Clinical Value of Platelets and Coagulation Parameters in Predicting the Severity of Delta Variant SARS-CoV-2.

INTRODUCTION: The present study aimed to analyze the clinical features and laboratory markers of patients with Delta variant SARS-CoV-2 and explore the role of platelet in predicting the severity of Delta. METHODS: This retrospective, observational study was conducted on 863 patients laboratory-confirmed Delta variant SARS-CoV-2. These cases were sub-classified based on disease severity into mild (n = 304), moderate (n = 537), and severe (n = 22). A series of laboratory findings and clinical data were collected and analyzed during hospitalization. RESULTS: Of 863 hospitalized patients with Delta, the median age was 38 years (interquartile range, 30-51 years) and 471 (54.58%) were male. The most common clinical symptoms mainly included cough, fever, pharyngalgia, expectoration, dyspnea, fatigue, and headache, and the commonest comorbidities were hypertension and diabetes. Among the hematological variables, neutrophil count, red blood cell count, and hemoglobin, were found to be statistically significant with regard to subcategories based of disease severity (p < 0.05). Among coagulation parameters, there was a statistically significant difference in D-dimer, fibrinogen, international normalized ratio, and prothrombin time (p < 0.05). Statistically significant differences were observed in platelet markers including platelet count, large platelet count, and plateletcrit (p < 0.05). Additionally, there was strong correlation between platelet and other parameters with disease severity. Logistical regression analysis and ROC curves showed that D-dimer was a single best marker of disease severity (p = 0.005, p < 0.0001); however, platelet (p = 0.009, p = 0.002) and plateletcrit (p = 0.002, p = 0.001) could also predict severe disease. Platelet was identified as an independent risk factor for severe Delta. CONCLUSION: Low platelet may be a marker of disease severity in Delta variant SARS-CoV-2 and may contribute to determine the severity of patients infected with Delta.

Circ-CBFB exacerbates hypoxia/reoxygenation-triggered cardiomyocyte injury via regulating miR-495-3p in a VDAC1-dependent manner.

A large body of literature has identified that circular RNAs play critical roles in regulating the occurrence and development of cardiovascular disease. In the present study, we intended to provide new ideas and perspectives on the functional role of circ-CBFB in hypoxia/reoxygenation (H/R)-injured cardiomyocytes. We observed that circ-CBFB expression was enhanced which was accompanied by a miR-495-3p reduction in response to H/R exposure. Functionally, deletion of circ-CBFB obviously potentiated cell viability and restrained cell apoptosis, which was accompanied by a remarkable elevation of antiapoptotic Bcl-2 but the repression of proapoptotic Bax and cleaved caspase-3 in response to H/R. Additionally, the absence of circ-CBFB dramatically prohibited H/R-evoked cardiomyocyte oxidative stress, as revealed by a decrease in reactive oxygen species overproduction, diminution in MAD content, and enhancement in SOD, CAT, and GSH-Px activities. Moreover, elimination of circ-CBFB resulted in improvement of mitochondrial dysfunction, as assessed by mitochondrial membrane potential, adenosine triphosphate production, and the release of cyto-c. Interestingly, circ-CBFB inversely regulated miR-495-3p expression via acting as a competing endogenous RNA. VDAC1 was identified to be a functional target of miR-495-3p and positively modulated by circ-CBFB. Mechanically, dissipation of miR-495-3p or augmentation of VDAC1 manifestly counteracted the beneficial effects of circ-CBFB knockdown on H/R-elicited cardiomyocyte insult. Collectively, these observations demonstrated that absence of circ-CBFB offered cardio-protection against H/R-triggered cardiomyocyte injury by relieving apoptosis, oxidative stress, and mitochondria dysfunction through miR-495-3p/VDAC1 axis. This work unveiled an innovative axis of circ-CBFB/miR-495-3p/VDAC1 in H/R-challenged cardiomyocyte damage, exerting its potential in providing new thoughts in acute myocardial infarction management.