Association between chronic tinnitus and brain-derived neurotrophic factor antisense RNA polymorphisms linked to the Val66Met polymorphism in BDNF.

Tinnitus is the sound heard in the ear or head of a person in the absence of external stimuli. Its etiopathogenesis is still not fully understood and the etiological causes responsible for tinnitus are quite variable. Brain-derived neurotrophic factor (BDNF) is one of the key neurotrophic factors in the growth, differentiation, and survival of neurons and in the developing auditory pathway, including the inner ear sensory epithelium. The regulation of BDNF gene is known to be managed by BDNF antisense (BDNF-AS) gene. BDNF-AS is located downstream of the BDNF gene and transcribes a long non-coding RNA. Inhibition of BDNF-AS upregulates BDNF mRNA, which increases protein levels and stimulates neuronal development and differentiation. Thus, BDNF and BDNF-AS both may play roles in the auditory pathway. Polymorphisms in both genes may have impact on hearing performance. A link was suggested between tinnitus and BDNF Val66Met polymorphism. However, there is no study questioning the relationship of tinnitus with BDNF-AS polymorphisms linked with BDNF Val66Met polymorphism. Therefore, this study aimed to scrutinize the role of BDNF-AS polymorphisms showing linkage with the BDNF Val66Met polymorphism in the course of tinnitus pathophysiology. Six BDNF-AS polymorphisms were analyzed on the tinnitus patients (n = 85) and the control subjects (n = 60) by Fluidigm Real-Time PCR using the Fluidigm Biomark microfluidic platform. When BDNF-AS polymorphisms were compared between the groups in terms of genotype and gender distribution, statistically significant differences were detected in rs925946, rs1519480, and rs10767658, polymorphisms (p less than 0.05). When the polymorphisms were compared by the duration of tinnitus, significant differences were found in rs925946, rs1488830, rs1519480, and rs10767658 polymorphisms (p less than 0.05). According to genetic inheritance model analysis, 2.33 and 1.53-fold risks were found for the rs10767658 polymorphism in the recessive and the additive models, respectively. For the rs1519480 polymorphism, a 2.25 fold risk was observed in the additive model. For the rs925946 polymorphism, 2.44 fold protective effect in dominant model, and 0.62 fold risk was found in the additive model. In conclusion, four of the polymorphisms in BDNF-AS gene (rs955946, rs1488830, rs1519480, and rs10767658) are potential gene loci that may play a role in the auditory pathway and affect auditory performance.

Prophylactic Anticoagulant Treatment Might Have an Anti-inflammatory Effect and Reduce Mortality Rates in Hospitalized COVID-19 Patients?

Objectives: COVID-19 associated coagulopathy and prophylactic anticoagulant therapy (PAT) are ongoing topics globally. Using PAT for anti-inflammatory effect may prevent thromboembolic events (TEEs). The objective of this study was to determine the anti-inflammatory effects of PAT in hospitalized COVID-19 patients. Methods: We conducted a retrospective observational study in a tertiary pandemic hospital. Patients were divided into two categories according to their PAT therapy status (PAT (+) and PAT (-)) and into three categories according to clinical features (mild: group 1; moderate: group: 2; and severe: group 3). We then evaluated laboratory parameters and clinical courses. Results: We included 662 hospitalized COVID-19 patients in this study. Enoxaparin sodium was given to all patients as PAT therapy. TEE was developed in five patients in the PAT (+) group. Pulmonary embolism developed in 3/5 patients and deep venous thrombosis in 2/5 patients. Disseminated intravascular coagulation (DIC) was detected in 54 patients in group 3. No statistically significant difference was found in 28-day mortality, development of DIC rates, intubation rates, and TEEs. Conclusions: The use of PAT in critically ill patients was not effective in reducing C-reactive protein, which is one of the biomarkers of inflammation.

Evaluation of the Hospitalized Coronavirus Disease 2019 Patients in First 3 Months of the Pandemic.

OBJECTIVE: Data about Turkish coronavirus disease 2019 patients are limited. We evaluated hospitalized coronavirus disease 2019 patients who were followed up in the first 3 months of the pandemic. MATERIAL AND METHODS: This retrospective, single-center, observational study included 415 confirmed hospitalized coronavirus disease 2019 patients. The patients were divided into groups, namely, mild, moderate, and critically ill patients. Symptoms at the time of admission, clinical, laboratory, and imaging findings were examined. RESULTS: In our study, 6.74% of coronavirus disease 2019 patients had severe disease, 59.5% were male, and the mortality rate was 11.3%. Diabetes mellitus and chronic obstructive pulmonary disease were more frequently seen in critically ill patient groups and hypertension in moderate patient groups. Anemia and aspartate aminotransferase levels were higher in non-survivors among mild coronavirus disease 2019 patients. In the moderate patients' group, aspartate aminotransferase, lactate dehydrogenase, international normalized ratio, ferritin, and D-dimer levels were higher and lymphocyte, hemoglobin levels were lower; in the critically ill patients' group, platelets were lower and uric acid levels were higher in non-survivor patients. CONCLUSION: In mild patients, anemia, lymphopenia, and increased aspartate aminotransferase levels; in moderate patients, leukopenia, anemia, and increased aspartate aminotransferase, lactate dehydrogenase, international normalized ratio, ferritin, and D-dimer levels; in the critically ill patient group, lower platelet and increased uric acid levels should be followed closely as they are mortality predictors.