Highlights The coronavirus disease 2019 (COVID-19) pandemic has resulted in unprecedented hazards to mental health globally. Relatively high rates of anxiety, depression, post-traumatic stress disorder, psychological distress, and stress were reported in the general population during the COVID-19 pandemic in eight countries. Common risk factors associated with mental distress during the COVID-19 pandemic include female gender, younger age group (≤40 years), presence of chronic/psychiatric illnesses, unemployment, student status, and frequent exposure to social media/news concerning COVID-19. Mitigation of COVID-19 induced psychological distress requires government intervention and individual efforts.

Preexisting noncommunicable diseases (eg, diabetes) increase the risk of COVID-19 infection, hospitalization, and death. Mood disorders are associated with impaired immune function and social determinants that increase the risk of COVID-19. Determining whether preexisting mood disorders represent a risk of COVID-19 would inform public health priorities.OBJECTIVE To assess whether preexisting mood disorders are associated with a higher risk of COVID-19 susceptibility, hospitalization, severe complications, and death.DATA SOURCES Systematic searches were conducted for studies reporting data on COVID-19 outcomes in populations with and without mood disorders on PubMed/MEDLINE,

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Farmland is one of the key factors affecting national or regional food security, and farmland suitability evaluation can provide critical information for the spatial layout of farmland. Previous studies have mainly focused on the role of natural factors in suitability evaluation, while ignoring the important influence of socio-economic activities. This study selects natural factors such as elevation and slope and non-agriculturalization sensitivity factors to build a farmland suitability evaluation framework of “natural non-agriculturalization sensitivity”, quantify the farmland suitability, and uses GIS technology to classify the evaluation results into four levels: highly, moderately, barely, and unsuitable. The results show that the non-agriculturalization sensitivity of farmland in Hubei Province shows the spatial characteristics of multi-point clustering, with density increasing from west and north to central and east; the overall farmland suitability in Hubei Province is high, and the areas of highly, moderately, barely, and unsuitable farmland account for 2.32%, 67.69%, 11.49%, and 18.50%, respectively. In terms of spatial distribution, there are obvious spatial differences in the farmland suitability, with highly and moderately suitable areas mainly distributed in the central and eastern regions and barely suitable and unsuitable areas mainly distributed in the western, northeastern, and southeastern parts of Hubei Province.

Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder caused by mutation in fibrillin-1 (FBN1). However, the molecular mechanism underlying MFS remains poorly understood. The study aimed to explore how the L-type calcium channel (Ca V 1.2) modulates disease progression of MFS and to identify a potential effective target for attenuating MFS. KEGG enrichment analysis showed that the calcium signaling pathway gene set was significantly enriched. We demonstrated that FBN1 deficiency exhibited inhibition on both the expression of Cav1.2 and proliferation of vascular smooth muscle cells (VSMCs). Then, we examined whether FBN1 mediates Cav1.2 via regulating TGF-β1. Higher levels of TGF-β1 were observed in the serum and aortic tissues from patients with MFS. TGF-β1 modulated Cav1.2 expression in a concentration-dependent manner. We evaluated the role of Cav1.2 in MFS by small interfering RNA and Cav1.2 agonist Bay K8644. The effect of Cav1.2 on cell proliferation was dependent on c-Fos activity. These results demonstrated FBN1 deficiency decreased the expression levels of Cav1.2 via regulation of TGF-β1, and downregulation of Cav1.2 inhibited cell proliferation of human aortic smooth muscle cells (HASMCs) in MFS patients. These findings suggest that Cav1.2 may be an appealing therapeutic target for MFS.