Table_1_The causal relationship between air pollution, obesity, and COVID-19 risk: a large-scale genetic correlation study.xlsx

ObjectiveObservational evidence reported that air pollution is a significant risk element for numerous health problems, such as obesity and coronavirus disease 2019 (COVID-19), but their causal relationship is currently unknown. Our objective was to probe the causal relationship between air pollution, obesity, and COVID-19 and to explore whether obesity mediates this association.MethodsWe obtained instrumental variables strongly correlated to air pollutants [PM2.5, nitrogen dioxide (NO2) and nitrogen oxides (NOx)], 9 obesity-related traits (abdominal subcutaneous adipose tissue volume, waist-to-hip ratio, body mass index, hip circumference, waist circumference, obesity class 1-3, visceral adipose tissue volume), and COVID-19 phenotypes (susceptibility, hospitalization, severity) from public genome-wide association studies. We used clinical and genetic data from different public biological databases and performed analysis by two-sample and two-step Mendelian randomization.ResultsPM2.5 genetically correlated with 5 obesity-related traits, which obesity class 1 was most affected (beta = 0.38, 95% CI = 0.11 - 0.65, p = 6.31E-3). NO2 genetically correlated with 3 obesity-related traits, which obesity class 1 was also most affected (beta = 0.33, 95% CI = 0.055 - 0.61, p = 1.90E-2). NOx genetically correlated with 7 obesity-related traits, which obesity class 3 was most affected (beta = 1.16, 95% CI = 0.42-1.90, p = 2.10E-3). Almost all the obesity-related traits genetically increased the risks for COVID-19 phenotypes. Among them, body mass index, waist circumference, hip circumference, waist-to-hip ratio, and obesity class 1 and 2 mediated the effects of air pollutants on COVID-19 risks (p ConclusionOur study suggested that exposure to heavy air pollutants causally increased risks for obesity. Besides, obesity causally increased the risks for COVID-19 phenotypes. Attention needs to be paid to weight status for the population who suffer from heavy air pollution, as they are more likely to be susceptible and vulnerable to COVID-19.</p

Image_1_The causal relationship between air pollution, obesity, and COVID-19 risk: a large-scale genetic correlation study.pdf

ObjectiveObservational evidence reported that air pollution is a significant risk element for numerous health problems, such as obesity and coronavirus disease 2019 (COVID-19), but their causal relationship is currently unknown. Our objective was to probe the causal relationship between air pollution, obesity, and COVID-19 and to explore whether obesity mediates this association.MethodsWe obtained instrumental variables strongly correlated to air pollutants [PM2.5, nitrogen dioxide (NO2) and nitrogen oxides (NOx)], 9 obesity-related traits (abdominal subcutaneous adipose tissue volume, waist-to-hip ratio, body mass index, hip circumference, waist circumference, obesity class 1-3, visceral adipose tissue volume), and COVID-19 phenotypes (susceptibility, hospitalization, severity) from public genome-wide association studies. We used clinical and genetic data from different public biological databases and performed analysis by two-sample and two-step Mendelian randomization.ResultsPM2.5 genetically correlated with 5 obesity-related traits, which obesity class 1 was most affected (beta = 0.38, 95% CI = 0.11 - 0.65, p = 6.31E-3). NO2 genetically correlated with 3 obesity-related traits, which obesity class 1 was also most affected (beta = 0.33, 95% CI = 0.055 - 0.61, p = 1.90E-2). NOx genetically correlated with 7 obesity-related traits, which obesity class 3 was most affected (beta = 1.16, 95% CI = 0.42-1.90, p = 2.10E-3). Almost all the obesity-related traits genetically increased the risks for COVID-19 phenotypes. Among them, body mass index, waist circumference, hip circumference, waist-to-hip ratio, and obesity class 1 and 2 mediated the effects of air pollutants on COVID-19 risks (p ConclusionOur study suggested that exposure to heavy air pollutants causally increased risks for obesity. Besides, obesity causally increased the risks for COVID-19 phenotypes. Attention needs to be paid to weight status for the population who suffer from heavy air pollution, as they are more likely to be susceptible and vulnerable to COVID-19.</p

Image_2_The causal relationship between air pollution, obesity, and COVID-19 risk: a large-scale genetic correlation study.pdf

ObjectiveObservational evidence reported that air pollution is a significant risk element for numerous health problems, such as obesity and coronavirus disease 2019 (COVID-19), but their causal relationship is currently unknown. Our objective was to probe the causal relationship between air pollution, obesity, and COVID-19 and to explore whether obesity mediates this association.MethodsWe obtained instrumental variables strongly correlated to air pollutants [PM2.5, nitrogen dioxide (NO2) and nitrogen oxides (NOx)], 9 obesity-related traits (abdominal subcutaneous adipose tissue volume, waist-to-hip ratio, body mass index, hip circumference, waist circumference, obesity class 1-3, visceral adipose tissue volume), and COVID-19 phenotypes (susceptibility, hospitalization, severity) from public genome-wide association studies. We used clinical and genetic data from different public biological databases and performed analysis by two-sample and two-step Mendelian randomization.ResultsPM2.5 genetically correlated with 5 obesity-related traits, which obesity class 1 was most affected (beta = 0.38, 95% CI = 0.11 - 0.65, p = 6.31E-3). NO2 genetically correlated with 3 obesity-related traits, which obesity class 1 was also most affected (beta = 0.33, 95% CI = 0.055 - 0.61, p = 1.90E-2). NOx genetically correlated with 7 obesity-related traits, which obesity class 3 was most affected (beta = 1.16, 95% CI = 0.42-1.90, p = 2.10E-3). Almost all the obesity-related traits genetically increased the risks for COVID-19 phenotypes. Among them, body mass index, waist circumference, hip circumference, waist-to-hip ratio, and obesity class 1 and 2 mediated the effects of air pollutants on COVID-19 risks (p ConclusionOur study suggested that exposure to heavy air pollutants causally increased risks for obesity. Besides, obesity causally increased the risks for COVID-19 phenotypes. Attention needs to be paid to weight status for the population who suffer from heavy air pollution, as they are more likely to be susceptible and vulnerable to COVID-19.</p

Image_3_The causal relationship between air pollution, obesity, and COVID-19 risk: a large-scale genetic correlation study.pdf

ObjectiveObservational evidence reported that air pollution is a significant risk element for numerous health problems, such as obesity and coronavirus disease 2019 (COVID-19), but their causal relationship is currently unknown. Our objective was to probe the causal relationship between air pollution, obesity, and COVID-19 and to explore whether obesity mediates this association.MethodsWe obtained instrumental variables strongly correlated to air pollutants [PM2.5, nitrogen dioxide (NO2) and nitrogen oxides (NOx)], 9 obesity-related traits (abdominal subcutaneous adipose tissue volume, waist-to-hip ratio, body mass index, hip circumference, waist circumference, obesity class 1-3, visceral adipose tissue volume), and COVID-19 phenotypes (susceptibility, hospitalization, severity) from public genome-wide association studies. We used clinical and genetic data from different public biological databases and performed analysis by two-sample and two-step Mendelian randomization.ResultsPM2.5 genetically correlated with 5 obesity-related traits, which obesity class 1 was most affected (beta = 0.38, 95% CI = 0.11 - 0.65, p = 6.31E-3). NO2 genetically correlated with 3 obesity-related traits, which obesity class 1 was also most affected (beta = 0.33, 95% CI = 0.055 - 0.61, p = 1.90E-2). NOx genetically correlated with 7 obesity-related traits, which obesity class 3 was most affected (beta = 1.16, 95% CI = 0.42-1.90, p = 2.10E-3). Almost all the obesity-related traits genetically increased the risks for COVID-19 phenotypes. Among them, body mass index, waist circumference, hip circumference, waist-to-hip ratio, and obesity class 1 and 2 mediated the effects of air pollutants on COVID-19 risks (p ConclusionOur study suggested that exposure to heavy air pollutants causally increased risks for obesity. Besides, obesity causally increased the risks for COVID-19 phenotypes. Attention needs to be paid to weight status for the population who suffer from heavy air pollution, as they are more likely to be susceptible and vulnerable to COVID-19.</p

DataSheet_1_Multi-omics profiling reveal responses of three major Dendrobium species from different growth years to medicinal components.docx

Dendrobium is a perennial herb found in Asia that is known for its medicinal and ornamental properties. Studies have shown that the stem is the primary medicinal component of Dendrobium spp. To investigate the effect of the species and age of Dendrobium (in years) on the content of its medicinal components, we collected the stems of 1-to-4-year-old D. officinale, D. moniliforme, and D. huoshanense, sequenced the transcriptome, metabolome, and microbiome, and analyzed the data in a comprehensive multi-omics study. We identified 10,426 differentially expressed genes (DEGs) with 644 differentially accumulated metabolites (DAMs) from 12 comparative groups and mapped the flavonoid pathway based on DEGs and DAMs. Transcriptomic and metabolomic data indicated a general trend of the accumulation of flavonoids exhibiting pharmacological effects in the three Dendrobium species. In addition, joint metabolome and microbiome analyses showed that actinobacteria was closely associated with flavonoid synthesis with increasing age. Our findings provide novel insights into the interactions of flavonoids of Dendrobium with the transcriptome and microbiome.</p

Magnetic Nano-Fe₃O₄-Supported 1-Benzyl-1,4-dihydronicotinamide (BNAH): Synthesis and Application in the Catalytic Reduction of α,β-Epoxy Ketones

A novel magnetically recoverable organic hydride compound was successfully constructed by using silica-coated magnetic nanoparticles as a support. An as-prepared magnetic organic hydride compound, BNAH (1-benzyl-1,4-dihydronicotinamide), showed efficient activity in the catalytic reduction of α,β-epoxy ketones. After reaction, the magnetic nanoparticle-supported BNAH can be separated by simple magnetic separation which made the separation of the product easier

Kidney tissue injury over time following 30min of bilateral renal ischenmia-reperfusion injury.

<p>C57BL/6 mice were subjected to sham or bilateral ischemia by clamping the renal pedicles for 30 min and then removing the clamps and confirming reperfusion. Mice were sacrificed at various times and kidney samples were collected. (A and B) BUN and serum creatinine were measured to determine renal function.The data shown were the means±SD. n = 6 per group. *<i>P</i> <0.05, vs sham; **<i>P</i> <0.01, vs sham(C) Photomicrograps of H & E-stained kidney sections (200×). All fields were chosen form cortex and outer medulla. Tubular damage is marked with arrows.</p

Renal SDF-1 protein levels following LC treatment.

<p>Kidney homogenates from mice subjected to I/R injury and treated with LV or LC were analysed for SDF-1 protein using ELISA. LC treatment resulted in an increase of SDF-1 levels compared with the concentration found in homogenates from LV-treated animals that reached statistical significance (n  =  4-6 per group, **<i>P</i> <0.01). Animals were sacrificed 24 h following ischaemia.</p

Regional location of SDF-1 in I/R kidney. (A) Immunohistochemistry staining of SDF-1 in the kidney also showed that IR-induced expression of SDF-1 was further distributed into the surrounding corticomedullary and outer medullary region compared to sham-operated mice.

<p>The kidney sections from sham-operated mice were used as control. (upper panels original magnification 200×; bottom panels 400×). (B) Quantification of SDF-1 positive area. Values are means ± SD. **<i>P</i> <0.01, vs sham.</p

IKKε Knockout Prevents High Fat Diet Induced Arterial Atherosclerosis and NF-κB Signaling in Mice

<div><p>Aims</p><p>Atherosclerosis is a public health concern affecting many worldwide, but its pathogenesis remains unclear. In this study we investigated the role of IKKε during the formation of atherosclerosis and its molecular mechanism in the mouse aortic vessel wall.</p><p>Methods and Results</p><p>C57BL/6 wild-type or IKKε knockout mice bred into the ApoE knockout genetic background were divided into 4 groups: (1) wild-type (WT), (2) ApoE knockout (AK), (3) IKKε knockout (IK), (4) or both ApoE and IKKε knockout (DK). Each group of mice were fed with a high fat diet (HFD) for 12 weeks from 8 weeks of age. Immunohistochemistry and Western blotting analysis demonstrated obvious increases in the expression of IKKε in the AK group compared with the WT group, especially in the intima. Serum lipid levels were significantly higher in the AK and DK groups than in the other two groups. Staining with hematoxylin-eosin and Oil Red, as well as scanning electron microscopy revealed less severe atherosclerotic lesions in the DK group than in the AK group. Immunofluorescence and Western blot analysis demonstrated obvious increases in the expression of NF-κB pathway components and downstream factors in the AK group, especially in the intima, while these increases were blocked in the DK group.</p><p>Conclusion</p><p>The knockout of IKKε prevented significant atherosclerosis lesions in the mouse aorta from in both wild-type and ApoE knockout mice fed a HFD, suggesting that IKKε may play a vital role in HFD-induced atherosclerosis and would be an important target for the treatment of atherosclerosis.</p></div