Juvenile myoclonic epilepsy (JME) is one of the most common idiopathic generalized epilepsy syndromes, yet its molecular pathogenesis remains incompletely understood. Circular RNAs (circRNAs) are stable non-coding RNAs with important regulatory roles and increasing relevance in neurological disorders. In this study, we investigated for the first time the association between selected circRNAs (hsa_circ_0000218, hsa_circ_0000229, hsa_circ_0000249, hsa_circ_0002010, and hsa_circ_0000143) and JME. Total RNA was isolated from peripheral blood samples of 41 patients with JME and 41 healthy controls, followed by RNase R treatment and quantitative real-time PCR analysis. Expression levels of hsa_circ_0002010 and hsa_circ_0000143 were significantly upregulated in patients with JME compared with controls (both p < 0.001), whereas hsa_circ_0000249 was significantly downregulated ( p < 0.001). No significant differences were observed for hsa_circ_0000218 or hsa_circ_0000229. Sex-specific analyses revealed differential expression patterns, and hsa_circ_0002010 and hsa_circ_0000249 were associated with drug resistance. Our findings suggest that certain circRNAs may be involved in molecular pathways related to JME and may provide preliminary information to inform future studies exploring their potential relevance in JME.

Aim: In this study, the effects of muscarinic acetylcholine receptor (mAChR) agonist carbachol on the proliferation of cisplatin-resistant (A2780cis) and cisplatin-free (SKOV-3) ovarian cancer cell line were for the first time investigated to further evaluate the potential therapeutic effect of metronomic chemotherapy. Material and Methods: The inhibitory effect of carbachol on cell proliferation was detected using the xCELLigence Real-Time Cell Analyzer (RTCA) dual plate (DP) system. A preliminary study was conducted to determine the dose of carbachol 100 µM, cisplatin 1 µM, and two combination studies were carried out with 100 µM carbachol + cisplatin 1 µM and 100 µM carbachol + 10 µM atropine, over cancer cells without drugs was used as the control group. The cell proliferation curve was monitored for 96 hours. The cell index value of inhibition in cell proliferation was automatically measured every hour for each well using RTCA 1.2.1 software. Results: Co-administration of carbachol with cisplatin caused a decrease in cell number in both A2780cis and SKOV-3 cell lines in a time-dependent manner (p

Amaç: Bu çalışmada apoptotik uyarıcı Fas hücre yüzey ölüm reseptörü (FAS) ve FAS ligandı genleri (FASLG) polimorfizmlerinin tekrarlayan gebelik kaybı (TGK) etiyolojisindeki yeri araştırıldı.Gereç ve Yöntem: Bu vaka-kontrol çalışmasında, TGK tanısı almış 70 kadın ve kontrol grubu olarak 70 kadından genomik DNA izole edildi. Her iki gruptaki FAS -670 A>G, FAS -1377 G>A ile FASLG -124 A>G polimorfizmlerinin genomik dağılımı ve allel frekansları real-time PCR yöntemi ile belirlenerek karşılaştırıldı.Bulgular: Çalışmamızda, FASLG -124 A>G polimorfizmi için TGK ve kontrol gruplarının genotip frekans farkının istatistiksel olarak anlamlı olduğu saptandı. Ancak FAS −670 A>G ve FAS-1377 G>A genotipleri ile TGK arasında istatistiksel düzeyde anlamlı bir ilişki saptanmadı. FASLG −124 A>G polimorfizmi için A allelini taşıyanlarda hastalığın görülme olasılığı A allelini taşımayanlara göre 3,94 kat daha yüksek bulundu.Sonuç: Bulgularımız, apoptozla ilişkili FASLG -124 A>G polimorfizminin TGK oluşumuna katkısı olabileceğini düşündürmektedir.

Purpose: Epilepsy is a common neurological disorder characterized by recurrent seizures, complex molecular mechanisms, and clinical heterogeneity. Despite significant advances in neuroimaging techniques and antiseizure therapies, the diagnosis and management of epilepsy still largely rely on clinical findings, electroencephalography, and neuroimaging. However, these conventional approaches remain insufficient for accurately predicting disease progression, treatment response, and drug resistance, emphasizing the need for reliable molecular biomarkers. This review aims to evaluate current evidence regarding peripheral blood-derived non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), with respect to their molecular functions, biomarker potential, and clinical applicability in epilepsy.Methods: Current evidence on peripheral blood-derived ncRNAs in epilepsy was reviewed, with particular emphasis on their roles in epilepsy-related molecular mechanisms, their potential as minimally invasive biomarkers, and the methodological and translational factors affecting their clinical application.Results: Increasing evidence indicates that dysregulated ncRNA expression is associated with key pathological processes involved in epilepsy, including neuroinflammation, oxidative stress, synaptic dysfunction, neuronal hyperexcitability, apoptosis, and blood-brain barrier impairment. Circulating ncRNAs detected in serum, plasma, and whole blood exhibit remarkable stability and may reflect pathological alterations occurring within the central nervous system, supporting their potential use as minimally invasive biomarkers and candidates for liquid biopsy approaches in epilepsy. However, small cohort sizes, variability in sample processing and normalization strategies, patient heterogeneity, antiseizure medication effects, and insufficient large-scale validation studies currently limit their clinical applicability.Conclusion: Peripheral blood-derived ncRNAs represent promising candidates for minimally invasive biomarker development in epilepsy. Nevertheless, standardized methodologies, well-characterized patient cohorts, and large-scale independent validation studies are required before ncRNA-based biomarkers can be translated into routine clinical practice.

Crimean–Congo hemorrhagic fever (CCHF) is a severe tick-borne viral disease with high mortality rates and no approved specific antiviral therapy or vaccine. Circular RNAs (circRNAs) are emerging regulators of gene expression and have been implicated in various infectious and inflammatory diseases; however, their role in CCHF remains unknown. In this study, we investigated circRNA expression profiles in peripheral blood samples from CCHF patients and healthy controls. Total RNA was isolated, enriched for circRNAs using RNase R treatment, and analyzed with the Arraystar Human circRNA Array V2 platform. Differential expression analysis was performed using the limma package in R, followed by RT-PCR validation and bioinformatic analyses. Compared with healthy controls, 15 circRNAs were significantly upregulated and 264 were significantly downregulated in CCHF patients. The most highly upregulated circRNAs included hsa_circ_011083, hsa_circ_092556, hsa_circ_001766, hsa_circ_001569, and hsa_circ_027934, whereas hsa_circ_405788, hsa_circ_104982, hsa_circ_002008, hsa_circ_406768, and hsa_circ_037139 were among the most downregulated. Additionally, 641 and 455 differentially expressed circRNAs were identified in fatal–control and fatal–nonfatal comparisons, respectively. Functional enrichment analyses revealed associations with immune response, inflammatory signaling, and host–virus interaction pathways. To our knowledge, this is the first study to characterize circRNA expression patterns in CCHF, providing novel insights into disease pathogenesis and identifying potential biomarkers associated with disease severity and mortality.