Progression of COVID-19 to severe disease and death is insufficiently understood.
Summarize the prevalence of risk factors and adverse outcomes and determine their associations in COVID-19 patients ...who were hospitalized.
We searched Medline, Embase and Web of Science for case-series and observational studies of hospitalized COVID-19 patients through August 31, 2020. Data were analyzed by fixed-effects meta-analysis using Shore's adjusted confidence intervals to address heterogeneity.
Seventy-seven studies comprising 38906 hospitalized patients met inclusion criteria; 21468 from the US-Europe and 9740 from China. Overall prevalence of death % (95% CI) from COVID-19 was 20% (18-23%); 23% (19-27%) in the US and Europe and 11% (7-16%) for China. Of those that died, 85% were aged≥60 years, 66% were males, and 66%, 44%, 39%, 37%, and 27% had hypertension, smoking history, diabetes, heart disease, and chronic kidney disease (CKD), respectively. The case fatality risk %(95% CI) were 52% (46-60) for heart disease, 51% (43-59) for COPD, 48% (37-63) for chronic kidney disease (CKD), 39% for chronic liver disease (CLD), 28% (23-36%) for hypertension, and 24% (17-33%) for diabetes. Summary relative risk (sRR) of death were higher for age≥60 years sRR = 3.6; 95% CI: 3.0-4.4, males 1.3; 1.2-1.4, smoking history 1.3; 1.1-1.6, COPD 1.7; 1.4-2.0, hypertension 1.8; 1.6-2.0, diabetes 1.5; 1.4-1.7, heart disease 2.1; 1.8-2.4, CKD 2.5; 2.1-3.0. The prevalence of hypertension (55%), diabetes (33%), smoking history (23%) and heart disease (17%) among the COVID-19 hospitalized patients in the US were substantially higher than that of the general US population, suggesting increased susceptibility to infection or disease progression for the individuals with comorbidities.
Public health screening for COVID-19 can be prioritized based on risk-groups. Appropriately addressing the modifiable risk factors such as smoking, hypertension, and diabetes could reduce morbidity and mortality due to COVID-19; public messaging can be accordingly adapted.
Med1 binds to a nuclear receptor and regulates transcription. Elevated Med1 protein expression promotes cancer growth in hormone-dependent breast and prostate cancers. Med1 protein expression was ...investigated by deubiquitinating enzymes (DUBs) overexpression in breast cancer cell lines. Various DNA constructs of SRT-DUBs were overexpressed in the MCF7 cell line, and Med1 protein expression was investigated by western blotting. The cell growth and in vitro invasion assay were performed in BRCA1-associated protein 1 (BAP1) wild type and mutant (C91A) overexpressed cells. Ubiquitination of the Med1 protein was observed, and Med1 protein expression and transcriptional activity were verified by various DUBs overexpressed. Although Med1 protein expression increased upon the overexpression of BAP1, it was not affected by the overexpression of BAP1 mutant (C91A). BAP1 was increased by the E2 treatment, which has an important effect on the breast cancer growth, and cell growth was decreased by BAP1 C91A overexpression. However, metastatic capacities were decreased by BAP1. In addition, the binding between the Med1 and the BAP1 protein was observed. These data suggested that BAP1 regulated Med1 protein expression in breast cancer cells and involved in cancer cell growth and metastasis by binding to Med1 protein.
Prior studies have shown that plant-based diets are associated with lower risk of cardiovascular risk factors and incident cardiovascular disease, but risks differed by quality of plant-based diets. ...No prospective studies have evaluated the associations between different types of plant-based diets and incident metabolic syndrome (MetS) and components of MetS. Furthermore, limited evidence exists in Asian populations who have habitually consumed a diet rich in plant foods for a long period of time.
Analyses were based on a community-based cohort of 5,646 men and women (40-69 years of age at baseline) living in Ansan and Ansung, South Korea (2001-2016) without MetS and related chronic diseases at baseline. Dietary intake was assessed using a validated food frequency questionnaire. Using the responses in the questionnaire, we calculated 4 plant-based diet indices (overall plant-based diet index PDI, healthful plant-based diet index hPDI, unhealthful plant-based diet index uPDI, and pro-vegetarian diet index). Higher PDI score represented greater consumption of all types of plant foods regardless of healthiness. Higher hPDI score represented greater consumption of healthy plant foods (whole grains, fruits, vegetables, nuts, legumes, tea and coffee) and lower consumption of less-healthy plant foods (refined grains, potatoes, sugar-sweetened beverages, sweets, salty foods). Higher uPDI represented lower consumption of healthy plant foods and greater consumption of less-healthy plant foods. Similar to PDI, higher pro-vegetarian diet score represented greater consumption of plant foods but included only selected plant foods (grains, fruits, vegetables, nuts, legumes, potatoes). Higher scores in all plant-based diet indices represented lower consumption of animal foods (animal fat, dairy, eggs, fish/seafood, meat). Over a median follow-up of 8 years, 2,583 participants developed incident MetS. Individuals in the highest versus lowest quintile of uPDI had 50% higher risk of developing incident MetS, adjusting for demographic characteristics and lifestyle factors (hazard ratio HR: 1.50, 95% CI 1.31-1.71, P-trend < 0.001). When we further adjusted for body mass index (BMI), those in the highest quintile of uPDI had 24%-46% higher risk of 4 out of 5 individual components of MetS (abdominal obesity, hypertriglyceridemia, low high-density lipoprotein HDL, and elevated blood pressure) (P-trend for all tests ≤ 0.001). Greater adherence to PDI was associated with lower risk of elevated fasting glucose (HR: 0.80, 95% CI 0.70-0.92, P-trend = 0.003). No consistent associations were observed for other plant-based diet indices and MetS. Limitations of the study may include potential measurement error in self-reported dietary intake, inability to classify a few plant foods as healthy and less-healthy, lack of data on vegetable oil intake, and possibility of residual confounding.
In this study, we observed that greater adherence to diets consisting of a high intake of refined carbohydrates, sugars, and salty foods in the framework of plant-based diets was associated with an elevated risk of MetS. These results suggest that considering the quality of plant foods is important for prevention of MetS in a population that habitually consumes plant foods.
Alfvén mode Pc1 waves undergo mode conversion to the fast mode due to induced Hall current in the ionosphere. The fast mode Pc1 waves are trapped and propagate across the magnetic field through the ...ionospheric waveguide. This process is called Pc1 wave ducting (PWD). Ducting is expected to be in any direction, but most of the existing literature investigated only PWDs toward the equator. In this paper, we report the rare observations of PWD propagating from sub-auroral latitudes and pervading the polar cap using Swarm satellites, ground magnetometers, and Defense Meteorological Satellite Program (DMSP) satellites. We first identify the injection region of Pc1 wave where localized broadband transverse waves, isolated aurora, and energetic proton precipitations are concurrently observed. Then, we compare ducting characteristics in the ionosphere between the two hemispheres. For the three events investigated here, PWDs in the Southern Hemisphere (SH) pervaded the polar cap while Pc1 waves in the Northern Hemisphere (NH) did not. This hemispheric asymmetry is attributed to the plasma density in the SH sufficient to form the Pc1 waveguide. However, a sharp plasma density gradient on the propagation path still interrupts the ducting even in higher plasma density (> 105 cm-3) regions. The observation of two intersecting Swarm satellites indicates the PWD is not only elongated meridionally, but also can have a significant zonal extent beyond that of the injection region.
Ultra-processed food has low nutritional quality, is associated with development of chronic diseases, and may increase exposure to chemicals used in food packaging and production.
To assess ...associations of ultra-processed food consumption with exposure to phthalates and bisphenols, including newer replacements, in the general U.S. population.
Among 2212 National Health and Nutrition Examination Survey (NHANES) 2013–2014 participants (≥6 years), we classified items reported in a 24-h dietary recall according to the NOVA food processing classification system and calculated energy intake from ultra-processed food. Urinary concentrations of mono-benzyl (MBzP), mono-(3-carboxypropyl) (MCPP), mono-(carboxyisononyl) (MCNP), mono-(carboxyisoctyl) (MCOP), and four metabolites of di(2-ethylhexyl) (∑DEHP) phthalates and bisphenols A, F, and S were measured in spot urine samples. We estimated percent changes in natural log creatinine-standardized concentrations per 10% higher energy from ultra-processed food in covariate-adjusted multivariable linear regression models. We examined effect measure modification by age group, race/ethnicity, and poverty:income ratio and assessed associations with minimally processed food intake.
In adjusted models, higher energy from ultra-processed food was associated with higher urinary concentrations of MCPP, MCNP, and MCOP but not MBzP, ∑DEHP, or bisphenols. Each 10% higher energy from ultra-processed food was associated with 8.0% (95% CI: 5.6%, 10.3%) higher urinary MCOP concentrations, with a stronger association among children than adolescents or adults. Ultra-processed sandwiches/hamburgers, French fries/other potato products, and ice cream/pops were associated with higher concentrations of multiple chemicals. Higher energy from minimally processed food was associated with lower concentrations of MCPP, MCNP, MCOP, and bisphenols A and F.
Ultra-processed food consumption may increase exposure to currently used phthalates. Additional research is needed to determine whether minimally processed food diets or changes in food production practices can reduce phthalate and bisphenol exposures and related health effects, particularly among children who are more vulnerable to toxicants and tend to consume more ultra-processed food than adults.
•Ultra-processed food is related to higher levels of phthalates but not bisphenols.•Minimally processed food is related to lower levels of phthalates and bisphenols A and F.•Magnitudes of some associations are stronger among children.•Chemical exposures may contribute to adverse health effects of ultra-processed food.
Viral infection during pregnancy has been correlated with increased frequency of autism spectrum disorder (ASD) in offspring. This observation has been modeled in rodents subjected to maternal immune ...activation (MIA). The immune cell populations critical in the MIA model have not been identified. Using both genetic mutants and blocking antibodies in mice, we show that retinoic acid receptor–related orphan nuclear receptor gamma t (RORγt)–dependent effector T lymphocytes for example, T helper 17 (TH17) cells and the effector cytokine interleukin-17a (IL-17a) are required in mothers for MIA-induced behavioral abnormalities in offspring. We find that MIA induces an abnormal cortical phenotype, which is also dependent on maternal IL-17a, in the fetal brain. Our data suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD-like phenotypes.
Maternal immune activation (MIA) contributes to behavioural abnormalities associated with neurodevelopmental disorders in both primate and rodent offspring. In humans, epidemiological studies suggest ...that exposure of fetuses to maternal inflammation increases the likelihood of developing autism spectrum disorder. In pregnant mice, interleukin-17a (IL-17a) produced by T helper 17 (T
17) cells (CD4
T helper effector cells involved in multiple inflammatory conditions) induces behavioural and cortical abnormalities in the offspring exposed to MIA. However, it is unclear whether other maternal factors are required to promote MIA-associated phenotypes. Moreover, the underlying mechanisms by which MIA leads to T cell activation with increased IL-17a in the maternal circulation are not well understood. Here we show that MIA phenotypes in offspring require maternal intestinal bacteria that promote T
17 cell differentiation. Pregnant mice that had been colonized with mouse commensal segmented filamentous bacteria or human commensal bacteria that induce intestinal T
17 cells were more likely to produce offspring with MIA-associated abnormalities. We also show that small intestine dendritic cells from pregnant, but not from non-pregnant, females secrete IL-1β, IL-23 and IL-6 and stimulate T cells to produce IL-17a upon exposure to MIA. Overall, our data suggest that defined gut commensal bacteria with a propensity to induce T
17 cells may increase the risk of neurodevelopmental disorders in the offspring of pregnant mothers undergoing immune system activation owing to infections or autoinflammatory syndromes.
This study aims to understand the difference in trauma patients' use of health services in Korea according to insurance type and the Injury Severity Score. Andersen's behavioral model of health ...service use is employed to identify the factors influencing their use. Claims data from January 1 to December 31, 2016 were extracted from both the Health Insurance Review and Assessment Service and the automobile insurance screening center for all the medical treatments identified with the Korean Triage and Acuity Scale and Injury Severity Score. Using the Health Insurance Review and Assessment Service's remote statistical analysis system, hierarchical regression and negative binomial analyses were conducted to determine the effect of predisposing, enabling, and need factors on health service use. The results demonstrate that the use of Korean health services is relatively equitable since medical expenses for trauma patients are greatly influenced by need factors. However, the length of time trauma patients stay in the hospital appears to differ according to insurance type. This study suggests that healthcare policies need to increase coverage benefits and improve medical billing for patients with severe trauma, as well as develop a more robust screening system for patients with mild to moderate impairments.
Trophoblasts, the principal cellular component of the placenta, play an important role in nutrient and gas exchange. Previous studies have indicated that maternal immune activation (MIA) leads to an ...elevation in IL-17A cytokine levels in maternal serum, subsequently influencing fetal brain development during pregnancy. In this study, we aimed to elucidate the impact of the IL-17A cytokine on placental function. First, we treated JAR and JEG-3, which is a placenta cell line, with IL-17A in a concentration-dependent or time-dependent manner and observed cell morphology and viability. It was confirmed that treatment with IL-17A or a double-stranded RNA mimic (PolyI:C) had no effect on the morphology or cell viability. IL-17A treatment increased the expression of IL-17R at the mRNA and protein levels, and Poly(I:C) increased the levels of IFNγ and TNFα. Additionally, PPARγ, known as a metabolism regulator, was increased by IL-17A treatment. Also, we observed that the expression of Glut1 and Glut3 was increased by IL-17A treatment. To confirm this, we examined the expression of transporters in the placental tissue of the MIA rodent model, and we observed that mRNA expression of glut1 and glut3 was significantly increased. However, the expression of Gltu1 and Glut3 was observed to be significantly inhibited in the brains of MIA-induced offspring. This study suggests that IL-17A increases signaling through IL-17R in the placenta and fetal brain tissue; however, there is a mechanism for regulating the expression of glucose transporters by increased IL-17A in the placenta.
The pathophysiological roles of astrocytes in the reactive state are thought to have important significance in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). ...However, the detailed mechanisms underlying the transition of astrocytes from the resting state to the reactive state during neurodegenerative disease largely remain to be defined. Here, we investigated the pathways involved in activating astrocytes from the resting state to the reactive state in primary cultured astrocytes treated with oligomeric Aβ and in the hippocampus of 5XFAD mice. Treatment with oligomeric Aβ induced an increase in reactive astrocytes, as assessed by the protein level of glial fibrillary acidic protein (GFAP) and this increase was caused by STAT3 phosphorylation in primary cultured astrocytes. The administration of Stattic, an inhibitor of STAT3, rescued the activation of astrocytes in primary cultured astrocytes and in the hippocampus of 6-month-old 5XFAD mice as well as impairments in learning and memory. Collectively, these results demonstrated that reactive astrocytes in the AD brain are induced via STAT3 and the impairments in learning and memory observed in 5XFAD mice are rescued by STAT3 inhibition, suggesting that the inhibition of STAT3 phosphorylation in astrocytes may be a novel therapeutic target for cognitive impairment in AD.
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