Objective To explore cardiovascular disease in postmenopausal women with polycystic ovary syndrome(PCOS) phenotype.Methods This study was a prospective follow-up study which included subjects with PCOS phenotype admitted from Jan.1st, 2005 to Dec.31st, 2007 in Gynecology Department of Dongyang People's Hospital.These subjects were divided into two groups according to the presence or absence of PCOS phe -notype and were followed .Kaplan-Meier method was used to estimate survival rate .The survival difference be-tween the two groups was compared using the log-rank test.Multivariate Cox proportional hazards regression was used to determine the independent risk factors of major adverse cardiac events ( MACE) .Results 11 patients in non-PCOS phenotype group had MACE , and 6 patients in PCOS phenotype group had MACE .PCOS phenotype group had a significantly decreased MACE-free survival(χ2 =4.957,P=0.026).Multivariate Cox proportional hazards regression analysis showed that low level of HDL-C, presence of PCOS phenotype and high level of hs-CRP were independent predictors for MACE .Conclusion PCOS phenotype is an independent risk factor for car-diovascular disease in postmenopausal women , help to make further risk stratification and shows cardiovascular disease is closely related to PCOS .

0 05), and there was no significant influence on function of median nerve Conclusion Experiment study in rats showed that the distal nerves can be regenerated after multi nerves end to side neurorrhaphy on a trunk

Objective:To observe the effect of ginsenoside Rd pretreatment on the expressions of N-methyl-D-aspartate(NMDA)receptor subunit NR2 B protein and endonuclease G(EndoG)in basal ganglia region after cerebral focal ischemia-reperfusion in rats and to investigate possible mechanism of ginsenoside Rd in the treatment of ischemic stroke.Methods:A rat model of middle cerebral artery occlusion(MCAO)was induced by intraluminal filament method.The expressions of NR2B and EndoG in basal ganglia region for focal cerebral iSChemia 1 hour,and 1,6,24 and 72 hours reperfusion were detected by immunohistochemical staining and image analysis method.The effects of ginsenoside Rd on the expressions of FaxioG and NR2B and the volume of cerebral infarction were evaluated.Results:The positive expression of NR2B in basal ganglia region on the ischemic side in ischemia-reperfusion group was increased significantly.The expression of EndoG in the nucleus was notable;the positive expressions of NR2B and EndoG at different reperfusion time points in ginsenoside Rd pretreatment group were decreased significantly(P<0.05 or P<0.01),and the volume of cerebral infarction was reduced significantly(P<0.01).Conclusions:The expressions of NMDA receptor subunit NR2B protein and apoptosis-inducing factor EndoG were increased significantly after cerebral focal ischemia reperfusion;ginsenoside Rd pretreatment may significantly reduce the expressions of NR2B and EndoG.It reduces the volume of cerebral infarction by inhibiting excitatory neurotoxicity and blocking neuronal apoptosis,and thus plays a role in neuroprotection.

Objective To analyze the relation between lamivudine-resistant mutation types and HBV genotypes.Methods 95 cases with YMDD mutation were selected from out-patient clinic and sickroom in our hospital.Restriction endonuclease MboⅠand EarⅠwere used to identify HBV genotypes of PCR product, farther a phylogenesis tree was applied to check it.Results We could divide 95 cases into two parts, 75 cases(78.95%) were HBV C genotype and 20 cases(21.05%) were B genotype, these were verified by phylogenesis tree.With regard to the types of YVDD mutation、YIDD mutation and YMDD+YVDD+YIDD mutation, there were 11 cases, 5 cases, 4 cases in genotype B, respectively, but 35 cases, 27 cases, 13 cases in genotype C.We made the cha-test to check genotypes and types of YMDD mutation, ?2= 0.856, P=0.710. There were no significant differences.Conclusions Using MboⅠand EarⅠcan genotype HBV PCR product easily and reliably. It is no statistical significance between HBV B or C genotype and the types of YMDD mutation.

Objective: To investigate the infection state of hepatitis C virus genotype 6a in China.Methods: Three(95,126,150)HCV genotype 6a serum samples were identified by digesting 5′NCR with compound enzyme method.Then,HCV 5′NCR and NS5B fragments were amplified from these samples by RT-PCR assay and sequenced.The phylogenetic trees of the samples were analyzed and compared with 24 HCV complete gene sequences from GenBank.Results: The sequencing reports on 5′NCR showed "CA" bases in 3 serum samples(95,126,150) were inserted into-145 site,and the sequences of 3 serum samples had the highest homology with sequence Y12083(0.934,0.930,and 0.926,respectively).The results of the phylogenetic trees suggested these 3 serum samples belonged to HCV genotype 6a.The sequencing reports on NS5B showed the 3 serum samples also had the highest homology with HC-J4(0.934,0.930,and 0.926,respectively),and the results of the phylogenetic trees suggested these 3 serum samples belonged to HCV genotype 1b.To exclude the influence of amplification efficiency of primers,NS5B fragments were amplified by HCV genotype 6a specific primers and no amplification products appeared.Conclusion: There are different results of HCV genotype by analyzing 5′NCR and NS5B in 3 samples infected with HCV genotype 6a.It may be related with gene recombination.It suggests HCV genotype should be analyzed on more than two regions.

Objective: To develop a hepatitis C virus(HCV) reverse transcription-polymerase chain reaction (RT-PCR) assay using Uracil-DNA glycosylase (UDG) for amplicon contamination control and evaluate the temperature and UDG concentrations for anti-contamination. Methods: In this new HCV RT-PCR assay, reverse transcription, UDG anti-contamination and the first PCR were carried out at the same time. The layer candles were used to prevent the contamination in the second PCR. dU-DNA was used as quality control for UDG anti-contamination and templates to determine the sensitivity of the new HCV RT-PCR assay. HCV cDNA was detected by DNA enzyme immunoassay (DNA-EIA). Results: Complete degradation of amplicon DNA was observed on the conditions of 0.2 u UDG per reaction volume respectively at 37 ℃ and 42 ℃ for 40 min. The anti-contamination condition also could eliminate all detectible dU-DNA, including the highest concentration of amplicon DNA.The 1∶104 dilution of the HCV RNA sample containing 2.110?105copies/mL copies of RNA could be detected. Conclusion: Our results indicate that this new RT-PCR assay can control the contamination stringently and is sensitive as well.

Objective:To investigate the existence condition of hepatitis B surface antigen(HBsAg) termina-tion codon bias.Methods: A total of 174 reference sequences of all kinds of Hepatitis B virus(HBV) genotypes were chosen from GenBank,and compared by BioEdit.Then secondary structure of RNA was constructed and analyzed together.Results:(1) There were two types of HBsAg termination codon: TAA and TGA in 174 reference sequences.TAA was in 124 cases(71.26%);and TGA in 50 cases(28.74%).(2) There was codon bias selection in HBsAg termination codon,and it could affect the secondary structure of RNA and amino acid sequence encoding protein.Conclusion: HBsAg termination codon bias exists and may be related to RNA structure and the conservatiom of protein function in the evolutionary progress.

Objective To investigate the effects of total anthraquinone in rheum on aquaporin 2 and aquaporin 4 expression in rat kidney and explore its diuresis mechanism.Methods Thirty-two SD rats were randomly divided into control group,low dose group,medium dose group and high dose group.Total anthraquinone in rheum was administered to rats at different doses.Urinary volume of 24 h,Na+ concentration and osmolality were detected.Rats were sacrificed 5 days later.Blood samples were taken from the abdominal aorta to detect blood biochemical indicators. Kidneys of rats were removed to detect AQP2, AQP4 expression through immunohistochemistry,Western blot,and RT-PCR. Results Compared with control group,there were significantly increased 24 h urine output of rats in medium and high dose group[(16.21±1.96),(18.16±1.8) ml vs(13.85±1.25)ml,P＜0.05].24 h urine output in low-dose group did not change significantly.AQP2 protein and mRNA expression were significantly decreased in rats'kidneys of medium and high dose group (P＜0.01),The AQP4 protein and mRNA expression was significantly down-regulated in high dose group (P＜0.01).In medium does group,the AQP4 protein expression was down-regulated (P＜0.01),without significant decrease in the mRNA expression.Protein and mRNA expression of AQP2 and AQP4 did not significantly change in low dose group.Conclusion Total anthraquinone in rheum can reduce the expression level of AQP2 and AQP4 in rat kidney,which is probably one mechanism of diuresis caused by rheum.

Objective:To investigate the clinical manifestations and pathogenic gene mutation sites of familial cavernous hemangioma by a pedigree study of this disease.Methods:A family of cerebral cavernous hemangioma who was admitted to the Department of Neurology of the First Affiliated Hospital of Henan University of Science and Technology in April 2019 was diagnosed as cerebral cavernous hemangioma type 1 based on clinical manifestations and head magnetic resonance imaging (MRI), diffusion weighted imaging and susceptibility weighted imaging screening. According to Zabramski classification criteria, the family′s clinical data were collected and genes were sequenced.Results:A 58-year-old female proband had dizziness and headache as the main symptoms, her daughter and son had no clinical symptoms, and her granddaughter had clinical manifestations of cerebral hemorrhage and seizures. The proband and her family members showed multiple cavernous hemangioma on cranial MRI,and the p.L436fs mutation in the KRIT1 gene of familial cerebral cavernous malformation type 1 was confirmed through genetic examination, which was consistent with the Zabramski typing results based on head MRI. The mutation site of the familial spongiform malformation type 1 pathogenic gene was found to be p.L436fs in KRIT1 gene, which has not been reported in familial cerebral cavernous hemangioma type 1 until now.Conclusion:A new p.L436fs mutation of KRIT1 gene was found in familial cerebral cavernous malformation type 1, which expands understanding of the clinical manifestations and pathogenic gene mutation sites of familial cavernous hemangioma.