Human coronaviruses are RNA viruses that are sensitive to ultraviolet (UV) radiation. Sunlight contains UVA (320–400 nm), UVB (260–320 nm) and UVC (200–260 nm) action spectra. UVC can inactivate coronaviruses, including severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). The incidence and mortality of coronavirus disease 2019 (COVID-19) are considered to be correlated with vitamin D levels. Vitamin D synthesis in human skin is closely related to exposure to UVB radiation. Therefore, the incidence and mortality of COVID-19 are also considered to be correlated with Vitamin D levels. In this study, Spearman and Kendall rank correlation analysis tests were used to analyze the correlation between the average percent positive of five human coronaviruses (SARS-CoV-2, CoVHKU1, CoVNL63, CoVOC43, and CoV229E) in the U.S. and the corresponding sunlight UV radiation dose The results indicated that the monthly average percent positive of four common coronaviruses was significantly negatively correlated with the sunlight UV radiation dose. The weekly percent positive of SARS-CoV-2 during April 17, 2020 to July 10, 2020 showed a significant negative correlation with the sunlight UV radiation dose in census regions 1 and 2 of the U.S. while no statistical significance in the other regions. Additionally, sunlight UV radiation also showed some negative effects with respect to the early SARS-CoV-2 transmission.
Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) is a unique PPIase belonging to the parvulin family, and it isomerizes peptide bond between phospho-(Ser/Thr) and Pro. Pin1 has been linked to the pathogenesis of various human diseases; however, its exact biological functions remain unclear. The aim of the present study is to explore the expression pattern of Pin1 in patients with refractory epilepsy and in a chronic pilocarpine-induced epileptic mouse model. Using Western blot, immunofluorescence and immunoprecipitation analysis, we found that Pin1 protein was mainly distributed in neurons, demonstrated by colocalization with the dendritic marker, MAP2. However, the expression of Pin1 decreased remarkably in epileptic patients and experimental mice. Furthermore, the reciprocal coimmunoprecipitation analysis showed that Pin1 interacted with NR2A and NR2B-containing NMDA receptors not AMPA receptors in epileptic mouse models. Our results are the first to indicate that the expression of Pin1 in epileptic brain tissue could play important roles in epilepsy.
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