Plasma elaidic acid level is associated with periodontal health in American adults: A cross-sectional study.

Background: Whether there is an association between TFAs and periodontitis is unclear. The purpose of this study was to investigate the relationship between moderate/severe periodontitis and plasma level of elaidic acid, a major trans-fatty acid component, in American adults. Methods: The National Health and Nutrition Examination Survey (NHANES) years 2009-2010 were used to screen a total of 1,610 people. The independent variable of interest is plasma elaidic acid level, the dependent variable is periodontitis, and the covariates include socio-demographic variables, lifestyle variables, systemic diseases, etc. The distribution of variables in the covariate differences between the different independent groups according to tertile was investigated using a multiple linear regression model. To examine the association between plasma elaidic acid levels and moderate/severe periodontitis, three models were used. Results: Multiple logistic regression analysis showed a significant association between plasma elaidic acid level and moderate/severe periodontitis after adjustment for potential confounders (OR = 1.021, 95%CI: 1.004-1.039, P = 0.01394). Subjects with the highest tertile of plasma elaidic acid levels were 51.9% more likely to have periodontitis compared with subjects with the lowest tertile of plasma elaidic acid levels (OR = 1.519, 95% CI: 1.136-2.030, P = 0.00477). No possible sources of heterogeneity were identified in the subgroup analyses. Conclusion: Plasma elaidic acid levels are associated with periodontal disease in American adults.

The Rhinolophus affinis bat ACE2 and multiple animal orthologs are functional receptors for bat coronavirus RaTG13 and SARS-CoV-2

Bat coronavirus (CoV) RaTG13 shares the highest genome sequence identity with SARS-CoV-2 among all known coronaviruses, and also uses human angiotensin converting enzyme 2 (hACE2) for virus entry. Thus, SARS-CoV-2 is thought to have originated from bat. However, whether SARS-CoV-2 emerged from bats directly or through an intermediate host remains elusive. Here, we found that Rhinolophus affinis bat ACE2 (RaACE2) is an entry receptor for both SARS-CoV-2 and RaTG13, although RaACE2 binding to the receptor binding domain (RBD) of SARS-CoV-2 is markedly weaker than that of hACE2. We further evaluated the receptor activities of ACE2s from additional 16 diverse animal species for RaTG13, SARS-CoV, and SARS-CoV-2 in terms of S protein binding, membrane fusion, and pseudovirus entry. We found that the RaTG13 spike (S) protein is significantly less fusogenic than SARS-CoV and SARS-CoV-2, and seven out of sixteen different ACE2s function as entry receptors for all three viruses, indicating that all three viruses might have broad host rages. Of note, RaTG13 S pseudovirions can use mouse, but not pangolin ACE2, for virus entry, whereas SARS-CoV-2 S pseudovirions can use pangolin, but limited for mouse, ACE2s enter cells. Mutagenesis analysis revealed that residues 484 and 498 in RaTG13 and SARS-CoV-2 S proteins play critical roles in recognition of mouse and human ACE2. Finally, two polymorphous Rhinolophous sinicus bat ACE2s showed different susceptibilities to virus entry by RaTG13 and SARS-CoV-2 S pseudovirions, suggesting possible coevolution. Our results offer better understanding of the mechanism of coronavirus entry, host range, and virus-host coevolution.

PM2.5 promotes abdominal aortic aneurysm formation in angiotensin â ¡-infused apoe-/- mice.

BACKGROUND: Particulate matter 2.5 (PM2.5) has proven to be associated with morbidity and mortality from cardiovascular diseases. However, whether PM2.5 could promote the formation of abdominal aortic aneurysm (AAA) is unclear. Present study aimed to explore the relationship between PM2.5 exposure and AAA development. METHODS: Ang Ⅱ-infused apoe-/- mice were treated with PM2.5 or saline by intranasal instillation. Four weeks later, histological and immunohistological analyses were used to evaluate the effect of PM2.5 on AAA formation. Human aortic smooth muscle cells (HASMCs) were also employed to further analyze the adverse effect of PM2.5 in vitro. RESULTS: We found that PM2.5 could significantly increase the AAA incidence, the maximal abdominal aortic diameter and could promote the degradation of elastin. Additionally, the expression of senescence markers, P21 and P16 were also enhanced after PM2.5 exposure. We also found that PM2.5 significantly increased the AAA related pathological changes, MMP2 and MCP-1 expression in HASMCs. Meanwhile, PM2.5 could increase the expression of senescence markers P21, P16 and SA-ß-gal activity, also the reactive oxygen species levels in vitro. CONCLUSIONS: PM2.5 promoted the formation of AAA in an Ang Ⅱ-induced AAA model. The underlying mechanism might be cellular senescence after PM2.5 exposure.