👤 Yunus E Bayrak

Juvenile idiopathic arthritis (JIA) is the most common childhood chronic arthritis, and pain may persist despite controlled inflammation, potentially due to central sensitization. This study aimed to evaluate the effects of very early-onset arthritis on pain, behavior, and cognition using a collagen-induced arthritis model in juvenile rats. Thirty-six three-week-old male Wistar rats were divided into control, sham (saline), and arthritis (type II collagen with incomplete Freund's adjuvant) groups. Disease severity was monitored via joint thickness and VAS. Pain (hot plate, Randall-Selitto), behaviors (EPM, MFST), and cognition (PAT) were assessed. Locomotor activity was assessed. Joints were analyzed histologically (H&E); hippocampal BDNF and TNF-α were examined immunohistochemically. Arthritis severity progressed over six weeks, with increased joint thickness and VAS scores in the arthritis group (p < 0.05). Mechanical hyperalgesia showed a paw- and time-dependent pattern, with earlier changes in some paws and more consistent reductions during the late phase (weeks 4-6). Locomotor activity did not differ among groups, indicating no motor deficits. The arthritis group exhibited greater anxiety (EPM, p = 0.001) and depression-like behavior (FST, p = 0.004), while cognition (PAT) remained unaffected. Hippocampal TNF-α increased, whereas BDNF was unchanged. Very early-onset arthritis is associated with mechanical hyperalgesia and emotional disturbances, accompanied by hippocampal TNF-α alterations, and exhibits features consistent with central sensitization, without significant effects on cognition or hippocampal BDNF expression. Early juvenile arthritis showed mild severity with delayed mechanical hyperalgesia. Thermal hyperalgesia and locomotor deficits were not observed in arthritic rats. Hippocampal TNF-α increase was linked to anxiety and depression-like behaviors. Hippocampal BDNF levels remained stable, suggesting intact learning processes. Show less

This study investigates the genetic and clinical characteristics of hyperlipidemia in patients from Eastern Anatolia. A retrospective cohort of 205 patients (aged 3-71) underwent next-generation sequencing (NGS) to identify genetic variations in lipid metabolism genes (LDLR, APOB and LPL), which were then correlated with the patients' clinical data. Patients with obesity or chronic diseases were excluded. The LDLR c.1729T > C variant was detected in 12 patients. Severe hypertriglyceridemia was observed in patients with homozygous variants in GPIHBP1 and LPL. Elevated triglyceride levels have also been observed to be associated with variants such as APOA5 c.70C > T, thus highlighting their role in lipid metabolism. Phenotypic variation was observed based on the type of genetic variant and its zygosity. The study emphasizes the intricate relationship between lipid metabolism and genetic abnormalities, underscoring potential ramifications for personalized treatment strategies. The report calls for the incorporation of genetic screening into clinical practice with a view to improving diagnostics and outcomes, and it emphasizes the necessity for further research to achieve a full understanding of variants of uncertain significance (VUS) and their associated phenotypes. Show less