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Objective To detect the plasma plasminogen activator inhibitor-1(PAI-1)and urokinase-type plasminogen activator(uPA)levels in PCOS and control of different BMI.Methods This experiment is divided into PCOS group and control group,PCOS group also divided into obesity and without obesity.To assay plasma PAI-1 and serum uPA of PCOS with or without obesity by enzyme-linked immunosurbent assay(ELISA),and to meassure body mass index(BMI),waist hip ratio(WHR),blood glucose,fasting insulin and IRT.To evaluate insulin resistance with Homa Model and to measure insulin area under curve(AUC).Results LH/FSH,T,blood glucose,HOMA-IR,AUC and the plasma level of PAI-1 were significantly increased in PCOS as compared with normal control,and HOMA-IR,AUC and the plasma level of PAI-1 were also increased in obesity as compared with non-obesity of PCOS(P
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ObjectiveTo explore the molecular mechanism of neural tube defects (NTDs) caused by hyperglycemia and thiadiazole and the antagonistic effect of taurine MethodsThe pregnant mice were divided into hyperglycemia groups, thiadiazole group,taurine groups and control groups The mRNA and the protein of Pax3 or Cx43 gene were detected respectively by reverse transcription-polymerase chain reaction assay and immunohistochemical method ResultsAs compared with mice treated by thiadiazole-stomach-perfusing, NTDs were significantly increased from mice treated with glucose-injection when blood glucose levels were ≥ 13 4 mmol/L Elevated glucose and thiadiazole could cause changes in Pax3 and Cx43 expression Hyperglycemia had stronger developmental toxicity on mice embryos Expression of Pax3 (mRNA 0 97?0 20, protein 0 11?0 02) in hyperglycemia group was significantly decreased, while expression of Cx43 (mRNA 7 05?1 63, protein 0 94?0 05) was significantly increased, and the relationship of dose-effect was demonstrated In the thiadiazole group, the expression of Cx43 (mRNA 6 96?0 73, protein 0 92?0 12) was significantly stronger than control groups, but there were no significant differences in expression of Pax3 between thiadiazole and its control groups Both of their teratogenicity could be antagonized by taurine ConclusionsThis study suggests that congenital malformation associated with diabetic pregnancy is caused by disruption of regulatory genes,Pax3 and Cx43 expression in embryo in response to elevated glucose Thiadiazole can only disturb the regulation of Cx43 gene causing NTDs Taurine can correct the disruption caused by the two teratogens
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CLN3 gene product is an antiapoptotic membrane protein, the expressions of CLN3 in normal tissues and cells are at very low level. Juvenile-Batten disease is a neurodegenerative disease caused by accelerated apoptosis of photoreceptors and neurons resulting from deletion of 1.02 kb in the CLN3 gene. A number of observations showed that CLN3 mRNA and protein are overexpressed in a variety of human cancer cell lines. Blocking of CLN3 expression using an adenovirus-expressing antisense CLN3 inhibited growth and viability of cancer cells. CLN3 may regulate apoptosis through modulating ceramide synthesis or the expression of some down stream genes. More importantly, these results suggested that CLN3 is a novel molecular target for the etiology, progression and theraputics of cancer.
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Objectives:To observe the influence of PN treatment on the postoperative patients of advanced ovarian cancer. Methods:The patients were divided into two groups.Thirty cases of patients(PN group) were treated with PN after the operation for the ovarian cancer.Thirty five cases of patients(control group) were treated regularly without PN.The biochemical indicators,complications and mortality rate were compared between the two groups. Results:The biochemical indicators in PN group were better than those in control group.The incidence of complications and mortality rate in PN group were significantly lower than those in control group. Conclusions:PN can improve the general status of postoperative patients with advanced ovarian cancer and decrease the complication incidence and motality rate.