PubMed COVID-19 Clinical Care

CONCLUSION: Reconceptualizing COVID-19 as a 'collective trauma' can help healthcare workers understand the needs of post-COVID patients and enable them to respond empathetically. A trauma-informed model is complementary to this cohort as it

CONCLUSION: These factors should be considered in the assessment of individuals affected by coronavirus disease to provide comprehensive care.

CONCLUSION: the data show that the construction and implementation of smartphone use policies in the academic and hospital context to prevent smartphone addiction and control associated risk factors is necessary.

CONCLUSIONS: The pathophysiology of the COVID-19 infection and changes in health care delivery during the pandemic played a role in worsening outcomes in the patient population with ICH.

CONCLUSION: The COVID-19 vaccination had an impact on the value of HCC, which might be linked to the occurrence of systemic adverse effects following vaccinations.

Taiwan provided several COVID-19 vaccine platforms: mRNA (BNT162b2, mRNA-1273), adenoviral vector-based (AZD1222), and protein subunit (MVC-COV1901). After Taiwan shifted from its zero-COVID strategy in April 2022, population-based evaluation of

Emerging evidence suggests prolonged use of noninvasive respiratory support may increase mortality of patients with coronavirus disease 2019 (COVID-19)-associated acute respiratory distress syndrome who require extracorporeal membrane oxygenation

The COVID-19 pandemic increased women's vulnerability to intimate partner and sexual violence (IPV/SV), as well as challenging organizations' ability to respond. This research is based on a 2021 nationwide survey about the impacts of COVID-19 on IPV

Rift Valley fever virus (RVFV) could cause an emergency illness characterized by fever, muscle pain, and even death in humans or ruminants. However, there are no approved antiviral drugs that prevent or treat RVFV infection. While therapeutic

G3BP1 is an RNA binding protein that condenses untranslating messenger RNAs into stress granules (SGs). G3BP1 is inactivated by multiple viruses and is thought to antagonize viral replication by SG-enhanced antiviral signaling. Here, we show that