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Introduction Coagulation dysfunction and thromboembolism emerge as strong comorbidity factors in severe COVID‐19. However, it is unclear when particularly platelet activation markers and coagulation factors dysregulated during the pathogenesis of COVID‐19. Here, we sought to assess the levels of coagulation and platelet activation markers at moderate and severe stages of COVID‐19 to understand the pathogenesis. Methods To understand this, hospitalized COVID‐19 patients with (severe cases that required intensive care) or without pneumonia (moderate cases) were recruited. Phenotypic and molecular characterizations were performed employing basic coagulation tests including prothrombin time (PT), activated partial thromboplastin time (APTT), D‐Dimer, and tissue factor pathway inhibitor (TFPI). The flow cytometry‐based multiplex assays were performed to assess FXI, anti‐thrombin, prothrombin, fibrinogen, FXIII, P‐selectin, sCD40L, plasminogen, tissue plasminogen activator (tPA), plasminogen activator inhibitor‐1 (PAI‐1), and D‐Dimer. Results The investigations revealed induction of plasma P‐selectin and CD40 ligand (sCD40L) in moderate COVID‐19 cases, which were significantly abolished with the progression of COVID‐19 severity. Moreover, a profound reduction in plasma tissue factor pathway inhibitor (TFPI) and FXIII were identified particularly in the severe COVID‐19. Further analysis revealed fibrinogen induction in both moderate and severe patients. Interestingly, an elevated PAI‐1 more prominently in moderate, and tPA particularly in severe COVID‐19 cases were observed. Particularly, the levels of fibrinogen and tPA directly correlated with the severity of the disease. Conclusions In summary, induction of soluble P‐selectin, sCD40L, fibrinogen, and PAI‐1 suggests the activation of platelets and coagulation system at the moderate stage before COVID‐19 patients require intensive care. These findings would help in designing better thromboprophylaxis to limit the COVID‐19 severity.

Ramadan is the 9th month of the lunar calendar during which Muslims abstain from food and drink between dawn and sunset for 30 consecutive days. Ramadan fasting is observed by all healthy Muslim adults, as well many Muslims with type 2 diabetes (T2DM). Hypoglycemic events (HE) are a serious complication associated with diabetes management and are associated with increased cardiovascular disease risk. Conflicting results have been reported concerning the incidence of HE among people with T2DM observing Ramadan fasting. This review summarizes available scientific evidence on the occurrence of HE and the effects of different moderators on the incidence of HE among patients with T2DM during Ramadan. We conducted a systematic review of available observational studies and randomized controlled trials (RCTs) for patients with T2DM who fasted during Ramadan, with HE as the primary outcome. Ten databases were searched for relevant studies from inception until October 31, 2020. In total, 68 studies (35 RCTs and 33 observational studies) met the inclusion criteria. Non-sulfonylureas hypoglycemic medications showed superior effects in lowering the incidence of HE over sulfonylureas hypoglycemic medications. Variable moderators were associated with experiencing HE during Ramadan in both observational studies and RCTs, including sex, geographical location, body anthropometric indicators, season, dietary behaviors, fasting duration, time since diagnosis, and pre-fasting education. This comprehensive systematic review covered the largest number of observational and clinical studies investigating the impact of Ramadan on HE among patients with T2DM. The study highlights the significance of different moderators that influence the effect of Ramadan fasting on HE, including dietary behaviors, fasting time duration, sex, season, country, pre-fasting education, age, and time since diagnosis. The study also highlighted the impact of different hypoglycemic medications on HE and noted the superiority of non-sulfonylureas over sulfonylureas hypoglycemic medications in lowering the risk for hypoglycemia in people with T2DM during Ramadan fasting.

Purpose This study investigated the relationships between eating habits and sleep quality among university students. Methods In a cross-sectional study, university students completed a self-report questionnaire to assess eating habits and meal timing. We assessed subjective sleep quality using the Pittsburgh Sleep Quality Index (PSQI) questionnaire and examined the associations between eating habits and overall sleep quality and its components. Results Four hundred ninety-eight students participated in the study. Students who used to skip breakfast, ate late-night snacks, and replaced meals with snacks were at 1.20 times, 1.24 times, and 1.25 times higher likelihood of having poor overall sleep quality, respectively. Multiple logistic regression analysis showed that skipping breakfast (r = − 0.111, P = 0.007), late-night snacks (r = − 0.109, P = 0.007), replacing meals with snacks (r = − 0.126, P = 0.002), and irregular mealtimes (r = − 0.094, P = 0.018) were the best correlates with poor sleep quality. After adjustment to demographic variables, replacing meals with snacks followed by skipping breakfast were the best independent associations with poor sleep quality by the PSQI. Conclusions Eating habits and meal timing were significantly associated with sleep quality. We speculate that healthy eating habits may lead to improved sleep quality and sleep components among university students.

Cardiomyopathy is an irreparable loss and novel strategies are needed to induce resident cardiac progenitor cell (CPC) proliferation in situ to enhance the possibility of cardiac regeneration. Here, we sought to identify the potential roles of glycogen synthase kinase‐3β (GSK‐3β), a critical regulator of cell proliferation and differentiation, in CPC proliferation post‐myocardial infarction (MI). Cardiomyocyte‐specific conditional GSK‐3β knockout (cKO) and littermate control mice were employed and challenged with MI. Though cardiac left ventricular chamber dimension and contractile functions were comparable at 2 weeks post‐MI, cKO mice displayed significantly preserved LV chamber and contractile function versus control mice at 4 weeks post‐MI. Consistent with protective phenotypes, an increased percentage of c‐kit‐positive cells (KPCs) were observed in the cKO hearts at 4 and 6 weeks post‐MI which was accompanied by increased levels of cardiomyocyte proliferation. Further analysis revealed that the observed increased number of KPCs in the ischemic cKO hearts was mainly from a cardiac lineage, as the majority of identified KPCs were negative for the hematopoietic lineage marker, CD45. Mechanistically, cardiomyocyte‐GSK‐3β profoundly suppresses the expression and secretion of growth factors, including basic‐fibroblast growth factor, angiopoietin‐2, erythropoietin, stem cell factor, platelet‐derived growth factor‐BB, granulocyte colony‐stimulating factor, and vascular endothelial growth factor, post‐hypoxia. In conclusion, our findings strongly suggest that loss of cardiomyocyte‐GSK‐3β promotes cardiomyocyte and resident CPC proliferation post‐MI. The induction of cardiomyocyte and CPC proliferation in the ischemic cKO hearts is potentially regulated by autocrine and paracrine signaling governed by dysregulated growth factors post‐MI. A strategy to inhibit cardiomyocyte‐GSK‐3β could be helpful for the promotion of in situ cardiac regeneration post‐ischemic injury.