In order to investigate the mechanism of elevated vascular endothelial growth factor (VEGF) in peritoneal fluids from patients with endometriosis, macrophages were recovered from peritoneal fluids obtained at the time of diagnostic laparoscopy from infertile women with endometriosis (EMT group, n=20) and without endometriosis (control group, n=20). Macrophages were cultured in vitro. The VEGF levels of peritoneal fluid and the supernatant of macrophages culture were determined by enzyme linked immunoassay (ELISA). Meanwhile, the eutopic (n=20) and ectopic endometrium (n=20) from endometriosis patients, and normal edometrium (n=20) from non-endometriosis patients were obtained for the analysis of VEGF expression by labeled Streptavidin Biotin (LSAB). It was found that VEGF levels in peritoneal fluid and macrophages culture supernatant were significantly higher in EMT group than in control group (P<0.01). In normal endometrium, VEGF showed a cyclic changes and similar in eutopic and ectopic endometrium from patients with endometriosis. There was no difference in the intensity of VEGF in endometrium between two groups within each menstrual phase. It is suggested that altered VEGF production by peritoneal macrophages and ectopic endometrium secretion may contribute to the elevated VEGF levels in the peritoneal fluid of patients with endometriosis.
Ascitic Fluid/*metabolism ; Cells, Cultured ; Endometriosis/*metabolism ; Macrophages, Peritoneal/pathology ; Vascular Endothelial Growth Factor A/*biosynthesis

In order to explore the effects of metformin combined with cyproterone acetate (CPA) on the clinical features, endocrine and metabolism of the patients with polycystic ovarian syndrome (PCOS), 50 cases of non-obese PCOS were randomly subjected to CPA (CPA treatment group, n = 25) and CPA+ metformin (n = 25) treatment for 6 months. Before and after treatment the body mass index (BMI), waist : hip ratio (WHR), ovarian volume, serum gonadotrophin, androgen and sex hormone-binding globulin (SHBG) levels, and fasting lipid, glucose and insulin levels were measured. The results showed that all of the parameters in two groups were similar before treatment. After treatment for 6 months in the CPA+ metformin group, BMI and WHR were significantly decreased, while insulin sensitivity was significantly decreased as Compared with those before treatment. In CPA group, no significant changes were found before and after treatment. Combined use of CPA and metformin could result in the reduction of serum androstenedione and increases of serum SHBG levels as compared with the CPA treatment alone. It was concluded that combined use of CPA and metformin could improve the insulin sensitivity, and further suppress the hyperandrogenism in non-obese women with PCOS.
Androgen Antagonists/therapeutic use ; Androstenedione/blood ; Body Mass Index ; Cyproterone Acetate/*therapeutic use ; Drug Therapy, Combination ; Hypoglycemic Agents/*therapeutic use ; Insulin Resistance ; Metformin/*therapeutic use ; Polycystic Ovary Syndrome/*drug therapy

Objective:To investigate the effects of clinically achievable dose of lovastatin on prostate cancer PC3 cells.Methods:PC3 prostate cancer cells were treated with dimethyl sulfoxide(DMSO),or lovastain only,or lovastatin with mevalonic acid for 24,48 and 72 hours respectively.MTT assay was used to detect the cell viability.By means of [3H] thymidine incorporation tests,the effects of lovastatin on cell proliferation were analyzed.Western blot was used to detect activated casepase3,caspase7,and cleaved PARP(cPARP),the important molecules on the apoptosis pathway.Results:Cell proliferation of PC3 was significantly inhibited by 39.29%[(63.69%?3.69%) vs(102.98%?6.84%),P=0.000] after 48 h treatment with lovastatin at its clinically achievable dose of 2 ?mol/L.After 72 hours the cell proliferation was inhibited by 44.24% [(52.79%?9.88%) vs(97.03%?0.87%),P=0.048].The cell number was also markedly decreased(4.86?105 ? 0.10?105) vs(9.66?105?0.10?105),P=0.000] after 72 h treatment at this low concentration of 2 ?mol/L.The viability of PC3 cells was significantly decreased 50.12%(56.52%?6.40%) vs(106.64%?5.27%),P=0.000] and 60.05%(41.99%?11.64%) vs(102.94%?8.49%),P=0.000] after 48 h and 72 h treatment,respectively.In addition,2 ?mol/L lovastatin induced activation of casepase7 and led the death substrate PARP to cleavage.Conclusion:Clinically achievable dose of lovastatin inhibits prostate cancer PC3 cell proliferation and induces PC3 cell apoptosis.

Objective The surgery time for patients with infective endocarditis (IE) has been transformed.It has been supported that,for the patients with surgical indications,the surgery time should be as early as possible to improve the clinical outcome.The purpose of the research is to identify whether the patients with IE could get further benefit from early surgery.Methods Between June 1996 and July 2011,135 IE patients'data has been collected retrospectively,all of whom were verified through the modified Duke categories.The patients were devided into group A( the new therapeutic schedule group after 2008 ) and group B( the traditional therapeutic schedule group before 2008 ) by the year of 2008.The end points of observation were death associated with IE,cardiac failure,embolism,and re-infection.The comparison between the groups was by means of non-parameter rank and inspection test,variance analysis,t test,chi-square test,fisher exact test.The outcome comparison between the groups was via the Kaplan-Meier survival analysis.Results There were no significant differences in baseline data between the groups.No survival differences could be observed via the Kaplan-Meier analysis( Log Rank P =0.189).During the following-up visit,compared with the patients in group B,the mortality in group A is lower(9.4％ vs.23.0％,P=0.016),the incidence of heart failu re was less in group A (5.4％ vs.26.2％,P ＜0.001 ).No differences could be found in re-infection between the two groups(0 vs.4.9％,P =0.112 ). More patients in group A underwent surgery (67.6％ vs.32.8％,P ＜0.001 ).Conclusion The new therapeutic sehedule of IE coull reduce the mortality rate and promote the cardiae funetion.The incidence of re-infeetion didn't increase.

Obesity is an established risk factor for endometrial cancer. Leptin, a secreted protein of the ob gene by white adipose tissue, plays an important role in the regulation of food intake and energy consumption in the brain and acts as a potential growth stimulator in normal and neoplastic cancer cells. However, a direct role for leptin in endometrial cancer has not been demonstrated. In the present study, the effect of leptin on the proliferation of Ishikawa endometrial cancer cells was investigated as well as the possible mechanism(s) underlying this action in endometrial cancers which express both short and long isoforms of leptin receptors. The expression of leptin receptor (ObRb) in Ishikawa cells was detected by RT-PCR and Western blotting. The cells after serum starvation, were treated by leptin with various concentrations (0, 10, 50, 100, 150 ng/mL) for different durations (6, 12, 24 h). The effect of leptin treatment on cell proliferation was examined by MTT assay. Meanwhile, inhibitory effect of Janus tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) inhibitor AG490 or extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor PD98059 on the proliferation of Ishikawa cells induced by leptin was also studied. Ishikawa cells were treated with 100 ng/mL leptin for various periods (0, 20, 40, 60 min), and the levels of STAT3 phosphorylation and ERK1/2 phosphorylation were examined by Western blotting. The results showed that leptin induced the phosphorylation of STAT3 and the activation of ERK1/2 in a time- and dose-dependent manner in the Ishikawa endometrial cancer cells. Blocking STAT3 phosphorylation with the inhibitor AG490, or blocking ERK1/2 activation by the specific ERK1/2 kinase inhibitor, PD98059, abolished leptin-induced proliferation of Ishikawa cells. In addition, leptin was found to potently induce the invasion of endometrial cancer cells in a Matrigel invasion assay. Leptin-stimulated invasion was effectively blocked by pharmacological inhibitors of STAT3 (AG490) and ERK1/2 kinase (PD98059). These results suggested that leptin promotes endometrial cancer growth and invasiveness by activating STAT3 and ERK1/2 signaling pathways and therefore blocking its action at the receptor level can be a rational therapeutic strategy.

The effect of rosiglitazone on endocrine, metabolism and ovulatory performance in the paitents with polycystic ovary syndrome (PCOS) and insulin resistance was investigated. Twenty-five patients diagnosed as having polycystic ovary syndrome (PCOS) combined with insulin resistance were treated with rosiglitazone for 12 weeks. Before and after treatment, serum luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E2), testosterone (T), androstenedione (A), sex hormone binding globulin (SHBG), insulin and glucose concentration, total cholesterol, triglycerides (TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholestero (LDL-C), apolipoprotein A, apolipoprotein B levels and ovulatory performance were determined. The results showed that after treatment serum insulin levels was decreased significantly (P<0.01). The HDL-C was increased while LDL-C decreased significantly (P<0.05, P< 0.01). The serum LH, T, A concentrations and the ratio of LH/FSH were decreased, while SH-BG levels increased significantly (P<0.01). The ovulation rate during clomiphene citrate therapy was 72%, significantly higher than that before treatment. It is likely that reduction of hyperinsulinemia that is produce by rosiglitazone may effectively improve the endocrine, metabolism and ovulatory performance in the patients with PCOS and insulin resistance.
Adult ; Estradiol ; blood ; Female ; Follicle Stimulating Hormone ; blood ; Humans ; Hypoglycemic Agents ; therapeutic use ; Insulin Resistance ; Luteinizing Hormone ; blood ; Ovulation Induction ; Polycystic Ovary Syndrome ; drug therapy ; physiopathology ; Thiazolidinediones ; therapeutic use

In order to investigate the mechanism of elevated vascular endothelial growth factor (VEGF) in peritoneal fluids from patients with endometriosis, macrophages were recovered from peritoneal fluids obtained at the time of diagnostic laparoscopy from infertile women with endometriosis (EMT group, n=20) and without endometriosis (control group, n=20). Macrophages were cultured in vitro. The VEGF levels of peritoneal fluid and the supernatant of macrophages culture were determined by enzyme linked immunoassay (ELISA). Meanwhile, the eutopic (n=20) and ectopic endometrium (n=20) from endometriosis patients, and normal edometrium (n=20) from non-endometriosis patients were obtained for the analysis of VEGF expression by labeled Streptavidin Biotin (LSAB). It was found that VEGF levels in peritoneal fluid and macrophages culture supernatant were significantly higher in EMT group than in control group (P<0.01). In normal endometrium, VEGF showed a cyclic changes and similar in eutopic and ectopic endometrium from patients with endometriosis. There was no difference in the intensity of VEGF in endometrium between two groups within each menstrual phase. It is suggested that altered VEGF production by peritoneal macrophages and ectopic endometrium secretion may contribute to the elevated VEGF levels in the peritoneal fluid of patients with endometriosis.
Adult ; Ascitic Fluid ; metabolism ; Cells, Cultured ; Endometriosis ; metabolism ; Female ; Humans ; Macrophages, Peritoneal ; pathology ; Vascular Endothelial Growth Factor A ; biosynthesis

In order to explore the effects of metformin combined with cyproterone acetate (CPA) on the clinical features, endocrine and metabolism of the patients with polycystic ovarian syndrome (PCOS), 50 cases of non-obese PCOS were randomly subjected to CPA (CPA treatment group, n=25) and CPA+metformin (n= 25) treatment for 6 months. Before and after treatment the body mass index (BMI), waist: hip ratio (WHR), ovarian volume, serum gonadotrophin, androgen and sex hormone-binding globulin (SHBG) levels, and fasting lipid, glucose and insulin levels were measured. The results showed that all of the parameters in two groups were similar before treatment. After treatment for 6 months in the CPA+ metformin group, BMI and WHR were significantly decreased, while insulin sensitivity was significantly decreased as compared with those before treatment. In CPA group, no significant changes were found before and after treatment. Combined use of CPA and metformin could result in the reduction of serum androstenedione and increases of serum SHBG levels as compared with the CPA treatment alone. It was concluded that combined use of CPA and metformin could improve the insulin sensitivity, and further suppress the hyperandrogenism in non-obese women with PCOS.

Objective To elucidate the clinical characteristics and coronary angiographic findings of patients underwent PCI before and after drug-eluting stents(DES).Methods DESIRE(Drug-Eluting Stent Impact on revascularization) was a retrospective registry of patients who received revascularization therapy during July,2001 through June,2002(non-DES era) and July,2003 through February,2004(DES era).In this analysis,we used the DISIRE data to examine the clinical and angiographic features of patients who received PCI in the different era.Results Among 3763 patients in the registry,2180 patients were analyzed(763 were in the non-DES era and 1417 were in the DES era).In the DES era,more diseased vessels(1.31?0.54 vs 1.39?0.61,P

Serum C3, C4, IgG and IgM levels were evaluated in healthy post-menopausal women receiving short-term hormone replacement therapy (HRT) regimens and in untreated women. Serum C3, C4, IgM and IgG levels were assessed in 54 women receiving HRT therapy (CEE 0.625 mg+MPA 2.5 mg/day), and in 54 control women not receiving HRT. The results showed that the mean serum C3 and C4 levels were significantly higher in women receiving HRT than those untreated women (P＜0.01). There was significant difference in lgG and IgM levels between two groups. It was con-cluded that HRT might be involved in the development of cardiovascular diseases through inflamma- tory mechanisms, as suggested by increased serum levels of C3 and C4.