Natural life depends on biological rhythms that enable living creatures to thrive and survive. Biological rhythms or clocks allow species to adapt their physiological functions to external environmental changes. The environmental changes, creating a complex circadian (day) and circannual (year) rhythmicity, affect the whole organism, particularly the endocrine glands and the gonads. The hypothalamic-pituitary-gonadal axis is extremely susceptible to circannual rhythmicity, regulating the hormone levels (Santi et al., 2020). One of the most critical functions of annual hormone changes in nature is the optimisation of reproduction timing, thereby ensuring the highest survival chances of the offspring (Henkel et al., 2006; Roenneberg & Aschoff, 1990). Unlike other animal species, humans do not necessitate to set a season of fertility and can reproduce throughout the entire year. Although the human is not normally considered a seasonal breeder, many reports demonstrated the seasonal changes in gonadotropins, gonadal hormones and melatonin
Male infertility can be caused by environmental factors, genetic defects, physiological and endocrine deficiencies and testicular pathologies. Aluminium (Al) can cause male infertility through a number of mechanisms. The aim of our study was thus to determine whether vitamin E (VitE) has protective effects on Al-induced testicular damage, which was determined according to sperm counts and morphology and using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. Thirty-four male Wistar rats (250–300 g) were randomly assigned to control (no procedures performed; n = 6) or 0.2 mL intraperitoneal injection group ( n = 7 each; three times per week for 4 weeks): sham (distilled water), 10 mg/kg Al, 500 mg/kg VitE and 10 mg/kg Al plus 500 mg/kg VitE (Al + VitE). Sperm samples were evaluated for andrological parameters. The testes were examined by haematoxylin/eosin. The epithelial thickness and areas were calculated and Johnsen scores were determined for the germinal epithelium; the apoptotic indices were determined from TUNEL staining. For Al, the bonds between the germinal epithelial cells were broken in some tubules, and there were unidentified cells in the lumen of some tubules. For control, sham and VitE, normal morphology of the germinal epithelium was generally preserved. With Al + VitE, the full germinal epithelium cell series was maintained, with only mature sperm in the lumen. TUNEL-positive cells were significantly higher with Al compared to control and sham ( p < 0.05). For Al + VitE, the number of apoptotic cells was reduced compared to Al alone and was therefore similar to control, sham and VitE ( p > 0.05). Our findings show that Al caused testicular damage. VitE reduced the number of apoptotic cells during the damage caused by Al.
The use of stem or progenitor cells from bone marrow, or peripheral or umbilical cord blood is becoming more common for treatment of diabetic foot problems. These cells promote neovascularization by angiogenic factors and they promote epithelium formation by stimulating cell replication and migration under certain pathological conditions. We investigated the role of CD34 + stem cells from human umbilical cord blood in wound healing using a rat model. Rats were randomly divided into a control group and two groups with diabetes induced by a single dose of 55 mg/kg intraperitoneal streptozocin. Scarred areas 5 mm in diameter were created on the feet of all rats. The diabetic rats constituted the diabetes control group and a diabetes + stem cell group with local injection into the wound site of 0.5 × 106 CD34 + stem cells from human umbilical cord blood. The newly formed skin in the foot wounds following CD34 + stem cell treatment showed significantly improvement by immunohistochemistry and TUNEL staining, and were closer to the wound healing of the control group than the untreated diabetic animals. The increase in FGF expression that accompanied the local injection of CD34 + stem cells indicates that FGF stimulation helped prevent apoptosis. Our findings suggest a promising new treatment approach to diabetic wound healing.
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