SARS-CoV2, the COVID-19 Pandemic and Community Perceptions.

The purpose of this study was to describe knowledge and beliefs about SARS-CoV2 and COVID-19 and explore the gaps between current media coverage of health risks and what the general public knows about the virus and its outcome. A 37-question survey was developed and administered to a community collaborative group in a Midwestern state in the United States. Fifty-three participants completed the survey. When asked where participants found their information, a majority reported the internet (33.9%, n = 18/53) and radio and/or tv (28.3%, n = 15/53). Most participants showed a basic level of COVID-19 knowledge, but few could identify the 3 most frequent symptoms of COVID-19 (7.5%, n = 4/53). The results from this study highlight the continued need for increased public health communication. Educational efforts should focus on social media and internet outlets to address COVID-19 misinformation, strategies to address vaccine hesitancy, and the associated communication gap to help address related health disparities.

Mice with an absent stress response are protected against ischemic renal injury.

Inducible heat shock proteins (HSPs), regulated by heat shock factor-1 (HSF-1), protect against renal cell injury in vitro. To determine whether HSPs ameliorate ischemic renal injury in vivo, HSF-1 functional knockout mice (HSF-KO) were compared with wild-type mice following bilateral ischemic renal injury. Following injury, the kidneys of wild-type mice had the expected induction of HSP70 and HSP25; a response absent in the kidneys of HSF-KO mice. Baseline serum creatinine was equivalent between strains. Serum creatinine at 24 h reflow in HSF-KO mice was significantly lower than that in the wild type. Histology showed similar tubule injury in both strains after ischemic renal injury but increased medullary vascular congestion in wild-type compared with HSF-KO mice. Flow cytometry of mononuclear cells isolated from kidneys showed no difference between strains in the number of CD4(+) and CD8(+) T cells in sham-operated animals. At 1 h of reflow, CD4(+) and CD8(+) cells were doubled in the kidneys of wild-type but not HSF-KO mice. Foxp3(+) T-regulatory cells were significantly more abundant in the kidneys of sham-operated HSF-KO than wild-type mice. Suppression of CD25(+)Foxp3(+) cells in HSF-KO kidneys with the anti-CD25 antibody PC61 reversed the protection against ischemic renal injury. Thus, HSF-KO mice are protected from ischemic renal injury by a mechanism that depends on an increase in the T-regulatory cells in the kidney associated with altered T-cell infiltration early in reflow. Hence, stress response activation may contribute to early injury by facilitating T-cell infiltration into ischemic kidney.