Said Ali Atalay

Background: Differentiating ovarian endometriomas from hemorrhagic cysts matters because their management differs. Purpose: To evaluate whether a multiparametric magnetic resonance imaging (MRI) approach improves differentiation of endometriomas from hemorrhagic cysts over conventional subjective assessment. Material and Methods: In total, 83 hemorrhagic cystic ovarian lesions (45 endometriomas, 38 hemorrhagic cysts) on 1.5-T pelvic MRI were retrospectively evaluated by two independent blinded radiologists (with 20 and 7 years of experience in abdominopelvic and gynecological MRI) for quantitative T1 and T2 signal intensities (quantitative shading), intralesional and perilesional apparent diffusion coefficient (ADC), lesion size, and the T2 shading and dark-spot signs. ROC analysis, logistic regression, and inter-/intra-observer agreement were assessed, and models were compared with the DeLong test. Results: Endometriomas were larger (55.0 vs. 40.7 mm; P = 0.007), had lower intralesional ADC (1.054 vs. 1.563 ×10 ⁻³ mm ² /s; P = 0.002), and a greater T1–T2 signal difference ( P < 0.001), which had the highest single-parameter accuracy (AUC = 0.799). There was no statistically significant difference in the T2 shadowing sign between the groups (91.1% vs. 81.6%; P = 0.342). The T2 dark-spot sign was specific (100%) but insensitive (24.4%). Perilesional ADC did not differ ( P = 0.112) and showed poor inter-observer agreement (ICC = 0.064). A multiparametric model (quantitative shading, intralesional ADC, lesion size) outperformed conventional MRI (AUC = 0.894 vs. 0.670; DeLong P < 0.001), increasing sensitivity from 24.4% to 88.9% at comparable specificity. Conclusion: A multiparametric model combining quantitative shading, intralesional ADC and lesion size significantly improved differentiation over conventional MRI, whereas perilesional ADC showed no diagnostic utility at 1.5 T.

Subependimal dev hücreli astrositomlar, genellikle tuberoskleroz ile ilişkili, foramen Monro çevresinde yerleşen düşük dereceli tümörlerdir. BOS akımını tıkayarak hidrosefaliye yol açabilirler. MRG’de T1 izo/hipointens, T2 hiperintens olup belirgin kontrast tutulumu gösterirler. Cerrahi tedavi temel yaklaşımdır.

Bu vaka, sistemik malignite öyküsü bulunan bir hastada gelişen beyin metastazını tanımlamaktadır. MRG’de çevresel kontrastlanan, geniş vazojenik ödemle çevrili kitle görünümü tipiktir. Difüzyon ve perfüzyon bulguları metastatik özellikleri destekler. Tedavi; cerrahi, radyocerrahi ve sistemik tedavilerin kombinasyonunu içerir.

Kolloid kistler üçüncü ventrikülün ön kısmında yerleşen, genellikle benign ve yavaş büyüyen epitel kökenli lezyonlardır. BOS akımını engelleyerek akut hidrosefali ve ani başlangıçlı baş ağrısına yol açabilirler. BT’de hiperdens, MRG’de içeriklerine bağlı değişken sinyalli olup çoğu belirgin kontrastlanma göstermez.

Pyruvate kinase liver and red blood cells (PKLR) has emerged as a key gene associated with metabolic dysfunction-associated steatotic liver disease (MASLD). Through a computational drug repurposing approach, we identified JNK-IN-5A as a small molecule that significantly inhibits the c-Jun N-terminal kinase (JNK) family and suppresses PKL expression in HepG2 cells. In this study, we further evaluated JNK-IN-5A and its derivatives, including SET-151, SET-152, SET-162, and SET-130, as potential therapeutic candidates for MASLD. Building on our previously established HepG2 de novo lipogenesis (DNL) steatosis model, we demonstrated that JNK-IN-5A and its derivatives markedly reduced intracellular triacylglycerol (TAG) accumulation during DNL induction. These compounds also significantly inhibited the expression of key DNL pathway proteins, including PKL, FASN, ACACA, SCD1, SREBP1-c, and ChREBP. Global transcriptomic analyses revealed that SET-151, SET-152, and SET-162 exhibited superior anti-steatotic effects compared to SET-130 and JNK-IN-5A. These three derivatives uniquely downregulated genes involved in pyruvate metabolism, bile acid synthesis, fatty acid metabolism, and glycolysis pathways, effects not observed with JNK-IN-5A alone. Additionally, Compass analysis indicated that treatment with SET-151, SET-152, and SET-162 led to significant alterations in metabolic reactions related to lipid metabolism, whereas JNK-IN-5A showed minimal impact. Finally, we evaluated JNK-IN-5A and SET-152 in a high-sucrose, high-fat diet-induced in vivo rat model of MASLD. Both compounds significantly reduced hepatic lipid accumulation, liver stiffness, and key biochemical markers of MASLD. Collectively, our findings identified SET-152 as a promising drug candidate for the treatment of MASLD.