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To study the ability of human spermatogonial stem cells (hSSCs) to proliferate in vitro under mouse spermatogonial stem cell (mSSC) culture conditions. testosterone.

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Gender contributes to differences in incidence and progression of chronic kidney disease (CKD) and associated cardiovascular disease. To induce kidney damage in male and female Wistar rats (n = 12/group), a 0.25% adenine diet for 16 wk was used. Kidney function (blood urea nitrogen, plasma creatinine, proteinuria) and structure (glomerular damage, tubulointerstitial atrophy, fibrosis, inflammation); cardiovascular function (blood pressure, ventricular stiffness, vascular responses, echocardiography) and structure (cardiac fibrosis); plasma testosterone and estrogen concentrations; and protein expression for oxidative stress [heme oxygenase-1, inflammation (TNF-α), fibrosis (transforming growth factor-β), ERK1/2, and estrogen receptor-α (ER-α)] were compared in males and females. Adenine-fed females had less decline in kidney function than adenine-fed males, although kidney atrophy, inflammation, and fibrosis were similar. Plasma estrogen concentrations increased and plasma testosterone concentrations decreased in adenine-fed males, with smaller changes in females. CKD-associated molecular changes in kidneys were more pronounced in males than females except for expression of ER-α in the kidney, which was completely suppressed in adenine-fed males but unchanged in adenine-fed females. Both genders showed increased blood pressure, ventricular stiffness, and cardiac fibrosis with the adenine diet. Cardiovascular changes with adenine were similar in males and females, except males developed concentric, and females eccentric cardiac hypertrophy. In hearts from adenine-fed male and female rats, expression of ER-α and activation of the ERK1/2 pathway were increased, in part explaining changes in cardiac hypertrophy. In summary, adenine-induced kidney damage may be increased in males due to the suppression of ER-α. testosterone.

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The question of whether, as hormone therapies, spawning agents differ from each other to induce physiological pathways of gametogenesis and oocyte maturation in fish remains important, because it could modify undesirable changes, regulated by endocrine systems of individual fish. A series of experimental treatments were applied to investigate the underlying mechanism(s) in which female bunnei (Barbus sharpeyi) fish respond differently to hormone therapies. Female broodstocks were injected twice (with 12 h interval) by three different treatments namely A, B and C. The treatment A received carp pituitary extract (CPE) + luteinizing hormone-releasing hormone analogs (LHRHα2) (0.5 mg CPE kg(-1) BW for first injection and 2 mg CPE kg(-1) BW + 10 µg LHRHα2 kg(-1) for second injection), treatment B received CPE (0.5 and 3.5 mg kg(-1) BW), and treatment C received ovaprim (0.1 and 0.15 ml kg(-1) BW). Blood samples were collected at four different time intervals, including prior to injections, 6 h after first injection, 6 h after second injection and at the time of spawning, and serum steroid hormones, including testosterone, progesterone and estradiol-17β as well as cortisol, were measured. Results showed significant increases in serum estradiol-17β following all treatments, but the most profound response was found in treatments A and B. Testosterone was higher in larger broodfish than in small-sized broodfish (>1.5 vs. <1.5 kg) in all treatments. CPE led to higher concentration of testosterone rather than two other treatments. CPE also increases the progesterone following first injection and approximately remains unchanged till the end of experiment. Change in progesterone level was only significant after second injection of ovaprim as well as after spawning compared with previous time. Linear regression analyses indicated that cortisol had adverse effects on progesterone and testosterone levels of weight group <1.5 kg. These results suggest that among inducing agents, applied here, CPE can provide more reasonable response in reproduction of female B. sharpeyi. testosterone.

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To determine whether the central nervous system is involved in the effect of Chinese herbal medicine on sexual function recovery in orchidectomized rats. testosterone.

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We aimed to investigate the effect and mechanism of icariin on male sexual function. Forty-eight Crl:CD1(ICR) male mice were randomly divided into control, low-, medium- and high-dose icariin group (intragastric administration of 50, 100 and 200 mg/kg/d for 21 days). Mating experiment was then performed at a ratio of 1: 3 (male: female). The mating behaviours of male mice were recorded. The genital indexes and serum testosterone, nitric oxide (NO), hypothalamic dopamine (DA) and 5- hydroxy tryptophan (5-HT) concentrations were measured. The expression of endothelial nitric oxide (eNOS), phosphatidylinositol tallow alcohol 3-kinase (PI3K) and phosphorylated protein kinase (p-AKT) in penile tissue was detected by Western blot. All icariin groups exhibited shorter capture latency and ejaculation latency, increased number of capture and ejaculation, higher capture and ejaculation rate, and higher testicular and prostate indexes compared with controls (p < .001). These groups had higher serum testosterone and NO concentrations (p < .001), hypothalamic DA and 5-HT levels, and eNOS, PI3K and phosphorylated AKT expressions in penile tissue (p < .05). The effect of icariin was dose-dependently increased. Our study suggests that icariin improves the sexual function of male mice, which might be associated with the hypothalamic-pituitary-gonadal axis and the PI3K/AKT/eNOS/NO signalling pathway. testosterone.

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