Objectives: Premature ovarian failure (POF) rat models are essential for elucidating the hormonal and ovarian molecular mechanisms of human POF diseases and developing new therapeutic agents. This study aimed to compare the applicability of chronic immobilization stress (CIS) as a POF model with that of cisplatin and to examine the impact of AP39, a mitochondrial protective agent, on ovarian function in rats treated with cisplatin and CIS. Methods: Sixty Sprague–Dawley female rats were divided equally into six groups (10 per group): Control, Cisplatin, AP39, Cisplatin + AP39, CIS, and CIS + AP39. Ovarian dysfunction was induced with cisplatin (3 mg/kg) or CIS. Forced swim test, hormone concentrations, estrous cyclicity, histopathology, follicle counts, and molecular alterations in the ovary and mitochondria were analyzed. Results: In the CIS and cisplatin groups, mitochondrial biogenesis, egg quality, hormonal profile, estrous cycle, and folliculogenesis significantly declined. Nonetheless, most of the parameters with undesirable results did not normalize after AP39 administration. Conclusions The cisplatin- and CIS-treated rats exhibited unshared deteriorated hormonal pathways and similarly disrupted gene expression patterns. Our current CIS model did not meet the human POF criteria, which include decreased estradiol levels, despite having advantages in terms of ease of modeling and reproducibility and demonstrating pathological changes similar to those observed in human POF. Therefore, rather than using this model as an POF model, using it as a representation of stress-induced ovarian dysfunction would be more appropriate.

Objectives: Premature ovarian failure (POF) rat models are essential for elucidating the hormonal and ovarian molecular mechanisms of human POF diseases and developing new therapeutic agents. This study aimed to compare the applicability of chronic immobilization stress (CIS) as a POF model with that of cisplatin and to examine the impact of AP39, a mitochondrial protective agent, on ovarian function in rats treated with cisplatin and CIS. Methods: Sixty Sprague–Dawley female rats were divided equally into six groups (10 per group): Control, Cisplatin, AP39, Cisplatin + AP39, CIS, and CIS + AP39. Ovarian dysfunction was induced with cisplatin (3 mg/kg) or CIS. Forced swim test, hormone concentrations, estrous cyclicity, histopathology, follicle counts, and molecular alterations in the ovary and mitochondria were analyzed. Results: In the CIS and cisplatin groups, mitochondrial biogenesis, egg quality, hormonal profile, estrous cycle, and folliculogenesis significantly declined. Nonetheless, most of the parameters with undesirable results did not normalize after AP39 administration. Conclusions The cisplatin- and CIS-treated rats exhibited unshared deteriorated hormonal pathways and similarly disrupted gene expression patterns. Our current CIS model did not meet the human POF criteria, which include decreased estradiol levels, despite having advantages in terms of ease of modeling and reproducibility and demonstrating pathological changes similar to those observed in human POF. Therefore, rather than using this model as an POF model, using it as a representation of stress-induced ovarian dysfunction would be more appropriate.

Objectives: Premature ovarian failure (POF) rat models are essential for elucidating the hormonal and ovarian molecular mechanisms of human POF diseases and developing new therapeutic agents. This study aimed to compare the applicability of chronic immobilization stress (CIS) as a POF model with that of cisplatin and to examine the impact of AP39, a mitochondrial protective agent, on ovarian function in rats treated with cisplatin and CIS. Methods: Sixty Sprague–Dawley female rats were divided equally into six groups (10 per group): Control, Cisplatin, AP39, Cisplatin + AP39, CIS, and CIS + AP39. Ovarian dysfunction was induced with cisplatin (3 mg/kg) or CIS. Forced swim test, hormone concentrations, estrous cyclicity, histopathology, follicle counts, and molecular alterations in the ovary and mitochondria were analyzed. Results: In the CIS and cisplatin groups, mitochondrial biogenesis, egg quality, hormonal profile, estrous cycle, and folliculogenesis significantly declined. Nonetheless, most of the parameters with undesirable results did not normalize after AP39 administration. Conclusions The cisplatin- and CIS-treated rats exhibited unshared deteriorated hormonal pathways and similarly disrupted gene expression patterns. Our current CIS model did not meet the human POF criteria, which include decreased estradiol levels, despite having advantages in terms of ease of modeling and reproducibility and demonstrating pathological changes similar to those observed in human POF. Therefore, rather than using this model as an POF model, using it as a representation of stress-induced ovarian dysfunction would be more appropriate.

Objectives: Premature ovarian failure (POF) rat models are essential for elucidating the hormonal and ovarian molecular mechanisms of human POF diseases and developing new therapeutic agents. This study aimed to compare the applicability of chronic immobilization stress (CIS) as a POF model with that of cisplatin and to examine the impact of AP39, a mitochondrial protective agent, on ovarian function in rats treated with cisplatin and CIS. Methods: Sixty Sprague–Dawley female rats were divided equally into six groups (10 per group): Control, Cisplatin, AP39, Cisplatin + AP39, CIS, and CIS + AP39. Ovarian dysfunction was induced with cisplatin (3 mg/kg) or CIS. Forced swim test, hormone concentrations, estrous cyclicity, histopathology, follicle counts, and molecular alterations in the ovary and mitochondria were analyzed. Results: In the CIS and cisplatin groups, mitochondrial biogenesis, egg quality, hormonal profile, estrous cycle, and folliculogenesis significantly declined. Nonetheless, most of the parameters with undesirable results did not normalize after AP39 administration. Conclusions The cisplatin- and CIS-treated rats exhibited unshared deteriorated hormonal pathways and similarly disrupted gene expression patterns. Our current CIS model did not meet the human POF criteria, which include decreased estradiol levels, despite having advantages in terms of ease of modeling and reproducibility and demonstrating pathological changes similar to those observed in human POF. Therefore, rather than using this model as an POF model, using it as a representation of stress-induced ovarian dysfunction would be more appropriate.

INTRODUCTIONThe risk of surgery-related infection is a persistent problem in orthopaedics and infections involving implants are particularly difficult to treat. This study explored the responses of bone and soft tissue to antimicrobial-coated screws. We investigated whether such screws, which have never been used to fix bony tissues, would result in a cytotoxic effect. We hypothesised that the coated screws would not be toxic to the bone and that the likelihood of infection would be reduced since bacteria are not able to grow on these screws.

METHODSTitanium screws were inserted into the left supracondylar femoral regions of 16 rabbits. The screws were either uncoated (control group, n = 8) or coated with a polyvinylpyrrolidone-polyurethane interpolymer with tertiary amine functional groups (experimental group, n = 8). At Week 6, histological samples were obtained and examined. The presence of necrosis, fibrosis and inflammation in the bony tissue and the tissue surrounding the screws was recorded.

RESULTSLive, cellular bone marrow was present in all the rabbits from the experimental group, but was replaced with connective tissue in four rabbits from the control group. Eight rabbits from the control group and two rabbits from the experimental group had necrosis in fatty bone marrow. Inflammation was observed in one rabbit from the experimental group and five rabbits from the control group.

CONCLUSIONTitanium surgical screws coated with polyvinylpyrrolidone-polyurethane interpolymer were associated with less necrosis than standard uncoated screws. The coated screws were also not associated with any cytotoxic side effect.

Animals ; Bone Screws ; Coated Materials, Biocompatible ; Polyurethanes ; toxicity ; Povidone ; toxicity ; Rabbits ; Surgical Wound Infection ; prevention & control ; Titanium