Objective The goal of this randomized placebo-controlled clinical trial was to investigate the therapeutic efficacy of oral 25-hydroxyvitamin D 3 [25(OH)D 3 ] in improving vitamin D status in vitamin D deficient/insufficient patients infected with the SARS-CoV-2 (COVID-19) virus. Methods This is a multicenter randomized double blinded randomized placebo-controlled clinical trial. Participants were recruited from three hospitals that are affiliated to [Institution Blinded for Review], and [Institution Blinded for Review]. Results A total 106 hospitalized patients who had a circulating concentration of 25(OH)D <30 ng/ml were enrolled in this study. Within 30 and 60 days 79.4% (26 out of 34) and 100% (24 out of 24) of the patients who received 25(OH)D 3 became sufficient whereas ≤12.5% the patients in the placebo group became sufficient during 2 months follow-up. We observed an overall lower trend for hospitalization, ICU duration, needing ventilator assistance and mortality in the 25(OH)D3 group compared with placebo group but they weren’t statistically significant. Treatment with oral 25(OH)D 3 was associated with a significant increase in the lymphocyte percentage and decrease in the ratio of neutrophils to lymphocytes (NLR) in the patients. The lower NLR was significant associated with reduced ICU admission days and mortality. Conclusion Our analysis indicated that oral 25-hydroxyvitamin D 3 was able to correct vitamin D deficiency/insufficiency in COVID-19 patients that resulted in improved immune function by increasing blood lymphocyte percentage. RCTs with a larger sample size and with higher dose of 25(OH)D3 maybe needed to confirm the potential effect of 25(OH)D3 on reducing clinical outcomes in COVID-19 patients. Ethics and Dissemination The study protocol was approved by the Ethics Committee of [Institution Blinded for Review]. (Approval Number: IR.TUMS.VCR.REC.1399.061). Dissemination plans include academic publications, conference presentations and social media. Trial registration The protocol was registered with the Iranian Registry of Clinical Trials (IRCT) on April 11, 2020 [Number Blinded for Review]. and U.S. National Institutes of Health [Number Blinded for Review] on May 11, 2020.

BackgroundHealth in early life is crucial for health later in life. Exposure to air pollution during embryonic and early-life development can result in placental epigenetic modification and foetus reprogramming, which can influence disease susceptibility in later life. Objectives: The aim of this paper was to investigate the placental adaptation in the level of global DNA methylation and differential gene expression in the methylation cycle in new-borns exposed to high fine particulate matter in the foetal stage.Study designThis is a nested case-control study. We enrolled pregnant healthy women attending prenatal care clinics in Tehran, Iran, who were residents of selected polluted and unpolluted regions, before the 14th week of pregnancy. We calculated the regional background levels of particle mass- particles with aerodynamics diameter smaller than 2.5 μm (PM2.5) and 10 μm (PM10)—of two regions of interest. At the time of delivery, placental tissue was taken for gene expression and DNA methylation analyses. We also recorded birth outcomes (the new-born’s sex, birth date, birth weight and length, head and chest circumference, gestational age, Apgar score, and level of neonatal care required).ResultsAs regards PM2.5 and PM10 concentrations in different time windows of pregnancy, there were significantly independent positive correlations between PM10 and PM2.5 in the first trimester of all subjects and placental global DNA methylation levels (p-value = 0.01, p-value = 0.03, respectively). The gene expression analysis showed there was significant correlation between S-adenosylmethionine expression and PM2.5 (p = 0.003) and PM10 levels in the first trimester (p = 0.03).ConclusionOur data showed prenatal exposures to air pollutants in the first trimester could influence placental adaptation by DNA methylation.

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