Healthcare workers' socio-psychological status after a year with COVID-19 pandemic: a cross-sectional face-to-face survey in Erzincan, Turkey.

Introduction: on January 7th 2020, SARS-CoV-2 was identified in Wuhan, China, and on March 11th, 2020, the World Health Organization declared it a "Pandemic". The aim of this research is to assess depression, anxiety, work, and social status in healthcare workers during the COVID-19 pandemic. Methods: the research was designed to be a cross-sectional face-to-face survey. The study included 111 healthcare employees and 222 non-healthcare workers between the ages of 18 and 65 who applied to the hospital. For some reason, no one was excluded from the research. Socio-demographic and lifestyle-related questions, depression, anxiety, work-social adjustment scores, and pandemic-social status-operation connections were all assessed using a self-report questionnaire containing psychometric measures. Results: the mean age of the participants in the study was 33.67±10.01 and 59% of the participants were female. PHQ9: 11.67±6.41, GAD7: 9.06±5.81, and W&SAS: 17.55±10.98 were the scores of the healthcare professional groups. PHQ9: 10.25±6.21, GAD7: 7.59±5.65, and W&SAS: 14.75±10.27 were the non-healthcare professional groups' results. When the PHQ9, GAD7, and W&SAS scores of both groups were compared, there was no statistically significant difference in the PHQ9 depression score between the two groups (p=0.107), the GAD7 (p<0.05) and W&SAS (p<0.05) scores of the healthcare professionals were statistically significantly higher. Conclusion: in comparison to the non-healthcare worker group, healthcare professionals had the same level of depression, greater levels of moderate and high anxiety, and higher levels of work-social adjustment disorder. Unlike the literature, we found that the degree of depression fell to the same level as the non-health professional group in our study, but it was still disadvantaged in terms of anxiety and work-social adjustment.

Effect of tocilizumab on ischemia-reperfusion-induced oxido-inflammatory renal damage and dysfunction in rats.

Ischemia-reperfusion-induced (I/R) renal damage is a pathogenic process that starts with ischemia, then progresses through oxidative stress and inflammation. Tocilizumab (TCZ), a recombinant human monoclonal antibody produced against the IL-6 receptor, will be tested against renal I/R injury. TCZ is known to lower the levels of proinflammatory cytokines and oxidant mediators while raising the amounts of antioxidant molecules. Our purpose is to evaluate the biochemical and histological effects of TCZ against I/R-induced oxido-inflammatory kidney damage and dysfunction in rats. Animals were divided into 3 groups as renal I/R (RIR), I/R+ TCZ (IRT), and healthy group (HG). TCZ was administered at a dose of 8 mg/kg to the IRT group (n=6) of the animals, and distilled water as a solvent was administered intraperitoneally (ip) to the RIR (n=6) and HG (n=6) groups. Then, two hours of ischemia and six hours of reperfusion were applied to the left kidneys of IRT and RIR animals. TCZ significantly inhibited the increase in the levels of malondialdehyde (MDA), nuclear kappa B (NF-κB), tumour necrosis factor alpha (TNF-α), interleukin 1-ß (IL-1ß), IL-6, creatinine (Cr) and blood urea nitrogen (BUN) and decrease in total glutathione (tGSH) with I/R in renal tissue. TCZ also attenuated severe histopathological damage due to I/R in renal tissue. TCZ protected renal tissue from I/R-induced oxidative and inflammatory damage. These results indicate that TCZ may be useful in the treatment of renal I/R injury.

Case report: cerebral thromboembolism in an unconscious COVID-19 patient in intensive care.

Although the severity of coronavirus disease 2019 (COVID-19) being more frequently related to acute respiratory distress syndrome and acute cardiac and renal injuries, thromboembolic events have been increasingly reported. Acute respiratory distress syndrome due to SARS-CoV-2 (Severe Acute Respiratory Syndrome - Corona Virus 2) often requires intensive care follow-up. As well as respiratory failure, the SARS-CoV-2 may cause central nervous system (CNS) involvement. The pandemic has raised many challenges in managing critically ill older adults, a population preferentially killed by COVID-19. The mortality and morbidity rates are extremely high in critically ill patients with COVID-19. Recent studies have reported the potential development of a hypercoagulable state in COVID-19. Viral infections and hypoxia may cause these state. It is increasingly reported that thromboembolic events are associated with a poor prognosis. Due to these thromboembolic complications, COVID-19 patients often have neurological symptoms. These symptoms may not be observed in intensive care patients who are sedated. We report one case who was sedated COVID-19 pneumonia and who was later diagnosed with cerebral venous thrombosis with cranial imaging when he could not awaken even though sedation was discontinued. Since COVID-19 causes intense thrombotic susceptibility due to cytokine storm, cerebrovascular thromboembolic complications associated with COVID-19 infection should be considered first and foremost for unconsciousness ventilated patients. Severe and potentially cerebral thrombosis may prolong the patient´s stay in intensive care.