ABSTRACT
[Objective] The aim of our study is to examine nodule prevalence in a population over 40 years old in order to explore the relation between prevalence of thyroid nodules and metabolic parameters.[Methods] A total of 1875 individuals who were over 40 years of age were received the questionnaire and underwent thyroid ultrasonography examinations.Height,weight,waist circumference,blood pressure were measured.Levels of fasting blood glucose,fasting serum insulin,glycated hemoglobin,blood lipids,thyroid stimulating hormone and free T4 were detected.Body mass index (BMI) and homeostasis model assessment-insulin resistance (HOMA-IR) were calculated.[Result] The study included a total of 1875 subjects (513 men and 1362 women).The age of subjects were between 41 and 113 years old,and the mean age was 57.4±7.1 years old.The prevalence of thyroid nodules was 51.2％,and the prevalence of thyroid nodules in women was significantly higher than that in men (53.4％ vs.45.2％,P=0.002).The prevalence of thyroid nodules was significantly higher in subjects with hypertriglyceridemia (59.2％ vs.49.5％,P=0.009) and hypertension (56.5％ vs.47.8％,P＜ 0.001).Result of multivariate binary logistic regression revealed that hypertension (OR=1.405,P=0.002),female sex (OR=1.490,P=0.001),older age (OR=1.028,P＜0.001),and hypertriglyceridemia (OR=1.589,P=0.005) were independent risk factors for thyroid nodules.The prevalence of thyroid nodules increased along with age,systolic blood pressure and serum triglyceride level.[Conclusion] The prevalence of thyroid nodules and metabolism-related diseases were high in population over 40 years old.After adjusted for age and sex,hypertriglyceridemia and hypertension were possible independent risk factors for thyroid nodules especially in women.In general,hypertriglyceridemia and hypertension might play an important role in the pathological process of thyroid nodules.
ABSTRACT
Objective Association between the 45T/G and 276G/T single nueleotide polymorphisms of adiponectin gene and the occurrence of type 2 diabetes in Chinese population was studied. Methods 20 studies consisting 22 ease-control comparisons about 45T/G polymorphism and nine case-control studies about 276G/T polymorphism that were based on our inclusion criterion and available in the literature were reviewed. Results Results from Meta-analysis demonstrated a large heterogeneity among the studies both on 45T/G and 276G/T polymorphisms and a significant association was observed between 45T/G polymorphism at exon 2 of the adiponectin gene and type 2 diabetes among the Chinese population. 45Gallele appeared to be one of the genetic risk factors for susceptibility to type 2 diabetes with a random effects odds ratio ( OR ) of 1.43 ( 95 % CI : 1.17-1.75 ), and the G allele carriers were more susceptible to the disease with an OR of 1.38 ( 95 % CI : 1.04-1.84 ). Results from Meta-analysis, however, showed no association between the 276G/T polymorphism and type 2 diabetes in the Chinese populationr while the random effects OR of the allele 276T to susceptibility of disease was 0.83 (95% CI: 0.61-1.13).Conclusion The current paper on Meta-analysis demonstrated a correlation between the 45T/G single nucleotide polymorphism and the occurrence of type 2 diabetes in Chinese population, which was different from the findings that such an association with 276G/T polymorphism could not be demonstrated in the same ethnic population.
ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the correlation between the beta-fibrinogen gene-455G/A polymorphism and cerebral infarction in Chinese population by means of meta-analysis.</p><p><b>METHODS</b>Genetic association studies on evaluating the beta-fibrinogen gene -455G/A polymorphism and cerebral infarction involving Chinese population published before December 2005 were collected from database of PubMed, EMBASE, and CNKI. All the data in literature were abstracted based on the defined selection criteria by two independent investigators. Publication bias was tested by funnel plot and the odd ratios of all studies were combined dependent on the result of heterogeneity test among the individual studies. The software Review Manager (Version 4.2) was used for meta-analysis.</p><p><b>RESULTS</b>Eleven studies including 1405 patients and 1600 controls met the selection criteria. There was no publication bias in 11 reviewed studies. Heterogeneity test of reviewed studies showed statistically significant differences (chi2=24.58, P=0.006) among the ORs of individual studies. The combined OR of 11 studies of susceptibility to cerebral infarction in -455A allele carriers compared with the -455G/G wild homozygotes was 1.33 (95%CI 1.04-1.71, P=0.02). In the patients with cerebral infarction in 6 studies, the summarized average plasma fibrinogen level of allele A carrier was 0.29 g/L (95%CI 0.14-0.44, P=0.0002) higher than that of -455G/G homozygous ones.</p><p><b>CONCLUSIONS</b>beta-fibrinogen gene -455G/A polymorphism might contribute to susceptibility of cerebral infarction in Chinese population; allele A increases the individual susceptibility to the disease.</p>
Subject(s)
Humans , Asian People , Genetics , Cerebral Infarction , Blood , Fibrinogen , Genetics , Polymorphism, GeneticABSTRACT
<p><b>OBJECTIVE</b>The results of studies on association between -148C/T polymorphism in promoter region of beta-fibrinogen gene and susceptibility to cerebral infarction in Chinese population are controversial. In this study, we summarize the results of published works in this field by a meta-analysis. Data sources Genetic association studies evaluating the beta-fibrinogen gene -148C/T polymorphisms and cerebral infarction involving Chinese population published before December 2005 were collected from PubMed, EMBASE and CNKI. Study selection Case control studies involving unrelated, Han subjects aged from 18 to 80 years, and the internationally recognized diagnostic standard of cerebral infarction and genotype frequencies in control group consistent with Hardy-Weinberg equilibrium were used. Publication bias was tested by funnel plot and the odds ratios of all studies were combined dependent on the result of heterogeneity test among the individual studies. The software Review Manager (Version 4.2) was used for meta-analysis.</p><p><b>RESULTS</b>Eleven studies including 1223 patients and 1433 controls met the selection criteria. There was no heterogeneity among the odds ratios (ORs) of individual studies (chi(2) = 17.82, P = 0.06). The combined OR of susceptibility to cerebral infarction in -148T allele carriers compared to the wild homozygote was 1.32 (95% CI 1.12 to 1.55, P = 0.0008). In the patients with cerebral infarction, the average plasma fibrinogen level of allele T carrier was 0.42 g/L (95% CI 0.29 to 0.54, P < 0.001), higher than that of -148C/C homozygous ones.</p><p><b>CONCLUSIONS</b>beta-fibrinogen gene -148C/T polymorphism might contribute to susceptibility to cerebral infarction in Han Chinese. To reach a definitive conclusion, further gene to gene and gene to environment interactions studies on beta-fibrinogen polymorphisms and cerebral infarction with large sample size are required.</p>
Subject(s)
Humans , Cerebral Infarction , Genetics , China , Ethnology , Fibrinogen , Genetics , Genetic Predisposition to Disease , Polymorphism, GeneticABSTRACT
<p><b>BACKGROUND</b>Some single nucleotide polymorphisms (SNPs) in the peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha gene have been reported to be associated with type 2 diabetes in different populations, and studies on Chinese patients yielded controversial results. The objective of this case-control study was to explore the relationship between SNPs of PGC-1alpha and type 2 diabetes in the southern Chinese population and to determine whether the common variants: Gly482Ser and Thr394Thr, in the PGC-1alpha gene have any impacts on interaction with myocyte enhancer factor (MEF) 2C.</p><p><b>METHODS</b>The SNPs in all exons of the PGC-1alpha gene was investigated in 50 type 2 diabetic patients using polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) and direct sequencing. Thereafter, 263 type 2 diabetic patients and 282 healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). A bacterial two-hybrid system and site-directed mutagenesis were used to investigate whether Gly482Ser and Thr394Thr variants in the PGC-1alpha gene alter the interaction with MEF2C.</p><p><b>RESULTS</b>Three frequent SNPs (Thr394Thr, Gly482Ser and Thr528Thr) were found in exons of the PGC-1alpha gene. Only the Gly482Ser variant had a different distribution between diabetic patients and healthy subjects, with the 482Ser allele more frequent in patients than in controls (40.1% vs 29.3%, P < 0.01). Even in controls, the 482Ser (A) carriers were more likely to have higher levels of total cholesterol and low-density lipoprotein cholesterol than the 482Gly (G) carriers. The 394A-482G-528A haplotype was associated with protection from diabetes, while the 394A-482A-528A was associated with the susceptibility to diabetes. The bacterial two-hybrid system and site-directed mutagenesis revealed that the 482Ser variant was less efficient than the 482Gly variant to interact with MEF2C, whereas the 394Thr (A) had a synergic effect on the interaction between 482Ser variant and MEF2C.</p><p><b>CONCLUSIONS</b>The results suggested that the 482Ser variant of PGC-1alpha conferred the susceptibility to type 2 diabetes in the southern Chinese population. The underlying mechanism may be attributable, at least in part, to the altered interaction between the different variants (Gly482Ser, Thr394Thr) in the PGC-1alpha gene and MEF2C.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Asian People , Genetics , China , Diabetes Mellitus, Type 2 , Ethnology , Genetics , Genotype , Heat-Shock Proteins , Genetics , Metabolism , MEF2 Transcription Factors , Myogenic Regulatory Factors , Metabolism , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha , Polymerase Chain Reaction , Polymorphism, Single Nucleotide , Polymorphism, Single-Stranded Conformational , Protein Binding , Transcription Factors , Genetics , MetabolismABSTRACT
<p><b>BACKGROUND</b>The decreased degradation of extra-cellular matrix proteins plays an important role in the onset of diabetic nephropathy. Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1), which are members of the matrix metalloproteinase family, are associated with this process. Angiotensin II (AII) plays an important role in the development of diabetic nephropathy also. This research aimed to investigate the effect of angiotensin II receptor blocker on glucose-induced mRNA expressions of MMP-9 and TIMP-1 in rat mesangial cells.</p><p><b>METHODS</b>Rat mesangial cells were cultured and divided into 5 groups: normal glucose (group NG), high glucose (group HG), group NG + AII, NG + AII + saralasin (group NG + AII + S, saralasin is the AII receptor blocker) and HG + saralasin (group HG + S). After the cells were incubated for 24 hours, AII concentrations in the supernatant were measured by radioimmunoassay and the expression of MMP-9 and TIMP-1 mRNA was assayed by reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>AII concentrations were higher in group HG ((56.90 +/- 13.54) pg/ml) and group HG + S ((51.30 +/- 5.96) pg/ml) than in group NG ((37.89 +/- 8.62) pg/ml, P < 0.05), whereas there was no significant difference between group HG and group HG + S. The expression of MMP-9 mRNA and MMP-9/TIMP-1 mRNA ratio in group NG + AII (MMP-9, 0.33 +/- 0.04; MMP-9/TIMP-1, 0.40 +/- 0.06) and group HG (MMP-9, 0.36 +/- 0.02; MMP-9/TIMP-1, 0.45 +/- 0.03) were decreased more significantly than those in group NG (MMP-9, 0.72 +/- 0.02; MMP-9/TIMP-1, 1.21 +/- 0.07). These values in group NG + AII + S (MMP-9, 0.71 +/- 0.02; MMP-9/TIMP-1, 1.18 +/- 0.05) were higher than those in group NG + AII, and the values in group HG + S (MMP-9, 0.71 +/- 0.02; MMP-9/TIMP-1, 1.16 +/- 0.05) were higher than those in group HG (all were P < 0.05). TIMP-1 mRNA expression was increased more significantly in group NG + AII (0.81 +/- 0.03) and group HG (0.80 +/- 0.03) than in group NG (0.59 +/- 0.02), but it was lower in group NG + AII + S (0.60 +/- 0.01) than in group NG + AII and also lower in group HG + S (0.61 +/- 0.01) than in group HG (all were P < 0.05).</p><p><b>CONCLUSIONS</b>High glucose stimulates AII production. Both high glucose and AII induce a decrease in MMP-9 mRNA expression and MMP-9/TIMP-1 mRNA ratio as well as an increase in TIMP-1 mRNA expression, which can be reversed by saralasin, suggesting that high glucose can aggravate impaired matrix degradation by altering gene expression of MMP-9 and TIMP-1 and that the effect of high glucose may be mediated by AII.</p>
Subject(s)
Animals , Rats , Angiotensin II Type 1 Receptor Blockers , Pharmacology , Angiotensin Receptor Antagonists , Cells, Cultured , Gene Expression , Glucose , Pharmacology , Matrix Metalloproteinase 9 , Genetics , Mesangial Cells , Cell Biology , Metabolism , RNA, Messenger , Genetics , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Saralasin , Pharmacology , Tissue Inhibitor of Metalloproteinase-1 , GeneticsABSTRACT
Objective To induce mouse embryonic stem(ES)cells to differentiate into insulin-secreting cells by means of a 5-step model system.Methods E14.1 mouse ES cells were cultured in the presence of leukemia inhibitory factor(LIF)for 2 days(step 1),then the cells were cultured in hanging drops to form embryonic bodies(EBs)and the resulting EBs were cultured in suspension for 6 days in the presence of basic fibroblast growth factor bFGF(step 2).Subsequently the EBs were cultured in the medium containing glucagon- like peptide 1(GLP-1),hepatocyte growth factor(HGF),nerve growth factor(NGF)and nicotinamide for 10 days(step 3).After that,the EBs were dissociated into single cells,and the cells were cultured in monolayer in the presence of GLP-1,betacellulin,activin A,bFGF and nicotinamide for 10 days(step 4).Finally,the cells were cultured in low-glucose medium containing nicotinamide for 4 days(step 5).Insulin and some other islet- related genes expressions were investigated using RT-PCR and insulin expression was also investigated by DTZ- staining and immunohistochemistry.The percentage of insulin-secreting cells was evaluated by flowcytometry and insulin concentrations were measured by RIA.Results mRNA expression of insulin became visible at step 3 and more evident at step 5.Additionally,at step 5,mRNAs of glucagon,somatostatin,pancreatic polypeptide(PP), pancreatic duodenal homeobox 1(PDX-1),beta-cell E box transactivator 2(Beta2)and neurogenin 3(Ngn3) were detected.DTZ-staining positive cells and insulin immunohistochemical staining positive cells were observed. The percentage of insulin-positive cells was(24.0?2.5)%(n=6).In the presence of 5.6 mmol/L and 25 mmol/L glucose,insulin concentrations were(0.05?0.01)?g/L and(0.13?0.02)?g/L respectively(n= 6).Conclusion E14.1 mouse ES cells can be induced to differentiate into insulin-secreting cells by the 5-step model system.Insulin-secreting cells can release insulin into culture medium when treated with glucose,and insulin concentrations increase with rising concentration of glucose.