In this study, we wanted to investigate the effectiveness of combining disease‐modifying anti‐rheumatic drugs (DMARD) with hyperbaric oxygen therapy (HBOT) in reducing inflammation in a rheumatoid arthritis (RA) model using rats. We divided 56 male Sprague–Dawley rats into seven groups and induced RA using complete Freund's adjuvant. Some groups received HBOT, whereas others were given etanercept or leflunomide. We started the treatment on the 10th day after inducing RA and continued it for 18 days. To evaluate the effectiveness of the treatments, we measured paw swelling and used X‐rays to examine the joints before and after the treatment. We also analysed the levels of two inflammatory markers, tumour necrosis factor (TNF)‐α and interleukin (IL)‐1β, using an enzyme‐linked immunosorbent assay. Additionally, we conducted histological analysis and assessed the expressions of anti‐IL‐1β and anti‐TNF‐α antibodies. All the treatment groups showed a significant decrease in arthritis scores, paw swelling and levels of TNF‐α and IL‐1β. The X‐ray images revealed improvements in joint structure, and the histopathological analysis showed reduced inflammation and collagen abnormalities. Combining DMARD with HBOT had similar effects to individual therapies, suggesting a cost‐effective and potentially safer approach for improving outcomes in rats with RA.

To evaluate hyperbaric oxygen therapy (HBO) based on ovarian histology, total antioxidant status (TAS), total oxidant status (TOS), and anti-müllerian hormone (AMH), in the ovarian insufiency (POI) model created with cyclophosphamide (CYP). The rats were separated into 3 groups of the control group (n=6), the CYP group (n=6), and the CYP+HBO group (n=6). The rats in the CYP group and the CYP+HBO group were injected intraperitoneally with 200 mg/kg CYP on day 1, followed by 8 mg/kg/day for 14 days to create POI. From the 15^th day onwards, the rats in the CYP+HBO group were placed in a hyperbaric cabin and exposed to 100% oxygen at 2.4 atm pressure for one h, and were then returned to their cages at the end of the hour. A statistically significant decrease was determined in the primordial and primary follicle counts in the CYP group compared with the control group (p<0.05). In the CYP+HBO group, a statistically significant increase was determined in the primordial and primary follicle counts (p<0.05). The serum AMH levels were seen to be significantly decreased in the CYP group compared with both the control group and the CYP+HBO groups. The HBO was seen to decrease TOS and increase TAS. HBO could be an alternative treatment to minimize the effect of ovarian follicle loss caused by CYP, which is used for treating tumors that commonly occur in young females of reproductive age.

Background/Aim: Loss of smell, also known as anosmia, is a prevalent and often prolonged symptom following infection with SARS-CoV-2. While many patients regain olfactory function within weeks, a significant portion experience persistent anosmia lasting over a year post-infection. The underlying mechanisms responsible for this sensory deficit remain largely uncharacterized. Previous studies, including genome-wide association studies (GWAS), have identified genetic variants near the UGT2A1 and UGT2A2 genes that are linked to anosmia in COVID-19 patients. However, the role of epigenetic changes in the development and persistence of smell loss has not been well explored. In this study, we aimed to investigate epigenetic alterations in the form of DNA methylation in the UGT1A1 gene, which is a locus associated with olfactory dysfunction in COVID-19 patients. Methods: We analysed DNA methylation patterns in blood samples from two carefully matched cohorts of 20 COVID-19 patients each, which are differentiated by their olfactory function—those with normal smell (normosmia) and those suffering from smell loss (anosmia). The cohorts were matched for age and sex to minimize potential confounding factors. Results: Using quantitative analysis, we found significantly lower levels of DNA methylation in the UGT1A1 locus in the anosmia group compared to the normosmia group, with a 14% decrease in median methylation values in patients with smell loss (p < 0.0001). These findings highlight potential epigenomic alterations in the UGT1A1 gene that may contribute to the pathogenesis of anosmia following COVID-19 infection. Our results suggest that the methylation status at this locus could serve as a biomarker for olfactory dysfunction in affected individuals. Conclusion: This study is among the first to describe epigenetic changes associated with smell loss in COVID-19, providing a foundation for future research into targeted interventions and potential therapeutic strategies aimed at reversing persistent anosmia. Further investigations involving larger cohorts and additional loci may help elucidate the complex interaction between genetic, epigenetic, and environmental factors influencing long-term sensory impairment post-COVID-19.

Aim: To investigate the impact of alterations in the light-dark cycle on the activity of dentate gyrus neurons within the hippocampus. Methods: The Light/Dark cycle was implemented in controlled environments equipped with automated lighting systems, maintaining a consistent 12-hour duration for each phase. Wistar Albino male rats were categorized into two groups. The light group was exposed to light from 08:00 to 20:00 followed by darkness, while the dark group remained in darkness from 08:00 to 20:00 and was exposed to light during the subsequent 12 hours. All periods were examined concurrently at the same time of day on the 30th experimental day. Results: There was no statistical difference in the slopes of excitatory postsynaptic potentials (EPSP) and the amplitudes of population spikes (PS) across varying stimulation intensities (p>0.05), with the exception of the 1.5 mA intensity (p=0.04). The stimulus facilitation index for the EPSP slope was significantly greater in the light group compared to the dark group at 120, 140, and 160 ms (p<0.05). The enhancement observed in the night group relative to baseline values during the PTP, induction, and maintenance periods was significantly lower than that in the light group (p<0.001). Conclusion: The results suggest that variations in light-dark frequency can influence the electrical characteristics of dentate gyrus neurons, indicating the presence of an endogenous timing mechanism within the hippocampus that may regulate hippocampal Long-Term Potentiation (LTP).