9 ± 0.7 and 5.9 ± 0.7, respectively). Zygotes derived from the three experimental groups (n = 2914) were subjected to in vitro culture until hatching 4.5 days post coitum (dpc). Regardless of the mouse strain, no differences were observed among eCG and reCG treated females for overall cleavage rate 1.5 dpc (58.5% vs 60.5%), development rate 3.5 dpc (47.2% vs 48.9%) and hatching rate 4.5 dpc (49.5% vs 54.5) (P = NS). Control females from no-eCG treated group showed lower cleavage and development rates (36.4% and 29.7%, respectively; P less then 0.05). In conclusion, this study reports for the first time comparable superovulatory response and embryo development between recombinant and natural eCG treatment, which has important implications for reproductive technologies in several species.HT-2 toxin is widely found in moldy crops and is the major metabolite of T-2 toxin, which has been shown to exert various toxic effects in farm animals. However, little is known about the effects of HT-2 toxin on male reproduction, particularly spermatogenesis. This study aims to investigate the toxic effects of HT-2 toxin on goat spermatogonial stem cells (SSCs) and related autophagy-regulated mechanisms. Our results showed that HT-2 toxin exposure resulted in decreased cell viability and proliferation, disrupted SSCs self-renewal, and reduced germ cell-related gene expression. HT-2 toxin exposure also induced oxidative stress and cell apoptosis, as shown by ROS accumulation, increased antioxidant enzyme activity levels, decreased the mitochondrial membrane potential, and increased caspase-9 mRNA and Bcl/bax protein levels. Additionally, HT-2 toxin exposure increased the expression of the autophagy-inducing genes Atg5, Atg7 and Beclin1 and the number of autophagosomes, which indicated that HT-2 toxin induced autophagy in the goat SSCs. Moreover, we also examined a possible mechanism by which HT-2 toxin exposure induced higher expression of AMPK, mTOR and ULK at both the mRNA and protein levels. our results indicated that HT-2 toxin caused apoptosis and autophagy by activating AMPK-mTOR-ULK1 pathway, which further affected SSCs viability.We hypothesized that feeding a Saccharomyces cerevisiae fermentation product (SCFP) from -4 through +7 wk (calving = Day 0) facilitates early first postpartum ovulation and alters blood and follicular fluid concentrations of glucose, beta-hydroxybutyrate (BHB), free fatty acids (FFA), and steroid hormones favorable to subsequent fertility. Holstein cows were fed individually a SCFP product (n = 24) or served as controls (n = 23). Blood samples were collected at wk -4 and -2 from expected calving and at 1, 2, 5, and 7 wk postpartum to determine plasma concentrations of FFA and BHB. Early spontaneous ovulation (progesterone > 1 ng/mL or corpus luteum presence by postpartum median Day 33) or late ovulation was determined. Plasma FFA in weekly samples was not affected by SCFP supplementation, but FFA was greater (P less then 0.01; week by ovulation status) in late compared with early ovulating cows during and after postpartum wk 2. Plasma BHB in weekly samples was greater (P = 0.03) in SCFP than control cows an cows (P less then 0.05). Dry matter intake, daily milk yield, and yields of fat, protein, lactose, and total solids were less (P less then 0.01) in early compared with late ovulating cows, whereas milk fat percentage was increased (P less then 0.01) by SCFP supplementation. We conclude that elevated postpartum BHB and FFA in plasma, greater negative energy balance, and greater milk yield and components were associated with later postpartum ovulation, but metabolites and steroid hormones in blood and follicular fluid were unaffected by SCFP treatment or ovulation status except for androstenedione.Fumonisin B1 (FB1), as the most toxic fumonisin, is a common Fusarium mycotoxin contaminant of feed stuff and food, posing a potential health hazard to animals and humans. FB1 has been reported to cause hepatotoxicity, neurotoxicity, nephrotoxicity, immunotoxicity and embryotoxicity; however, little information is available on whether FB1 has toxic effects on mammalian oocytes. Herein, we adopted porcine oocytes as models to explore the effects and potential mechanisms of FB1 on mammalian oocytes during in vitro maturation. Porcine cumulus oocyte complexes (COCs) were exposed to 0, 20, 30 and 40 μM FB1 for 44 h during in vitro maturation, and the results reported that first polar body (PB1) extrusion was significantly inhibited when the FB1 concentration reached 30 (P less then 0.01) or 40 μM (P less then 0.001). Further cell cycle analysis revealed that meiotic progression was disrupted, with a larger proportion of the 30 μM FB1-treated oocytes being arrested at the germinal vesicle breakdown (GVBD) stagadversely affected oocyte maturation by disturbing cell cycle progression, destroying cytoskeletal dynamics and damaging mitochondrial function, which eventually induced oxidative stress and apoptosis in porcine oocytes.Paneth cells and Lgr5+ intestinal stem cells (Lgr5+ ISCs) constitute the stem cell niche and maintain small intestinal epithelial integrity by recognizing various niche factors derived from subepithelial cells and external antigens. Elesclomol Although it has been known that interferon-γ (IFN-γ), a Th1 cytokine, is associated with intestinal epithelial disruption during inflammation as a niche factor, dynamics of Paneth cells and Lgr5+ ISCs in response to IFN-γ remain to be understood. Here we show that CAG-tdTomato;Lgr5-EGFP (CT-LE) mice generated in this study enable to identify Paneth cells and Lgr5+ ISCs separately by fluorescence signals. Lgr5+ ISCs underwent cell death a little earlier than Paneth cells in response to IFN-γ by simultaneous tracking using CT-LE mice. In addition, the timing of cell death in most Paneth cells overlapped with Lgr5+ ISCs, suggesting that Paneth cell depletion is induced directly by IFN-γ. Taken together, we established a novel simultaneous stem cell niche tracking method and clarified the involvement of both Paneth cells and Lgr5+ ISCs in stem cell niche damage induced by IFN-γ, further contribute to understanding the mechanism for maintaining intestinal homeostasis by stem cell niche.