PubMed COVID-19 Clinical Care

SARS-COV-2 infection-induced excessive or uncontrolled cytokine storm may cause injury of host tissue or even death. However, the mechanism by which SARS-COV-2 causes the cytokine storm is unknown. Here, we demonstrated that SARS-COV-2 protein NSP9

LYB001 is an innovative recombinant SARS-CoV-2 vaccine that displays a repetitive array of the spike glycoprotein's receptor-binding domain (RBD) on a virus-like particle (VLP) vector to boost the immune system, produced using Covalink plug-and

CONCLUSIONS: This review provides preliminary evidence to support the current standard treatment practices in managing MIS-C pharmacologically. However, comprehensive investigation is required using clinical trials to provide stronger outcome

No abstract

CONCLUSIONS: COVID-19-specific aspects may impact health indicators differently depending on the work context.

This study compared social connectedness patterns and examined the relationships between objective or subjective social connectedness and mental health before and during the COVID-19 pandemic among community dwelling adults in South Korea. An

Respiratory epithelial cells fail to exhibit natural phenotypic and morphological characteristics when grown in standard cell culture conditions. To better understanding respiratory pathogen host-cell interactions in the airways, one approach is to

CONCLUSIONS: In this large cohort of hypoxemic patients with COVID-19, initiation of HFNO outside the ICU was safe, and clinical outcomes were similar to initiation in the ICU. Furthermore, the initiation of HFNO on wards saved time in ICU without

The continuous emergence of SARS-CoV-2 variants, particularly the newly circulating Omicron XBB subvariants, has led to a significant reduction in the neutralizing potency and breadth of antibodies. In this study, we report a SARS-CoV-2 human

Enterovirus D68 (EV-D68) is a re-emerging enterovirus that causes acute respiratory illness in infants and has recently been linked to Acute Flaccid Myelitis. Here, we show that the histone deacetylase, SIRT-1, is essential for autophagy and EV-D68