Aim: Polycystic ovary syndrome (PCOS) is associated with impaired fertility due to both ovarian dysfunction and alterations in uterine physiology. The aim of this study was to demonstrate the effect of PCOS on myometrium morphology and α-actin expression, which plays a role in the contraction mechanism, as well as on the ultrastructural morphology of myometrial smooth muscle cells (MSMCs).Material and Methods: Twenty-one female Sprague-Dawley rats (21 days old) were divided into control, vehicle and PCOS groups (n = 7 per group). PCOS was induced in the PCOS group by subcutaneous injections of 6 mg/100 g/day of dehydroepiandrosterone (DHEA) dissolved in 0.2 ml of sesame oil for 20 days. Light microscopic analyses of uterine tissue were performed. An ultrastructural examination of MSMCs was performed using transmission electron microscopy.Results: The PCOS group exhibited elevated epithelium thickness and stromal eosinophil infiltration. Masson trichrome staining revealed significant collagen deposition between the smooth muscle bundles in the myometrium, indicating fibrotic remodelling. Immunohistochemical analysis revealed decreased α-actin expression in the PCOS group. Ultrastructurally, MSMCs in the PCOS group demonstrated enlarged perinuclear spaces, while the morphology of dense bodies remained normal.Conclusion: PCOS induces significant remodelling of the myometrium, including increased collagen deposition, vascular dilation and early ultrastructural stress changes. These findings suggest that uterine dysfunction in PCOS may be caused by subtle yet functionally significant alterations to myometrial architecture. Further research incorporating functional contractility assays and contraction-related molecular pathways is required to clarify the mechanisms linking myometrial remodelling to impaired reproductive outcomes in PCOS.
Aim: Glioblastoma (GBM) is an aggressive primary brain tumor with limited treatment options. Ferroptosis, an iron-dependent cell death characterized by lipid peroxidation and oxidative stress, is a promising therapeutic target. This study investigated the anticancer effects of the imipridone derivative ONC212 in GBM cells and examined whether its cytotoxicity involves ferroptosis-related mechanisms.Material and Methods: U87 and U251 cells were treated with increasing ONC212 concentrations. Viability was assessed by CCK-8, proliferation by BrdU incorporation (24–72 h). Ferroptosis-associated changes were evaluated by measuring ferrous iron (Fe²⁺), malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS). Expression of ferroptosis-related genes GPX4 and ACSL4 was analyzed by qRT-PCR. Ferrostatin-1 (Fer-1) was used to confirm ferroptosis involvement.Results: ONC212 reduced viability in a time- and dose-dependent manner [IC₅₀ (95% CI): 18.7 µM (17.3-20.1), 9.6 µM (8.8-10.4), and 6.2 µM (5.7-6.7) at 24, 48, and 72 h, respectively]. BrdU incorporation decreased by 46.9% and 79.4% at 24 h and 72 h, respectively, following treatment with the 24-hour IC₅₀ concentration (18.7 µM). Ferroptosis-associated oxidative stress was evident through increased Fe²⁺, MDA, ROS, and GSH depletion. ONC212 upregulated ACSL4 (2.14‑fold) and reduced GPX4 expression by 62%. Fer-1 pretreatment partially reversed these alterations, supporting the involvement of ferroptosis-associated mechanisms. Similar results were obtained in U251 cells.Conclusion: ONC212 exerts potent cytotoxic and anti-proliferative effects in GBM cells and provides preliminary evidence suggesting that it induces ferroptosis-associated cell death through modulation of oxidative stress and ferroptosis‑associated gene expression. Targeting ferroptosis with ONC212 may represent a promising therapeutic strategy for GBM.
Subependymal giant cell astrocytoma (SEGA) usually arises near the foramen of Monro in patients with tuberous sclerosis complex (TSC). A 14-year-old boy presented with headache and a 6.2 × 5.8 cm extraventricular, cyst-dominant hemispheric lesion containing a mildly enhancing mural nodule. Microsurgical excision was performed. Histology demonstrated mixed spindle and polygonal epithelioid/ganglioid cells in a fibrillary, microvascular stroma. Tumor cells were positive for glial fibrillary acidic protein (GFAP) and cluster of differentiation 56 (CD56); epithelial membrane antigen (EMA), inhibin, and thyroid transcription factor-1 (TTF-1) were negative, and the Ki-67 labeling index was approximately 1%. No additional major or minor feature of TSC was identified using the 2021 International TSC Consensus criteria. At 12 months, the patient was neurologically intact and headache-free. Germline or tumor TSC1/TSC2 testing and postoperative contrast-enhanced magnetic resonance imaging (MRI) were unavailable. This case highlights the integrated assessment required for pediatric cystic tumors with mural nodules.
The anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly associated with a high risk of adverse cardiac events and mortality. The isolated origin of the left anterior descending artery from the pulmonary artery (ALADAPA) is even more infrequent. Although the clinical course is generally quieter than the classic ALCAPA syndrome, it carries a high risk of sudden cardiac death. Conditions that predispose individuals to thrombogenicity can precipitate this insidious condition. In this case report, we describe a fatal instance of ALADAPA syndrome, diagnosed for the first time post-cardiac arrest in a young woman following the use of high-dose oral contraceptive pills for emergency contraception.
Amyloidosis is characterized by the extracellular deposition of abnormally folded proteins. While localized forms occur in the head and neck, nasopharyngeal involvement is rare and can mimic malignancies.We present a rare case of primary localized nasopharyngeal amyloidosis. A 67-year-old female presented with nasal congestion, throat lump sensation, and left-sided conductive hearing loss. Endoscopy revealed a yellow-colored mass in the left nasopharynx. MRI showed a homogeneously enhancing lesion without destruction. Diagnosis was confirmed by histopathology demonstrating apple-green birefringence with Congo red staining. Systemic amyloidosis was excluded through comprehensive evaluation. The patient was managed with close follow-up, and no progression was observed over five years.Nasopharyngeal amyloidosis should be considered in the differential diagnosis of nasopharyngeal masses. Histopathological confirmation is essential, and systemic involvement must be meticulously excluded.
