PubMed COVID-19 Clinical Care

CONCLUSIONS: Overall, parents liked the concept of the RecMap website but had some suggestions to improve its usability (language, navigation, and website interface). These findings can be used to improve the RecMap website for parents and offer

CONCLUSION: Telehealth during the COVID-19 pandemic was associated with greater reliance on GP to prescribe cardiac medications and delays in obtaining prescriptions among cardiology clinic patients. Although most patients were satisfied with

Respiratory Syncytial Virus (RSV) is an important cause of respiratory infection in humans. Severe cases are common in children ≤2 years old, immunocompromised individuals, and the elderly. In 2020, RSV infection reduced in Rio Grande do Sul (RS)

CONCLUSIONS: Our data suggest that viral ARDS promotes cardiac inflammation by expanding the CCR2^(+) macrophage subset, and the associated cardiac phenotypes in mice can be elicited by activating the host immune system even without viral presence in

CONCLUSION: Based on bibliometric analysis and knowledge mapping, this study summarises development trends in the field of SIAD research, providing references for current and future research into SIAD.

BACKGROUND: Since the outbreak of COVID-19, how to reduce the risk of spreading viruses and other microorganisms while performing aerosolgenerating procedures (AGPs) has become a challenging question within the dental and dental hygiene communities

The COVID-19 pandemic has highlighted the need for mucosal vaccines as breakthrough infections, short-lived immune responses and emergence of new variants have challenged the efficacy provided by the first generation of vaccines against SARS-CoV-2

CONCLUSIONS: Long COVID was associated with financial disruption in the UK. If our findings reflect causal effects, extending employment protection and financial support to people with long COVID may be warranted.

CONCLUSIONS: This study demonstrates that certain immune response plasma proteins might play an important role in the pathophysiology of Long COVID and severity of fatigue after SARS-CoV-2 infection.

SARS-CoV-2 infection causes activation of endothelial cells (ECs), leading to dysmorphology and dysfunction. To study the pathogenesis of endotheliopathy, the activation of ECs in lungs of cynomolgus macaques after SARS-CoV-2 infection and changes in