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Diurnal cortisol slopes and blood pressure were not significantly improved. Conclusion The MB yoga intervention had a statistically significant effect on the health and well-being of nurses and HCPs, most specifically for measures of stress; perceived stress, burnout, vitality, sleep quality, serenity, and mindfulness.Introduction Communication skills training for people with traumatic brain injury (TBI) and their carers is recommended best practice. Delivery via telehealth could improve access to this training. This paper focuses on the acceptability of telehealth delivery of communication skills training. Methods A mixed-methods investigation of acceptability of telehealth to people with TBI and their carers was incorporated into a clinical trial. Thirty-six people with TBI (23 metropolitan and 13 regional) and their carers were recruited. Metropolitan participants were randomly allocated to telehealth or in-person intervention at a 13 ratio. Regional participants were allocated to telehealth. Telehealth and in-person participants were compared on retention, time to complete the programme, home practice completion and therapeutic alliance ratings. Participants completed semi-structured interviews regarding their views on telehealth, which were analysed using thematic analysis. Results There were no significant differences between telehealth and in-person participants in retention rate, time to complete the programme, degree of home practice completion or therapeutic alliance ratings. Three themes were identified 'telehealth delivery opens a window for access to rehabilitation in the context of my daily life', 'in-person delivery offers rehabilitation based on natural human interaction' and 'weighing telehealth against in-person delivery'. Discussion Participants found telehealth delivery acceptable, as indicated by the similarity between groups in the quantitative process measures, and as reported in interviews. Some reported a preference for in-person delivery if there had been a choice of delivery mode. Participants described characteristics of the two delivery modes which were relevant to their attitudes towards telehealth.Purpose The goal of the current study is to analyze the substance use trends in Generation Z youth (in both middle and high school environments) and to determine if any correlation exists between substance use behaviors and demographic variables. Methods Analysis is based on substance use data collected through the Pennsylvania Youth Survey (PAYS) from 2009 to 2017 and the 2016 US census data. Results Our results suggest that substance use in Gen Z adolescents is mainly linked to alcohol, marijuana, cigarettes, smokeless tobacco, vaping, and narcotic prescription drugs. Alcohol is the most prevalent high-risk substance used by 12th grade students with 69.8% of students having consumed alcohol over their lifetime. Vaping is the next highly used substance with 28.9% of students in 12th grade having vaped 30 day prior to the survey. Lorlatinib There is a significant correlation among adolescents between smoking cigarettes and using smokeless tobacco. A student using either alcohol, cigarettes or smokeless tobacco is highly likely to use the other two substances as well. Adolescents from counties with a high Caucasian population were at high risk for cigarette and smokeless tobacco use, while the opposite held true for counties with a high number of foreign-born persons or higher Asian or Hispanic populations. Higher median household incomes and higher adult education levels in a county were both protective factors against smokeless tobacco use. Conclusions Results of the study suggest that students start experimenting with high-risk substance use in early grades and to combat the prevalence, we suggest the importance of educating adolescents of the dangers of drug use in early grades.Objective Vascular calcification is a cardiovascular risk factor and accelerated in diabetes mellitus. Previous work has established a role for calcification-prone extracellular vesicles in promoting vascular calcification. However, the mechanisms by which diabetes mellitus provokes cardiovascular events remain incompletely understood. Our goal was to identify that increased S100A9 promotes the release of calcification-prone extracellular vesicles from human macrophages in diabetes mellitus. Approach and Results Human primary macrophages exposed to high glucose (25 mmol/L) increased S100A9 secretion and the expression of receptor for advanced glycation end products (RAGE) protein. Recombinant S100A9 induced the expression of proinflammatory and osteogenic factors, as well as the number of extracellular vesicles with high calcific potential (alkaline phosphatase activity, P less then 0.001) in macrophages. Treatment with a RAGE antagonist or silencing with S100A9 siRNA in macrophages abolished these responses,tion of microcalcification within plaques.Objective Arteriovenous fistulae (AVF) are the optimal conduit for hemodialysis access but have high rates of primary maturation failure. Successful AVF maturation requires wall thickening with deposition of ECM (extracellular matrix) including collagen and fibronectin, as well as lumen dilation. TAK1 (TGFβ [transforming growth factor-beta]-activated kinase 1) is a mediator of noncanonical TGFβ signaling and plays crucial roles in regulation of ECM production and deposition; therefore, we hypothesized that TAK1 regulates wall thickening and lumen dilation during AVF maturation. Approach and Results In both human and mouse AVF, immunoreactivity of TAK1, JNK (c-Jun N-terminal kinase), p38, collagen 1, and fibronectin was significantly increased compared with control veins. Manipulation of TAK1 in vivo altered AVF wall thickening and luminal diameter; reduced TAK1 function was associated with reduced thickness and smaller diameter, whereas activation of TAK1 function was associated with increased thickness and larger diameter. Arterial magnitudes of laminar shear stress (20 dyne/cm2) activated noncanonical TGFβ signaling including TAK1 phosphorylation in mouse endothelial cells. Conclusions TAK1 is increased in AVF, and TAK1 manipulation in a mouse AVF model regulates AVF thickness and diameter. Targeting noncanonical TGFβ signaling such as TAK1 might be a novel therapeutic approach to improve AVF maturation.Objective Metabolic dysregulation and inflammation are important consequences of obesity and impact susceptibility to cardiovascular disease. Anti-inflammatory therapy in cardiovascular disease is being developed under the assumption that inflammatory pathways are identical in women and men, but it is not known if this is indeed the case. In this study, we assessed the sex-specific relation between inflammation and metabolic dysregulation in obesity. Approach and Results Three hundred two individuals were included, half with a BMI 27 to 30 kg/m2 and half with a BMI>30 kg/m2, 45% were women. The presence of metabolic syndrome was assessed according to the National Cholesterol Education Program-ATPIII criteria, and inflammation was studied using circulating markers of inflammation, cell counts, and ex vivo cytokine production capacity of isolated immune cells. Additionally, lipidomic and metabolomic data were gathered, and subcutaneous fat biopsies were histologically assessed. Metabolic syndrome is associated with an increased inflammatory profile that profoundly differs between women and men women with metabolic syndrome show a lower concentration of the anti-inflammatory adiponectin, whereas men show increased levels of several pro-inflammatory markers such as IL (interleukin)-6 and leptin. Adipose tissue inflammation showed similar sex-specific associations with these markers. Peripheral blood mononuclear cells isolated from men, but not women, with metabolic syndrome display enhanced cytokine production capacity. Conclusions We identified sex-specific pathways that influence inflammation in obesity. Excessive production of proinflammatory cytokines was observed in men with metabolic syndrome. In contrast, women typically showed reduced levels of the anti-inflammatory adipokine adiponectin. These different mechanisms of inflammatory dysregulation between women and men with obesity argue for sex-specific therapeutic strategies.Objective The pathophysiology of hypertension remains incompletely understood. We investigated associations of circulating metabolites with longitudinal blood pressure (BP) changes in the Prospective Investigation of the Vasculature in Uppsala Seniors cohort and validated the findings in the Uppsala Longitudinal Study of Adult Men cohort. Approach and Results Circulating metabolite levels were assessed with liquid- and gas-chromatography coupled to mass spectrometry among persons without BP-lowering medication at baseline. We studied associations of baseline levels of metabolites with changes in BP levels and the clinical BP stage between baseline and a follow-up examination 5 years later. In the discovery cohort, we investigated 504 individuals that contributed with 757 observations of paired BP measurements. The mean baseline systolic and diastolic BPs were 144 (19.7)/76 (9.7) mm Hg, and change in systolic and diastolic BPs were 3.7 (15.8)/-0.5 (8.6) mm Hg over 5 years. The metabolites associated with diastolic BP change were ceramide, triacylglycerol, total glycerolipids, oleic acid, and cholesterylester. No associations with longitudinal changes in systolic BP or BP stage were observed. Metabolites with similar structures to the 5 top findings in the discovery cohort were investigated in the validation cohort. Diacylglycerol (362) and monoacylglycerol (180), 2 glycerolipids, were associated with diastolic BP change in the validation cohort. Conclusions Circulating baseline levels of ceramide, triacylglycerol, total glycerolipids, and oleic acid were positively associated with longitudinal diastolic BP change, whereas cholesterylester levels were inversely associated with longitudinal diastolic BP change. Two glycerolipids were validated in an independent cohort. These metabolites may point towards pathophysiological pathways of hypertension.Objective The aim of this study was to investigate if there is a causal relationship between circulating levels of TIM-1 (T-cell immunoglobulin and mucin domain 1) and incidence of stroke. Approach and Results Plasma TIM-1 was analyzed in 4591 subjects (40% men; mean age, 57.5 years) attending the Malmö Diet and Cancer Study. Incidence of stroke was studied in relation to TIM-1 levels during a mean of 19.5 years follow-up. Genetic variants associated with TIM-1 (pQTLs [protein quantitative trait loci]) were examined, and a 2-sample Mendelian randomization analysis was performed to explore the role of TIM-1 in stroke using summary statistics from our pQTLs and the MEGASTROKE consortium. A total of 416 stroke events occurred during follow-up, of which 338 were ischemic strokes. After risk factor adjustment, TIM-1 was associated with increased incidence of all-cause stroke (hazards ratio for third versus first tertile, 1.44 [95% CI, 1.10-1.87]; P for trend, 0.004), and ischemic stroke (hazards ratio, 1.42 [95% CI, 1.06-1.90]; P for trend, 0.011). Nineteen independent lead SNPs, located in three genomic risk loci showed significant associations with TIM-1 (P less then 5×10-8). A 2-sample Mendelian Randomization analysis suggested a causal effect of TIM-1 on stroke (β=0.083, P=0.0004) and ischemic stroke (β=0.102, P=7.7×10-5). Conclusions Plasma level of TIM-1 is associated with incidence of stroke. The genetic analyses suggest that this could be a causal relationship.
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