PubMed COVID-19 Clinical Care

No abstract

CONCLUSION: Qualitative data indicated restrictions had a predominantly negative impact on PA for children and youth, but inconsistent impacts on unstructured PA. The improved contextual understanding offered by our review will be foundational

CONCLUSIONS: The experimental results demonstrate that the proposed model has an excellent generalization ability and outperforms other state-of-the-art methods. It is expected to be a potent tool to assist clinicians in auxiliary diagnosis and to

CONCLUSIONS: The SARS-CoV-2 viral load trajectories in patients with HM can be stratified by treatment history for the underlying HM and severity of COVID-19. This article is protected by copyright. All rights reserved.

The previous acute respiratory diseases caused by viruses originating from China or the middle east (e.g., SARS, MERS) remained fast developing short diseases without major sequalae or any long-lasting complications. The new COVID-19, on the other

BACKGROUND The increasing number of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinfections has opened a new research direction related to analyzing long-term immune response and accurately characterizing individual cases of

CONCLUSIONS: Patients who had procedures deferred as a result of the healthcare system's response to the COVID-19 epidemic were impacted physically, financially, and psychologically. There should bea better crisis management strategyto ensure that

CONCLUSIONS: IPOS-COV is the first patient-centred measure adapted for severe COVID to support timely management. Future studies could further evaluate its responsiveness and clinical utility with clinimetric approaches.

Vaccine hesitancy is gaining attention due to the increasing spread of the COVID-19 pandemic in Malaysia. Malaysia is a majority Muslim country and religion has a significant influence on the acceptance or rejection of vaccines. This is clearly seen

CONCLUSION: Taken together the results imply that the immune system failed to control the disease progression in the absence of NOS2. Thus, our observations highlight a protective role of NOS2 in murine-β-coronavirus induced demyelination.