Zobrazení zdroje stránky Mcknightsauer3963

71, 95% CI, 0.58-0.88, P = 0.002). Moreover, patients with the rs9588884 GG genotype had lower levels of miR-20a compared with the rs9588884 CC genotype (P = 0.03). These findings indicate that the rs9588884 GG genotype was associated with lower levels of miR-20a and eventually related to the risk of CSCC in Chinese women.The double-ovarian stimulation strategy has been proposed to optimize the number of oocytes retrieved within the shortest possible timeframe. The objective of this study is to explore the effectiveness of luteal phase (LP) ovarian stimulation as compared to the previous follicular phase (FP) stimulation in a double stimulation strategy. We conducted an observational cohort study of women scheduled for a double stimulation protocol between March 2014 and June 2017, who had completed the FP controlled ovarian stimulation (COS 1) and started the LP stimulation (COS 2) in the same cycle. Women received equivalent daily doses of gonadotropins in combination with GnRH-antagonist protocol for both the COS 1 and the COS 2 performed during the same cycle. Ovulation was triggered using GnRH-agonist in the two stimulations. The primary outcome was the number of oocytes retrieved. A total of 77 patients were included in the analysis. The number of oocytes retrieved after COS 1 was significantly higher than after the COS 2 (5.25 ± 3.38 for COS 1 versus 3.83 ± 3.14 for COS 2; p = 0.001). The duration of the stimulation was significantly shorter, the total dose of injected gonadotropins was significantly lower, and the estradiol level on the trigger day was significantly higher with COS 1 as compared to COS 2. Stimulation during the LP in a double-successive stimulation strategy results in a lower ovarian response as compared to the FP equivalent daily dose stimulation.Tumor-associated macrophages and tumor-infiltrating lymphocytes are associated with survival in solid malignancies. Given the physiological link to peripheral immune cell counts, we evaluated if peripheral immune cell counts were predictors of outcomes in endometrial cancer. A retrospective study was completed for endometrial cancer cases between 2000 and 2010. Kaplan-Meier, bivariate, and multivariable Cox proportion hazard analyses were performed examining the relations between survival and peripheral immune cell counts. Three hundred ten patients were identified. In bivariate analyses, high monocyte counts (&gt; 0.7 × 109 cells/L) trended with decreased progression free survival (PFS) (p = 0.10) and poorer overall survival (OS) (p = 0.16). By contrast, high lymphocyte level (&gt; 1.5 × 109 cells/L) was associated with improved PFS (p = 0.008) and OS (p = 0.006). These findings were consistent for type I and type II endometrial cancers. In a multivariable Cox model, high monocyte level was associated with a greater risk of disease recurrence (hazard ratio (HR) = 1.63, p less then 0.035). Other significant predictors of recurrence were age, non-endometrioid histology, and the presence of lymph vascular space invasion (LVSI). [https://www.selleckchem.com/products/iacs-13909.html IACS13909] In a multivariable Cox model, high lymphocyte count trended with a lower risk of death (HR = 0.66, p = 0.07). Age, surgical stage, non-endometrioid histology, and LVSI were also associated with death in this model. In this sample of endometrial cancer patients, we found that high preoperative lymphocyte counts were associated with improved overall improved survival. High monocyte counts were associated with poorer disease-free survival outcomes. Further studies that focused on understanding tumor-antagonizing and pro-tumoral effects of lymphocytes and monocytes, respectively, in endometrial cancer are recommended.Accumulating research shows that ovarian cancer progression can be influenced by both gene mutations and endometriosis. However, the exact mechanism at hand is poorly understood. In the current study, we explored the expression of KRAS and SIRT1, two genes previously identified as altered in endometriosis and ovarian cancer. Human endometrial samples were obtained from regularly cycling women with endometriosis, ovarian cancer, and endometriosis-associated ovarian cancer between 18 and 50 of age undergoing hysterectomy, and immunohistochemical analyses were performed. The cytoplasmic expression of KRAS was low in eutopic endometrium from women without endometriosis or ovarian cancer; however, it was elevated in those who have been diagnosed with endometriosis, as well as ovarian cancer with or without the presence of endometriosis. Nuclear and cytoplasmic SIRT1 expression was also low within endometrium without either disease. However, nuclear SIRT1 expression was increased in those with endometriosis and ovarian cancer associated with endometriosis. Nuclear but not the cytoplasmic expression of SIRT1 correlated with KRAS expression in ovarian cancers associated with endometriosis. These results suggest roles of KRAS and SIRT1 in endometriosis and endometriosis-associated ovarian cancer. Cytoplasmic KRAS expression proves to be a key biomarker in both diseases, while nuclear SIRT1 may be a new biomarker specific to those with endometriosis and those with both endometriosis and ovarian cancer. Further research of these genes could aid in determining the pathogenesis of both diseases and help in clarifying the development of endometriosis-associated ovarian cancer.Obesity is closely related to reproductive disorders, which may eventually lead to infertility in both males and females. Ovarian granulosa cells play a critical role during the maintenance of oocyte development through the generation of sex steroids (mainly estradiol and progesterone) and different kinds of growth factors. However, the molecular mechanism of obesity-induced granulosa cell dysfunction remains poorly investigated. In our current study, we observed that high-fat diet feeding significantly increased the level of glucose-regulated protein 78 kDa (GRP78) protein expression in mouse granulosa cells; testosterone-induced estradiol generation was impaired accordingly. To further evaluate the precise mechanism of lipotoxicity-induced granulosa cell dysfunction, mouse primary granulosa cells were treated with palmitate, and the expression levels of ER stress markers were evaluated by real-time PCR and western blot. Lipotoxicity significantly increased ER stress but impaired the mRNA expression of granulosa cell function-related makers, including androgen receptor (Ar), cytochrome P450 family 19 subfamily A member 1 (Cyp19a1), hydroxysteroid 17-beta dehydrogenase 1 (Hsd17b1), and insulin receptor substrate 1 (Irs1).