Sabire Guler

Morphological and skeletal deformities compromise growth, swimming, feeding, welfare, and market value in farmed fish, but externally visible abnormalities may not reveal the underlying tissue lesions. This study characterized naturally occurring deformities in farmed rainbow trout (Oncorhynchus mykiss) using integrated macroscopic, radiographic, and histopathological evaluation. A total of 54 morphologically abnormal fish and one clinically normal fish were examined. Deformities were grouped by predominant external region, whole-body radiographs were evaluated for skeletal and structural abnormalities, and affected tissues were processed for routine histopathology. Caudal peduncle or tail-region deformities were most frequent (37.0%), followed by trunk/body deformities (25.9%), head-region deformities (24.1%), and specific or combined deformity patterns (13.0%). Vertebral compression was the dominant radiographic lesion (74.1%), followed by swim bladder anomalies (48.1%), contour irregularities (31.5%), combined deformity patterns (29.6%), and peduncle thickening (25.9%). Histopathology revealed ocular lesions compatible with cataract and microphthalmia, vertebral asymmetry and compression, cartilage and bone disorganization, intervertebral space loss, fibrosis, and skeletal muscle degeneration and atrophy. These findings show that visible deformities often reflect complex skeletal and soft-tissue pathology. Integrating radiography with histopathology provides a more informative framework for deformity assessment and welfare-oriented management in rainbow trout production.

Background/Objectives: Non-small-cell lung carcinoma (NSCLC) accounts for approximately 85% of lung cancers and remains a leading cause of cancer-related mortality. Although cisplatin is a cornerstone chemotherapeutic agent, its clinical effectiveness is limited by drug resistance and systemic toxicity. Capsaicin (CAP), a bioactive phytochemical derived from chili peppers, has demonstrated anticancer activity in several tumor types and has been investigated as a potential adjunct to conventional chemotherapy. Methods: An experimental study was conducted using A549 NSCLC cells and a xenograft mouse model. Cells were treated with CAP (50–300 µM), cisplatin (1 µg/mL), or their combination. Cell proliferation and apoptosis were evaluated using sulforhodamine B (SRB) assay, immunocytochemistry, and Western blot analysis. In vivo, tumor growth inhibition, histopathological alterations, and immunohistochemical expression of Ki-67 and cleaved caspase-3 were assessed. Results: Low CAP concentrations (50–100 µM) slightly increased proliferation, whereas concentrations ≥ 150 µM significantly reduced cell viability and induced apoptosis. Cisplatin monotherapy markedly suppressed proliferation and activated apoptosis. Bliss independence analysis demonstrated concentration-dependent synergy between CAP and cisplatin, with maximal synergy scores reaching 28.1 at 100 µM CAP. Combination treatment at CAP concentrations ≥ 150 µM produced the strongest antiproliferative effect in vitro and the highest tumor growth inhibition in vivo (88%). CAP did not further enhance cisplatin-induced apoptosis but significantly reinforced proliferation suppression with reduced Ki-67 expression. Conclusions: CAP exhibits biphasic dose-dependent effects in NSCLC and enhances cisplatin antitumor efficacy predominantly through proliferation suppression, supporting its further evaluation as an adjunctive phytochemical in cisplatin-based NSCLC therapy.

Background: Epilepsy is a chronic neurological disorder primarily affecting the central nervous system. However, growing evidence suggests that epilepsy also impacts peripheral organs, including the gastrointestinal tract. The intestinal barrier, essential for maintaining homeostasis and immune defense, is particularly susceptible to oxidative stress, which can disrupt junctional proteins, leading to increased permeability and barrier dysfunction. This study aimed to investigate the effects of epilepsy on duodenal morphology and intercellular junction integrity, as well as to evaluate the potential protective role of Rosa Canina Seed Oil (RSO) in mitigating these alterations. Methods: A pilocarpine‐induced rat model of epilepsy was employed in 47 male Sprague–Dawley rats, randomly assigned to eight experimental groups, and treated intragastrically with Rosa canina seed oil (RSO) at doses of 0.125, 0.25, or 0.5 mL/rat/day prior to epilepsy induction. Histomorphometric analysis was conducted to assess villus height, crypt depth, and mucosal surface area. Immunohistochemical staining was used to evaluate the expressions of key junctional and cytoskeletal proteins, including zonula occludens‐1 (ZO‐1), E‐cadherin, and vimentin. Correlation analysis was performed to explore associations between morphological parameters and protein expression levels. Results: Epileptic rats exhibited significant reductions in villus height, crypt depth, and absorptive surface area, along with downregulation of ZO‐1, E‐cadherin, and vimentin, indicating compromised barrier function. RSO treatment demonstrated a dose‐dependent protective effect, with moderate and high doses partially restoring intestinal morphology and tight junction integrity. Notably, higher doses of RSO significantly restored ZO‐1 levels and preserved vimentin expression, suggesting its role in stabilizing the epithelial barrier and cytoskeletal framework. Correlation analysis confirmed a strong association between epilepsy‐induced structural disruptions and barrier dysfunction ( p < 0.05), highlighting the potential protective effects of RSO. Conclusion: These findings demonstrate that epilepsy impairs intestinal barrier integrity by altering epithelial structure and junctional protein expression, leading to increased permeability. RSO treatment partially counteracted these effects, supporting epithelial stability and barrier function in a dose‐dependent manner.

The aim of the present study is to investigate the proliferative or apoptotic effects of different doses and durations of Royal jelly (RJ) on serous type epithelial ovarian cancer, which is the most common epithelial ovarian cancer. For this purpose, cells of the Skov-3 human ovarian adenocarcinoma cell line were grown in McCoy medium and seeded in 6-well plates. RJ was prepared as a stock solution (1000 mg RJ/10 ml dH₂O) and 1, 5, 10, 20, and 50 mg/ml RJ doses from the prepared stock solution were added to the medium for 24, 48, and 72 h incubated. After the treatment of RJ, the cell viability test (Tripan Blue), Ki-67 to determine the proliferative effect, cleaved-Caspase-3 and cleaved PARP expressions to determine its apoptotic effect were examined by immunocytochemical and immunofluorescence methods. In addition, findings were supported by the TUNEL method. As a result of the experiments, it was determined that 1 mg/ml and 24 h treatment of RJ did not affect cell proliferation and apoptosis, but generally, 50 mg/ml of RJ for 72 h inhibited proliferation in cancer cells and induced apoptosis. The use of royal jelly both monotherapeutically and in combination as an alternative treatment for ovarian cancer may provide the basis for new experimental protocols.

Consuming raw or undercooked mussels can lead to gastroenteritis and septicemia due to Vibrio contamination. This study analyzed the prevalence, density, species diversity, and molecular traits of Vibrio spp. in 48 fresh raw wild mussels (FRMs) and 48 ready-to-eat stuffed mussels (RTE-SMs) through genome analysis, assessing health risks. The results showed Vibrio prevalence rates of 12.5% in FRMs and 4.2% in RTE-SMs, with V. alginolyticus as the most common species (46.7%). It was determined that the seasonal distribution of Vibrio spp. prevalence in the samples was higher in the summer months. The genome sizes of the Vibrio spp. ranged from approximately 3.9 to 6.1 Mb, with the GC contents varying between 41.9% and 50.4%. A total of 22 virulence factor (VF) classes and up to six antimicrobial resistance (AMR) genes were detected in different Vibrio species. The presence of nine different biosynthetic gene clusters (BGCs), 27 prophage regions, and eight CRISPR/Cas systems in 15 Vibrio strains provides information about their potential pathogenicity, survival strategies, and adaptation to different habitats. Overall, this study provides a comprehensive understanding of the genomic diversity of Vibrio spp. isolated from FRM and RTE-SM samples, shedding light on the prevalence, pathogenicity, and toxicity mechanisms of Vibrio-induced gastroenteritis.

The formation of primordial follicles determines the pool size of follicles in the ovary, and is crucial for female reproductivity. Oocyte nest breakdown, and the formation of primordial follicles, largely depend upon the communication between oocytes and the surrounding pregranulosa cells. The neurogenic locus notch homolog protein (Notch) signaling pathway is the key player for this cell-to-cell communication, and is responsible for primordial folliculogenesis. However, different endocrine disruptors, including bisphenol A (BPA; a plasticizer and a constituent of reusable plastic containers) may affect the Notch signaling pathway, and might induce ovary dysfunction via Notch signaling. Consequently, we investigated the possible influence of BPA treatment on the proportional distribution of the follicular stages, follicle numbers, levels of apoptosis, and on Notch2 and Jagged2 expressions in the ovary. BPA was administered at doses of either 50 µg/kg/day or 50 mg/kg/day, at different time intervals, during neonatal and fetal periods in vivo. After collecting the ovaries from the various experimental groups, follicles were counted, and frequency of apoptosis was determined by TUNEL assay. In addition, Notch2 and Jagged2 expressions were assessed by immunohistochemical staining and qPCR. In summary, BPA treatment affected the follicle numbers and apoptosis level, and Notch2 and Jagged2 expressions varied with follicular stage. It was also observed that these parameters were dose and time dependent with respect to BPA exposure.

Folliculogenesis, steroidogenesis, ovulation, and vitellogenesis are regulated by the effect of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in the hypothalamus-pituitary-ovary axis and these hormones act via follicle stimulating hormone receptor (FSHR) and luteinizing hormone receptor (LHR) in the ovary. Poultry ration and food additives are essential in the regulation of reproductive activity. Phytase is a supplement frequently added to laying hen diets to increase phosphorus (P) utilization. The aim of this study was to reveal the effects of a newly isolated microbial phytase together with different concentrations of calcium (Ca2+) and available phosphorus (AP) on ovarian FSHR and LHR expressions. For this purpose, 90 Lohmann LSL-White layers were first divided into three main diet groups (standard Ca2+ and AP, standard Ca2+ and low AP, low Ca2+ and AP) and then into three subgroups (no-phytase, commercial phytase, and microbial phytase). At the end of the experiment, all chickens were slaughtered and ovarian tissues were fixed in formalin. Routine avidin-biotin complex immunohistochemistry was performed using anti-FSHR and anti-LHR primary antibodies. Immunohistochemically, FSHR and LHR were expressed in granulosa/theca cells, oocytes, interstitial cells, and vitellus. While the expression intensity of the receptors increased in the microbial phytase-treated groups, the strongest expression was obtained in the granulosa/theca cells and oocytes in the standard Ca and low AP group. In conclusion, we suggest that the addition of newly isolated microbial phytase to diets of laying hens and feeding standard Ca and low AP may have positive effects on reproductive performance by increasing the FSHR and LHR expression in ovaries.

Background/aim: The study aims to profile the dual-specificity phosphatases (DUSP) expression in response to Transforming growth factor ß1 (TGFß1)-induced epithelial- mesenchymal transition (EMT) in ovarian adenocarcinoma cells. Materials and methods: The ovarian adenocarcinoma cell line SKOV3 was used as a TGFß1-induced EMT model. Cells were incubated with 5 ng/mL TGFß1 to induce EMT. EMT was confirmed with real-time qPCR, western blot, and immunofluorescence analyses of various EMT markers. Western blot was used to analyze phospho- and total MAPK protein levels. Typical and atypical DUSPs mRNA expression profile was determined by real-time qPCR. Results: The epithelial marker E-cadherin expressions were decreased and mesenchymal EMT markers Snail and Slug expression levels were increased after TGFß1 induction. Phosphorylation of ERK1/2 and p38 MAPK were enhanced in response to TGFß1 treatment. The expression of DUSP2, DUSP6, DUSP8, DUSP10, and DUSP13 were decreased while DUSP7, DUSP16, DUSP18, DUSP21, and DUSP27 were increased by TGFß1. Conclusion: TGFß1 induced EMT which was accompanied by increased activity of MAPKs, and led to marked changes in expressions of several DUSPs in SKOV3 cells.