes expression.

Animals ; Arecoline ; pharmacology ; Diabetes Mellitus, Experimental ; metabolism ; Diabetes Mellitus, Type 2 ; metabolism ; Glucose Transporter Type 4 ; metabolism ; Glucose-6-Phosphatase ; metabolism ; Insulin Resistance ; Interleukin-6 ; metabolism ; Intracellular Signaling Peptides and Proteins ; metabolism ; Liver ; drug effects ; metabolism ; Male ; Phosphoenolpyruvate Carboxykinase (GTP) ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear ; metabolism ; Receptors, Steroid ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo study the relationship between plasma homocysteine (Hcy) level and deep-vein thrombosis (DVT), and analyze the interaction of Hcy, folate and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism in patients with DVT.

METHODSTotally 69 patients with DVT and 111 healthy controls were included in our case-control study. We determined the MTHFR C677T genotypes by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP), measured the serum folate and vitamin B12 by radioimmunoassay (RIA), and measured the plasma homocysteine level by fluorescence polarization immunoassay (FPIA).

RESULTSThe frequency of the MTHFR C677T TT genotype had no significant difference between DVT group and control group (P > 0.05). The plasma Hcy level was significantly higher in DVT group than in control group (13.03 +/- 8.74 mumol/L vs 10.14 +/- 4.30 mumol/L, P < 0.05). Both serum folate and VitB12 of patients with DVT were not significantly different from those of controls. The odds radios (OR) of hyperhomocysteinemia for DVT was 2.53 (95% CI 1.08-5.92). The interaction of low folate level and TT genotype increased the risk of DVT (OR = 3.12, 95% CI 1.17-8.38).

CONCLUSIONHyperhomocysteinemia may be an independent risk factor for DVT in Han nationality, while serum folate level and MTHRF C677T genotype are not. An interaction between serum folate level and MTHFR genotype that affect the Hcy level is an important risk factor for DVT.

Adult ; Aged ; Aged, 80 and over ; Female ; Folic Acid ; blood ; Genetic Predisposition to Disease ; Homocysteine ; blood ; genetics ; Humans ; Hyperhomocysteinemia ; blood ; genetics ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Middle Aged ; Polymorphism, Restriction Fragment Length ; Venous Thrombosis ; blood ; etiology ; genetics ; Vitamin B 12 ; blood

Objective To detect the effective connectivity of resting- state functional magnetic resonance imaging (fMRI) in normal adults. Methods 36 normal adults were performed resting-state fMRI scanning, and 5 brain netwokes were included as regions of interests. Independent component (ICA) was used to evaluate the effective connectivity, and multivariate Granger causality analysis (mGCA) was used to analyze the casuality between the networks. All preprocessing steps were carried out using Statistical Parametric Mapping 5.0 software. Results 5 classic resting brain networks including default mode network (DMN), memory network (MeN), motor network (MoN), auditory network (AN) and executive control network (ECN) were aquired. The mGCA presented significant casuality between DMN and other 4 networks, MeN and ECN, AN and MoN, ECN and AN. Conclusion There are specific brain effective connectivity of resting-state fMRI in normal adults, and there is significant causal link between these networks.

BACKGROUNDInterleukin-13 (IL-13) is recognized to be a key modulator in the pathogenesis of Th2-induced allergic inflammation. Transcription factors GATA3 and NFAT1 have been both implicated in the regulation of Th2 cytokines. We previously demonstrated the GATA3-NFAT1 association during human T cell activation. However, the function of the GATA3-NFAT1 complex in Th2 cytokines regulation is still unknown. Small interference RNA (siRNA) was constructed to knock down GATA3 expression in Hut-78 cells to investigate the possible role of GATA3-NFAT1 complex in IL-13 transcription.

METHODSCells were stimulated with anti-CD3 plus anti-CD28 antibodies to mimic in vivo antigen-mediated co-stimulation; the expression of IL-13 mRNA was determined by real-time PCR; chromation immunoprecipitation (CHIP) assay was employed to investigate the NFAT1 binding to IL-13 promoter.

RESULTSGATA3 siRNA suppressed the expression of GATA3 both in mRNA and protein levels in Hut-78 cells. The binding of NFAT1 to IL-13 promoter was inhibited by GATA3 siRNA in activated T cells, which was followed by the reduction of IL-13 transcription.

CONCLUSIONGATA3-NFAT1 complex may play an important role in the regulation of IL-13 transcription in human T cells.

Cells, Cultured ; GATA3 Transcription Factor ; antagonists & inhibitors ; genetics ; Humans ; Interleukin-13 ; genetics ; NFATC Transcription Factors ; metabolism ; Promoter Regions, Genetic ; RNA, Small Interfering ; genetics ; T-Lymphocytes ; metabolism ; Transfection

OBJECTIVETo study the relationship between human herpesvirus 6 (HHV-6) and oral squamous cell carcinoma.

METHODSThe serum anti-HHV-6 antibody titers from oral squamous cell carcinoma patients and control subjects were detected by indirect immunofluorescence assay. HHV-6 DNA in peripheral blood mononuclear cells from oral squamous cell carcinoma patients and control subjects was amplified by PCR with primers from sequence of HHV-6 and the specificity was confirmed by Southern-blot hybridization with an internal probe oligonucleotide. An immunohistochemical staining using rabbit anti-HHV-6 antibody was used to detect HHV-6 antigen in oral tumor tissues from oral squamous cell carcinoma patients.

RESULTSSignificantly higher proportion of patients with oral carcinoma (16/16) had IgG antibody to HHV-6 in sera compared with those (12/16) in control subjects, and geometric mean titer of these two groups was 1:118 and 1:64 respectively (P less than 0.05). The detectable rate of HHV-6 DNA in peripheral blood mononuclear cells for the above groups was 10/16 and 6/16 respectively (P less than 0.05). HHV-6 antigens were positive in 9 out of 12 oral tumor cases and in only 2 out of 8 pericancerous tissues the difference between these two groups was also significant (P less than 0.05).

CONCLUSIONThese results demonstrated the frequent presence of HHV-6 in oral squamous cell carcinoma, therefore, HHV-6 possibly play a role in the pathogenesis of oral squamous cell carcinoma.

Antibodies, Viral ; blood ; Carcinoma, Squamous Cell ; virology ; DNA, Viral ; blood ; Herpesviridae Infections ; complications ; virology ; Herpesvirus 6, Human ; genetics ; immunology ; isolation & purification ; Humans ; Immunoglobulin G ; blood ; Infant ; Mouth Neoplasms ; virology

Proliferation of vascular smooth muscle cells (VSMCs) is often accompanied by changes in intracellular actin distribution. The changes are controlled by the signal transduction pathways of protein kinase C/mitogenic activated protein kinase (PKC-MAPK), but the mechanism is unclear. In order to study the effect of insulin on the intracellular signal transduction (PKC-MAPK) probably involved in the modulation of proliferation and redistribution of actins in the VSMCs, the DNA synthesis, MAPK activities and its gene expression, and the redistribution of intracellular actins were investigated in the isolated VSMCs of SHR pretreated with PKC inhibitor and/or insulin, respectively. We found that insulin treatment resulted in proliferation of the VSMCs and an increase in [(3)H] TdR incorporation. Meanwhile, the activities and expression of MAPK increased significantly compared to the control group. These effects of insulin were blocked by PKC inhibitor. In addition, insulin caused a redistribution of the intracellular actins in VSMCs, which was also inhibited by PKC inhibitor. It is, therefore, suggested that these effects of insulin on VSMCs proliferation and distribution of the intracellular actins may be mediated by the MAPK signal transduction pathway.
Actins ; metabolism ; Animals ; Cell Division ; drug effects ; In Vitro Techniques ; Insulin ; pharmacology ; Mitogen-Activated Protein Kinases ; physiology ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; drug effects ; enzymology ; metabolism ; Protein Kinase C ; physiology ; Rats ; Rats, Inbred SHR ; Tissue Distribution