Decreased growth differentiation factor 9, bone morphogenetic protein 15, and forkhead box O3a expressions in the ovary via ulipristal acetate

SUMMARY OBJECTIVE: Folliculogenesis is a complex process involving various ovarian paracrine factors. During folliculogenesis, vitamin D3 and progesterone are significant for the proper development of follicles. This study aimed to investigate the effects of vitamin D3 and selective progesterone receptor modulator ulipristal acetate on ovarian paracrine factors. METHODS: In the study, 18 female Wistar-albino rats were randomly divided into three groups: control group (saline administration, n=6), vitamin D3 group (300 ng/day vitamin D3 oral administration, n=6), and UPA group (3 mg/kg/day ulipristal acetate oral administration, n=6). Ovarian tissue was analyzed by histochemistry and immunohistochemistry. For quantification of immunohistochemistry, the mean intensities of growth differentiation factor 9, bone morphogenetic protein 15, and forkhead box O3a expressions were measured by Image J and MATLAB. Blood samples were collected for the analysis of serum anti-Müllerian hormone levels by ELISA. RESULTS: Atretic follicles and hemorrhagic cystic structures were observed in the UPA group. After immunohistochemistry via folliculogenesis assessment markers, growth differentiation factor 9, bone morphogenetic protein 15, and cytoplasmic forkhead box O3a expressions decreased in the UPA group (p<0.05). Anti-Müllerian hormone level did not differ significantly between the experimental groups (p>0.05). CONCLUSION: Ulipristal acetate negatively affects folliculogenesis via ovarian paracrine factors. The recommended dietary vitamin D3 supplementation in healthy cases did not cause a significant change.

Dose-dependent ultrastructural changes in rat cornea after oral methylphenidate administration

To investigate dose-dependent ultrastructural changes in rat cornea after oral methylphenidate [Ritalin] administration. This study was conducted in the Department of Anatomy, Gazi University Faculty of Medicine, Ankara, Turkey between March and May 2005, with a total of 27 female prepubertal Wistar albino rats, divided into 3 different dose groups [5mg/kg, 10 mg/ kg, 20 mg/kg], and their control groups. They were treated orally with methylphenidate, and eye tissue was removed to process for electron microscopic studies. We observed that all cells, and prominently basal cells of the corneal epithelium show dose-dependent degenerative changes such as apoptotic bodies, chromatin condensation, and ondulation in their nuclei and crystolysis of the mitochondrion. In the stroma, the most evident finding was the increase of the collagen fiber. In addition to dose-dependent changes related to the apoptotic process, which is chromatin condensation in their nuclei, electron dense material accumulation, and pericellular edema in the cytoplasm were also seen. In the endothelial cell lines, disruption of the junctional complexes, vacuolization in the cell cytoplasms, and crystolysis of the mitochondrion's with rough endoplasmic reticulum cisternae activity were observed. Ritalin is inducing an evident degeneration, especially in epithelium cells with increasing doses. Ultrastructural cell organelle composition degeneration with stromal fibrosis has a negative effect on cornea dehydration. In light of these findings, we believe that the Ritalin treatment doses need to be kept to a minimum to maintain healthy cornea ultrastructure and related physiology

comparative study of the ultrastructure of submandibular, parotid and exocrine pancreas in diabetes and fasting

To comparatively analyze the ultrastructural changes in the submandibular and parotid glands and in the exocrine pancreas following diabetes induced by Streptozotocin exposure and the effects of fasting and insulin treatment on these alterations. For experimental procedure, we included 48 Sprague-Dawley type rats in July 2001-March 2002 at Gazi University, Turkey. We divided the rats into 8 groups following the infusion of Streptozotocin. While the degeneration manifested itself as accumulation of secretions within the mucous cells in the submandibular gland, lipid droplets were absent, being replaced by vacuolar structures. The parotid gland and exocrine pancreas, having similar properties, were affected similarly. Diabetes-induced loss of granules was observed in the serous cells in both glands. There was diffuse lipid accumulation within these cells. Regarding granule content, we observed the most prominent degenerative changes in the parotid gland. While cellular loss was observed in neither the submandibular, nor the parotid gland, we noted presence of apoptotic cells was noted in the pancreas. State of fasting was found to cause alterations within the glands indicating increased activity. While insulin treatment was seen to restore the structure to normal in general in both of the 3 glands. This study demonstrated that both of the 3 glands are affected by diabetes and concomitant fasting, and this effect manifests itself via the granule content

ultrastructural alterations in rat corneas with experimentally-induced diabetes mellitus

To examine the ultrastructural changes of rat corneas in streptozotocin [STZ] induced diabetes mellitus and the follow-up insulin treatment. Sprague-Dawley type rats was used for experimental procedures during the period from January to April 2003 at Baskent University, Ankara, Turkey. Rats were studied in 4 groups; group 1: controls, group 2: sham controls [single dose IV sodium citrate], group 3: STZ-induced diabetes mellitus [single dose 45 mg/kg STZ intravenously], group 4: diabetes mellitus + insulin treatment [8 U/day]. We observed degenerative changes in the epithelial layer, stromal keratocytes and endothelial cells in diabetic group. In contrast, the corneal layers have revealed positive alterations in the insulin-treated group. The statistical analyses showed significant narrowing in the epithelial layer in the diabetic group [p=0.002], whereas thickening was observed in the epithelial basement membrane and Descemet's membrane [p=0.002]. It was determined that diabetes mellitus causes degenerative changes in cornea, which are positively influenced by short-term insulin treatment