PURPOSE: The aim of this article was to determine the features of pathomorphological changes in testicles and uterus of rats associated with thyroid hormone (TH) levels. MATERIAL AND METHODS: Experimental dysfunction of thyroid gland was induced in rats by daily administration of thyroxin in a dose of 50 ug/100 g (hyperthyroidism) and mercazolil in a dose of 5 ug/100g (hypothyroidism). Thyroid and sex hormone profiles were determined. Microscopy and morphometry of testicles in males and uterus in females were performed. The quantity of spermatids and spermatozoa as well as total number of spermatogenic cells was calculated. RESULTS: Hypothyroidism reduced TH concentrations in female rats and increased sex hormones while hyperthyroidism augmented TH and sex hormone levels. In hypothyroid male rats, a decreased TH and unchanged testosterone levels were found out while in hyperthyroid ones there were increased TH and decreased testosterone levels. There was a gender difference in terms of TH changes in hyperthyroidism, i.e. T3 and T4 elevation was more outlined in male than in female rats. The most significant histopathological changes were established in the uterus of hyperthyroid female rats and presented with signs of an acute vascular insufficiency, inflammation, hypertension and fibrosis. Hypothyroidism exerted a crucial effect on pathomorphological changes in rat testicles consisting in atrophy of spermatogenic epithelium, vascular insufficiency, hypertension and fibrosis as well. CONCLUSION: TH level significantly influences on the pathomorphological changes in the male and female reproductive system.
Technologies based on autologous induced pluripotent stem cells (iPSCs) can become promising methods that provide tissue regeneration after a stroke which is currently one of the most acute social and medical problems. Transplantation of neural stem cells obtained from iPSCs by the method of directed differentiation can potentially stop the degradation of nerve tissue and significantly accelerate the regeneration processes. The advantage of using iPSCs is their ability to differentiate into various cell types. At the moment, there are proven methods for obtaining, cultivating and modifying these cells (genome editing), it is possible to create lines with various new properties. Knockout of genes for TNFaR1 and ASIC1a receptors can become such a genomic modification. TNFaR1 is the major receptor for Tumor Necrosis Factor (TNF), which is an essential multifunctional pro-inflammatory cytokine. TNFaR1 activation triggers the apoptosis program in the cell. ASIC1 is a transmembrane protein that is an essential component of acid-sensing ion channel (ASICs) complexes. These channels are receptor-activators of various intracellular systems (including apoptosis) in response to acidosis (lowered pH). Since strokes are accompanied by inflammatory and acidotic shock in the areas of nerve tissue damage, inactivation of the TNFaR1 and ASIC1 genes in the transplanted cells may increase cell survival and engraftment after transplantation. In this work, we describe the method of TNFaR1 and ASIC1a gene knockout using the CRISPR/Cas9 system in iPSCs, followed by the production of neural stem cells. The production of such knockout human neural stem cells (with the subsequent possibility of differentiation into neurons or glia) can also serve as the basis for fundamental studies of these genes, their products, and the basis for screening systems for drugs against stroke.
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