Background: Ischaemia–reperfusion (IR) injury, which can be encountered during surgical procedures involving the abdominal aorta, is a complex process that affects distant organs, such as the heart, liver, kidney, and lungs, as well as the lower extremities. In this study, we aimed to contribute to the limited literature by investigating the protective effect of dexmedetomidine, which was administered through different routes, on kidney tissue in rats with spinal cord IR injury. Methods: A total of 30 rats were randomly divided into five groups: control (C group), IR (IR group), IR-intraperitoneal dexmedetomidine (IRIPD group), IR-intrathecal dexmedetomidine (IRITD group), and IR-intravenous dexmedetomidine (IRIVD group). The spinal cord IR model was established. Dexmedetomidine was administered at doses of 100 μg/kg intraperitoneally, 3 μg/kg intrathecally, and 9 μg/kg intravenously. Histopathologic parameters in kidney tissue samples taken at the end of the reperfusion period and biochemical parameters in serum were evaluated. Results: When examined histopathologically, tubular dilatation was found to be significantly reduced in the IRIVD, IRITD, and IRIPD groups compared with the IR group (p = 0.012, all). Vascular vacuolization and hypertrophy were significantly decreased in the IRIVD, IRITD, and IRIPD groups compared with the IR group (p = 0.006, all). Tubular cell degeneration and necrosis were significantly reduced in the IRIVD, IRITD, and IRIPD groups compared with the IR group (p = 0.008, p = 0.08, and p = 0.030, respectively). Lymphocyte infiltration was significantly decreased in the IRIVD and IRITD groups compared with the IR group (p = 0.006 and p = 0.06, respectively). Conclusion: It was observed that dexmedetomidine administered by different routes improved the damage caused by IR in kidney histopathology. We think that the renoprotective effects of dexmedetomidine administered intravenously and intrathecally before IR in rats are greater.

Background: In the post-acute COVID-19 syndrome, many patients suffer from palpitations, effort-associated fatigue, and even sudden death. The mechanism of heart involvement in this syndrome is uncertain. The main purpose of the study was to identify possible cardiac involvement causes in patients with post-acute COVID-19 by using biomarkers such as NT-proBNP and nitric oxide (NO) and cardiac imaging modalities. Methods: In this cross-sectional study, a total of 105 participants were included according to the existence of symptoms, and 40 of these participants were asymptomatic patients. The ages of the participants ranged from 20 to 50 years. All patients were healthy before COVID-19. The symptoms were defined as palpitations and/or fatigue association with exercise in post-acute COVID-19 term. The comparison of the two groups was made by using biochemical parameters (NT-proBNP, Troponin I, NO) and imaging techniques (echocardiography, cardiovascular magnetic resonance (CMR) and cardiac positron emission tomography (PET)). Results: The symptomatic patients had higher NT-proBNP levels compared with asymptomatic patients (132.30± 35.15; 76.86± 16.79, respectively; p < 0.001). Interestingly, the symptomatic patients had lower NO levels than asymptomatic patients (9.20± 3.08; 16.15± 6.02, respectively; p < 0.001). Echocardiography and CMR were normal. However, we found regional increased 18F-FDG uptake on cardiac PET to be compatible with myocardial fatigue. Conclusion: We found elevated NT-proNBP levels, low serum NO levels, and increased 18F-FDG uptake on cardiac PET in post-acute COVID syndrome. Cardiac PET could replace or be added to CMR for detecting subtle subacute/chronic myocarditis. The follow-up of patients with post-acute COVID-19 could target the possibility of risk of heart failure.

Introduction: Oxidative stress has an important role in the pathophysiology of Alzheimer’s disease (AD), the most common type of dementia. Boric acid (BA) contributes significantly to the protection of the brain by reducing lipid peroxidation and supporting antioxidant defense. We aimed to evaluate the therapeutic potential of BA treatment in AD rats. Materials and Methods: Four groups were formed as Control (C), Alzheimer’s (A), Alzheimer’s + Boric acid (ABA), Boric acid (BA). Intracerebroventricular injection of Streptozotocin (STZ) was preferred to create an AD. After 4 weeks, BA was applied 3 times every other day. The Radial Arm Maze Test (RAMT) was used to evaluate memory and learning abilities. Biochemical and histopathological evaluations were made in the hippocampus. Results: Initial RAMT inlet/outlet (I/O) numbers were similar. Two weeks after STZ injection, I/O numbers decreased in group A and ABA compared to group C and BA (p< 0.05). After the second BA application, I/O numbers increased in the ABA group compared to the A group (p< 0.05). In group A, PON-1, TOS and OSI levels were higher and TAS levels were lower than in groups BA and C. After BA treatment, PON-1 and OSI levels were lower in the ABA group than in the A group (p< 0.05). Although there was an increase in TAS value and a decrease in TOS, this did not make a statistical difference. The thickness of the pyramidal cell in CA1 and the granular cell layers in the dentate gyrus, and the number of intact and degenerated neurons in the pyramidal cell layer were similar between the groups. Discussion: Significant improvement in learning and memory abilities after BA application is promising for AD. Conclusion: These results show that BA application positively affects learning and memory abilities, and reduces oxidative stress. More extensive studies are required to evaluate histopathological efficacy.