Endometriosis (EMs) is a common cause for female infertility, leading to the need for in vitro fertilization (IVF). In clinics, we found the operative oocyte retrieval to be more or less difficult in women with EMs. We hypothesized that EMs may be involved in the insufficient cumulus expansion that partially explained the lower oocyte retrieval in EMs-related infertile women undergoing assisted reproductive technology (ART). To explore whether the insufficient cumulus expansion exists in EMs-related infertile women and whether there is a possible relationship between the insufficient cumulus expansion and the clinical phenomenon of difficulty in oocyte retrieval. Those infertile women undergoing IVF recorded in our database between January 2013 and October 2017 were included. The expression levels of cumulus expansion-related genes (HAS2/PTGS2/PTX3/TNFAIP6) in the cumulus cells (CCs) from 19 infertile women with EMs and 24 controls were analyzed by real-time PCR. After that, 635 women with EMs-associated infertility (the EMs group) and 4634 women with male factor-associated infertility (the control group) were included in the retrospective analysis. The clinical outcomes were compared between the two groups. The relative mRNA levels of cumulus expansion-related genes were significantly decreased in the CCs from those infertile women with EMs when compared to the control group (all p  less then  0.05), especially the expression of PTGS2. The mean oocyte retrieval rates (proportion of obtained oocytes in punctured follicles) were (76.33 ± 2.58)% and (71.80 ± 0.58)% (p  less then  0.01). The mean numbers of flushing times per follicle were 1.11 ± 0.65 and 3.86 ± 1.53 (p  less then  0.001). The lower expression of cumulus expansion-related genes in CCs suggests the insufficient cumulus expansion in EMs-related infertile women, which partially explains a possible mechanism related to poor oocyte retrieval.Reproductive health of men has declined over time including reduced semen quality specifically sperm count, increased incidence of infertility, and testicular cancers. Our recent findings suggest that these disease states possibly arise as a result of disruption of testicular stem cells biology by perinatal insults including exposure to endocrine disrupting chemicals. Testicular stem cells include relatively quiescent, very small embryonic-like stem cells (VSELs), and actively dividing spermatogonial stem cells (SSCs). Both VSELs and SSCs express estrogen receptors and are directly vulnerable to endocrine disruption. Exposing mice pups to estradiol (20 μg/pup/day on days 5-7) or diethylstilbestrol (2 μg/pup/day on days 1-5) affected spermatogenesis during adult life with reduced numbers of tubules in stage VIII, tetraploid cells and sperm. These mice were infertile and majority of diethylstilbestrol treated mice revealed testicular cancer-like changes. An increase in VSEL numbers, observed by both flow cytometry and qRT-PCR, was associated with marked reduction of c-KIT positive spermatogonial cells. VSELs undergo epigenetic changes due to endocrine disruption that results in blocked differentiation (impaired spermatogenesis) leading to reduced sperm count and infertility, and their excessive self-renewal initiates cancer-like changes in adult life.  https://www.selleckchem.com/products/ly3023414.html  Thus, testicular dysgenesis syndrome (TDS) has a stem cell rather than a genetic basis.Conventional assisted reproductive technology (ART) cycles may delay cancer treatment and compromise survival, and also increase patients' psychological burden as a result of delayed chemotherapy. The aim of this study was to compare the success rates of random start and conventional start GnRH antagonist protocols in terms of oocyte and embryo outputs in cancer patients. Data of 111 patients with a newly diagnosed cancer who underwent ART for fertility preservation at a university-based infertility clinic between January 2010 and September 2019 were reviewed. The study group underwent random start controlled ovarian hyperstimulation (RS-COH) and the control group underwent conventional start COH (CS-COH). The main outcome measures were the number of total oocytes, MII oocytes, and embryo yield. A total of 46 patients (41.5%) underwent RS-COH and 65 (58.5%) underwent CS-COH. Baseline characteristics were similar between the groups. The most common cancer type in both groups was breast cancer (60.9% vs. 52.3%, respectively). The median duration of stimulation was significantly longer in RS-COH than in CS-COH (12 vs. 10 days; P = 0.005). The median number of MII oocytes was significantly higher in RS-COH than in CS-COH (7 vs. 5 oocytes, respectively; P = 0.020). The MII/AFC ratio was significantly higher in the RS-COH group compared to the CS-COH group (74% and 57% respectively; p = 0.02). In the linear regression analyses, RS-COH protocol did not have a significant impact on MII/AFC (standardized ß coefficient - 0.514; P = 0.289 adjusted R2 for the model = 0.779), oocyte yield (standardized ß coefficient - 0.070; P = 0.829 adjusted R2 for the model = 0.840), and MII rate (standardized ß coefficient - 0.504; P = 0.596 adjusted R2 for the model = 0.271). In conclusion, RS-COH protocol is as effective as CS-COH protocols for fertility preservation in cancer patients.Reduced activity of trophoblast cells is well-recognized to lead to preeclampsia (PE) progression. This study aims to evaluate the roles of histone deacetylase sirtuin 2 (SIRT2) in activity of trophoblast cells and the molecules involved. Differentially expressed genes in placental tissues between PE patients and healthy individuals were screened using microarray analyses. SIRT2 and atypical chemokine receptor 2 (ACKR2) were downregulated while miR-146a was upregulated in PE patients. SIRT2 was localized in placental syncytiotrophoblasts. Upregulation of SIRT2 enhanced viability, migration and invasion, while reduced apoptosis of HTR-8/SVneo cells. SIRT2 was found to trigger p65 deacetylation level and suppress miR-146a expression according to the luciferase and ChIP assays, whereas miR-146a was found to target ACKR2. Downregulation of p65 promoted migration and invasion of cells. Overexpression of miR-146a inhibited cell viability and blocked the function of SIRT2. ACKR2 was downregulated in tissues from PE women and its upregulation blocked the role of miR-146a.