Background: The ABO blood group system has been associated with multiple infectious diseases, including hepatitis B, dengue haemorrhagic fever and so on. Coronavirus disease 2019 (COVID-19) is a new respiratory infectious disease and the relationship between COVID-19 and ABO blood group system needs to be explored urgently. Methods: A hospital-based case-control study was conducted at Zhongnan Hospital of Wuhan University from 1 January 2020 to 5 March 2020. A total of 105 COVID-19 cases and 103 controls were included. The blood group frequency was tested with the chi-square statistic, and odds ratios (ORs) with 95% confidence intervals (CIs) were calculated between cases and controls. In addition, according to gender, the studied population was divided into two subgroups, and we assessed the association between cases and controls by gender. Finally, considering lymphopenia as a feature of COVID-19, the relationship between the ABO blood group and the lymphocyte count was determined in case samples. Results: The frequencies of blood types A, B, AB, and O were 42.8, 26.7, 8.57, and 21.9%, respectively, in the case group. Association analysis between the ABO blood group and COVID-19 indicated that there was a statistically significant difference for blood type A (P = 0.04, OR = 1.33, 95% CI = 1.02-1.73) but not for blood types B, AB or O (P = 0.48, OR = 0.90, 95% CI = 0.66-1.23; P = 0.61, OR = 0.88, 95% CI = 0.53-1.46; and P = 0.23, OR = 0.82, 95% CI = 0.58-1.15, respectively). An analysis stratified by gender revealed that the association was highly significant between blood type A in the female subgroup (P = 0.02, OR = 1.56, 95% CI = 1.08-2.27) but not in the male subgroup (P = 0.51, OR = 1.14, 95% CI = 0.78-1.67). The average level of lymphocyte count was the lowest with blood type A in patients, however, compared with other blood types, there was still no significant statistical difference. Conclusions: Our findings provide epidemiological evidence that females with blood type A are susceptible to COVID-19. However, these research results need to be validated in future studies.
improves endothelial function in hyperlipidemic rats by reducing oxidative/nitrative stress and differential regulation of eNOS/iNOS activity. Am J Physiol Endocrinol Metab 293: E1703-E1708, 2007. First published September 25, 2007 doi:10.1152/ajpendo.00462.2007.-Plasma adiponectin level is significantly reduced in patients with metabolic syndrome, and vascular dysfunction is an important pathological event in these patients. However, whether adiponectin may protect endothelial cells and attenuate endothelial dysfunction caused by metabolic disorders remains largely unknown. Adult rats were fed with a regular or a high-fat diet for 14 wk. The aorta was isolated, and vascular segments were incubated with vehicle or the globular domain of adiponectin (gAd; 2 g/ml) for 4 h. The effect of gAd on endothelial function, nitric oxide (NO) and superoxide production, nitrotyrosine formation, gp91 phox expression, and endothelial nitric oxide synthase (eNOS)/inducible NOS (iNOS) activity/expression was determined. Severe endothelial dysfunction (maximal vasorelaxation in response to ACh: 70.3 Ϯ 3.3 vs. 95.2 Ϯ 2.5% in control, P Ͻ 0.01) was observed in hyperlipidemic aortic segments, and treatment with gAd significantly improved endothelial function (P Ͻ 0.01). Paradoxically, total NO production was significantly increased in hyperlipidemic vessels, and treatment with gAd slightly reduced, rather than increased, total NO production in these vessels. Treatment with gAd reduced (Ϫ78%, P Ͻ 0.01) superoxide production and peroxynitrite formation in hyperlipidemic vascular segments. Moreover, a moderate attenuation (Ϫ30%, P Ͻ 0.05) in gp91 phox and iNOS overexpression in hyperlipidemic vessels was observed after gAd incubation. Treatment with gAd had no effect on eNOS expression but significantly increased eNOS phosphorylation (P Ͻ 0.01). Most noticeably, treatment with gAd significantly enhanced eNOS (ϩ83%) but reduced iNOS (Ϫ70%, P Ͻ 0.01) activity in hyperlipidemic vessels. Collectively, these results demonstrated that adiponectin protects the endothelium against hyperlipidemic injury by multiple mechanisms, including promoting eNOS activity, inhibiting iNOS activity, preserving bioactive NO, and attenuating oxidative/nitrative stress. metabolic syndrome; endothelial dysfunction; cytokine; nitric oxide; endothelial nitric oxide synthase; inducible nitric oxide synthase METABOLIC SYNDROME IS CHARACTERIZED by a group of metabolic and hemostatic abnormalities, including impaired glucose tolerance, hyperinsulinemia, hypertension, dyslipidemia, oxidant stress, and endothelial dysfunction (7). This cluster generates an increased risk of macroangiopathy, which is the leading cause of mortality for patients with metabolic syndrome and type 2 diabetes (3). Therefore, the discovery of therapeutic interventions that block or attenuate metabolic disorder-induced macroangiopathy holds great promise in reducing metabolic syndrome-related death.Endothelial dysfunction is an early pivotal event in the development, progression, and manifestat...
The effects of interleukin-33 (IL-33) on the immune system have been clearly demonstrated; however, in cardiovascular diseases, especially in coronary artery disease (CAD), these effects have not yet been clarified. In this study, we investigate the genetic role of the IL-33-ST2L pathway in CAD. We performed three-stage case-control association analyses on a total of 4,521 individuals with CAD and 4,809 controls via tag SNPs in the genes encoding IL-33 and ST2L-IL-1RL1. One tag SNP in each gene was significantly associated with CAD (rs7025417(T) in IL33, padj = 1.19 × 10(-28), OR = 1.39, 95% CI: 1.31-1.47; rs11685424(G) in IL1RL1, padj = 6.93 × 10(-30), OR = 1.40, 95% CI: 1.32-1.48). Combining significant variants in two genes, the risk for CAD increased nearly 5-fold (padj = 8.90 × 10(-21), OR = 4.98, 95% CI: 3.56-6.97). Traditional risk factors for CAD were adjusted for the association studies by SPSS with logistic regression analysis. With the two variants above, both located within the gene promoter regions, reporter gene analysis indicated that the rs7025417 C>T and rs11685424 A>G changes resulted in altered regulation of IL33 and IL1RL1 gene expression, respectively (p < 0.005). Further studies revealed that the rs7025417 genotype was significantly associated with plasma IL-33 levels in the detectable subjects (n = 227, R(2) = 0.276, p = 1.77 × 10(-17)): the level of IL-33 protein increased with the number of rs7025417 risk (T) alleles. Based on genetic evidence in humans, the IL-33-ST2L pathway appears to have a causal role in the development of CAD, highlighting this pathway as a valuable target for the prevention and treatment of CAD.
The cleanup of oily wastewater and crude-oil spills is a global challenge. Traditional membrane materials are inefficient for oil/water separation under harsh conditions and limited by sorption speeds because of the high viscosity of crude oil. Herein, a kind of Graphene-wrapped polyphenylene sulfide fibrous membrane with superior chemical resistance and hydrophobicity for efficient oil/water separation and fast adsorption of crude oil all-weather is reported. The reduced graphene oxide (rGO)@polyphenylene sulfide (PPS) fibrous membrane can be applied in the various harsh conditions with Joule heating and solar heating. In addition, the oil(dichloromethane)/water separation flux of rGO@PPS reached 12 903 L m–2h–1, and the separation efficiency reached 99.99%. After 10 cycles, the rGO@PPS still performed high separation flux and filtration efficiency. More importantly, the rGO@PPS still retained its high conductivity, excellent filtration efficiency, and stable hydrophobicity after acid or alkali treatment. Moreover, the rGO@PPS can be heated by solar energy to absorb viscous crude oil during the day, while at night, the crude oil can be adsorbed by Joule heating. The time to adsorb crude oil can be reduced by 98.6% and 97.3% through Joule heating and solar heating, respectively. This all-weather utilization greatly increases the adsorption efficiency and effectively reduces energy consumption.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.