Obesity is a growing global public health concern, with its prevalence rapidly increasing in Turkey, leading to severe consequences. Genetic factors, particularly mutations in structural genes and microRNAs (miRNAs) involved in gene expression regulation have been widely investigated in obesity research. This study aimed to explore the role of obesity-associated miRNAs and their potential interaction with vascular response alterations. A total of 60 obese and pre-obese patients and 26 age- and sex-matched healthy controls from the General Surgery Department of Fırat University Medicine School were included. The expression levels of 93 miRNAs were analyzed in 86 samples using the Fluidigm Biomark RT-PCR system, with 5S RNA as the housekeeping gene. Significant differences were observed in weight, BMI, cholesterol, triglyceride levels, and lymphocyte counts between the groups (p < 0.0001). Several miRNAs, including hsa-miR-148a-3p, hsa-miR-503-3p, hsa-miR-34a-5p, and hsa-miR-199a-3p, were significantly downregulated in obese patients. Additionally, gender-specific differences in miRNA expression were identified. These findings indicate that miRNAs play a crucial role in obesity pathophysiology and could serve as potential biomarkers and therapeutic targets for obesity treatment.

The pathophysiology of Alzheimer's disease (AD) is not fully understood and that new biomarkers for the condition should be presented. Our study aimed to determine the blood levels of some biochemical molecules and peptide proteins in AD, which is accepted as the most common cause of dementia in the world, and to elucidate the relationship between them. The study consisted of 2 groups: 40 newly diagnosed AD patients and 40 healthy individuals. Plasma levels between the 2 groups and the correlation between them were statistically analyzed. The median brain-derived neurotrophic factor (BDNF) level in the AD group was found to be higher and statistically significant compared to the control group (p = 0.033). According to our literature review, this is the first article in which these molecules have been studied together in AD patients. In this study, we revealed the importance of these parameters and especially the instrumental role of BDNF in the form and function of the brain in AD patients. Interestingly, in the patient group, all parameters in our study showed a positive and significant positive relationship with one another (p < 0.001).

We aimed to determine the potential damage mechanisms of exposure to widely used sodium hypochlorite (NaOCl) and the effects of Thymus vulgaris on this exposure. Rats were divided into six groups: control, T. vulgaris, 4% NaOCl, 4% NaOCl + T. vulgaris, 15% NaOCl, and 15% NaOCl + T. vulgaris. Serum and lung tissue samples were taken after applying NaOCl and T. vulgaris by inhalation twice a day for 30 min for four weeks. The samples were examined biochemically (TAS/TOS), histopathologically, and immunohistochemically (TNF-α). In serum TOS values, the mean of 15% NaOCl was significantly higher than in 15% NaOCl + T. vulgaris. This was the opposite in terms of serum TAS values. Histopathologically, there was a significant increase in lung injury in 15% NaOCl; significant improvement was observed in 15% NaOCl + T. vulgaris. Immunohistochemically, there was a significant increase in TNF-α expression in both 4% NaOCl and 15% NaOCl; significant decreases were observed in both 4% NaOCl + T. vulgaris and 15% NaOCl + T. vulgaris. The use of sodium hypochlorite, which is harmful to the lungs and is widely used in homes and industries, should be limited. In addition, using T. vulgaris essential oil by inhalation may protect against the harmful effects of sodium hypochlorite.

This research aimed to explore the protective and therapeutic properties of safranal in mitigating inflammation and oxidative stress induced by elevated acetaminophen (APAP) doses in a rat model. The protective and therapeutic effects of safranal were determined by histopathologically and examining some biochemical parameters such as aspartate transaminase (AST), alanine transaminase (ALT), glutathione, glutathione peroxidase, catalase, malondialdehyde, interleukin-6, tumor necrosis factor-α, and interleukin-1β. Male Wistar–Albino rats were subject to random allocation, forming five groups, each comprising seven rats (n = 7) in the study. Group 1 was the control group. APAP was administered in Group 2 to induce hepatotoxicity. Rats in Groups 3, 4, and 5 received intraperitoneal injections of safranal at doses of 0.025, 0.05, and 0.1 mL/kg/day for 14 days, respectively. On the 15th day, to induce APAP-induced hepatotoxicity, four groups (Groups 2, 3, 4, and 5) acquired a single intraperitoneal injection of 600 mg/kg APAP. The presence of APAP-induced hepatotoxic effect was proven by elevated AST and ALT levels, which are typical biomarkers of liver function in addition to the demonstration of histopathological changes. The findings suggest that pre-treatment with safranal may offer a protective effect against hepatotoxicity by attenuating oxidative stress and the inflammatory response.