OBJECTIVES: In this study, we investigated whether a high-fat diet (HFD) affected the bone implant connection (BIC) in peri-implant bone. MATERIALS AND METHODS: Four male rabbits were used in this study. Dental implant surgery was introduced into each tibia, and four implants were integrated into each animal. In both the normal diet (ND) group (n=2) and HFD group (n=2), 8 implants were integrated, for a total of 16 integrated implants. The animals continued with their respective diets for 12 weeks post-surgery. Afterward, the rabbits were sacrificed, and the BIC was assessed histomorphometrically. RESULTS: Histologic and histomorphometric analyses demonstrated that BIC was not impaired in the HFD group compared to the ND group. CONCLUSION: Within the limitations of this study, we found that HFD did not decrease the BIC in rabbit tibias.
Animals ; Dental Implants ; Diet ; Diet, High-Fat* ; Humans ; Male ; Osseointegration* ; Rabbits ; Tibia

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.

A 39-year-old female patient presented to our hospital with epigastric pain lasting for two months. Laboratory results showed impaired glucose tolerance. Ultrasonography of the patient showed a hypoechoic, diffusely enlarged pancreas. CT revealed a large pancreas, with multiple calcifications. On MRI, a diffusely enlarged pancreas was seen hypointense on both T1- and T2-weighted images with heterogeneous enhancement after gadolinium administration. A biopsy of the pancreas revealed primary amyloidosis of islet cells. Decreased signal on T1-weighted images without inflammation findings on CT and MRI were clues for the diagnosis.
Adult ; Amyloidosis/*diagnosis ; Contrast Media/diagnostic use ; Diagnosis, Differential ; *Diagnostic Imaging ; Female ; Glucose Tolerance Test ; Humans ; Islets of Langerhans/*pathology ; Pancreatic Diseases/*diagnosis