Background Some microRNAs are involved in diabetes pathology and some are known to have role in stroke. MiR-503 causes endothelial dysfunction in diabetic patients, predisposing to ischemia. There has been no study evaluating Mir-503 level in diabetic patients with or without ischemic stroke. Methods We designed a cross-sectional study to assess and compare serum level of MiR-503 in 4 groups of diabetic patients with ischemic stroke (I), non-diabetic patients with stroke (II), diabetic patients (III), and healthy controls (IV) in acute phase and 3 months later. Results Our data analysis showed that mean relative expression of MiR-503 in group (I) was significantly higher than 3 other groups ( p < 0.05). The level of miR-503 was related to the patients’ fasting blood glucose, Cholesterol level, NIHSS score and acute–phase modified Rankin Scale (mRS) (r = 0.49, p = 0.001, r = 0.5, p = 0.009, r = 0.45, p = 0.009, r = 0.48, p = 0.003, CI = 95%). Relative expression of miR in patients with mRS ≤ 2 (good outcome) was lower than in patients with mRS > 2 (poor outcome) ( p = 0.008). After 3 months, level of miR decreased significantly only in group (I) ( p = 0.002). Mean relative expression of miR-503 in chronic phase was not significantly different among groups ( p -value> 0.05). There was no relation between miRNA level and mRS in chronic phase. Conclusion Hyperglycemia and ischemia together raise the level of MiR-503 acutely but it does not remain at high level after 3 months. Although higher miR was related to more disability in acute phase, it does not affect long-term outcome in ischemic patients. As MiR-503 is stable enough in blood it can be used as a potential diagnostic marker of an ischemic stroke in diabetic patient. Its level also is an indicator of stroke severity and patients’ short-term outcome. It is recommended to study whether antagomiR-503 is a new therapeutic agent reducing the severity of and disability due to stroke.

Background: Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders with significant impact on quality of life (QOL). Considering the role of stress in the clinical course of IBS, we investigated associations between stress coping skills and symptoms and QOL in IBS patient. Methods: A cross-sectional study was conducted on 95 IBS patients referring to tertiary care centers. Coping skills (Jalowiec coping scale), IBS symptom severity scale, disease-specific QOL (IBS-QOL), and symptoms of depression and anxiety (Hospital Anxiety and Depression Scale [HADS]) were evaluated by questionnaires. Bivariate and multivariate analyses were performed to investigate association among these parameters. Results: Disease severity was positively correlated with emotive ( r = 0.30) and fatalistic ( r = 0.41) and negatively correlated with optimistic ( r = −0.25) and confrontive ( r = −0.24) coping strategies. Psychological dysfunction (total HADS score, B [95% (confidence interval) CI] = 2.61 [0.001–5.21]) and fatalistic coping (B [95% CI] = 35.27 [0.42–70.13]) were significant predictors of IBS severity. Conclusions: However, IBS patients involved in this study utilized adaptive coping strategies more frequently. Our study showed that use of maladaptive coping strategies had positive correlation with symptom severity and degree of anxiety and depression among patients, while implementation of optimistic strategies were found to be negatively correlated to severity of symptoms and also utilization of adaptive coping styles was associated with lesser degree of anxiety and depression.

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Introduction. Coronavirus disease 2019 (COVID-19) identified in December 2019 in Wuhan, China, is associated with high mortality rates worldwide. Hypothesis/Gap Statement. Thrombotic problems, such as coagulopathy, are common in COVID-19 patients. Despite anticoagulation, thrombosis is more common in patients in the intensive care unit and patients with more severe disease. Although the exact mechanisms of coagulopathy in COVID-19 patients are still unclear, studies showed that overactivation of the renin-angiotensin system (RAS), cytokine storm, endothelial damage, formation of neutrophil extracellular traps (NETs), and also extracellular vesicles (EVs) in response to COVID-19 induced inflammation can lead to systemic coagulation and thrombosis. Aim. The management of COVID-19 patients requires the use of basic and readily available laboratory markers, both on admission and during hospitalization. Because it is critical to understand the pathophysiology of COVID-19 induced coagulopathy and treatment strategies, in this review we attempt to explain the underlying mechanism of COVID-19 coagulopathy, its diagnosis, and the associated successful treatment strategies. Conclusion. The exact mechanisms behind COVID-19-related coagulopathy are still unclear, but several studies revealed some mechanisms. More research is needed to determine the best anticoagulant regimen and to study other therapeutic options.