163 research outputs found
AlterG-Training1_APS_JAP_supplement_rev2.docx
No full textThis document serves as supplementary material to the manuscript titled "Cardiovascular and metabolic responses to exercise testing during lower-body positive pressure running" by Tim Brüssau*, Robert Oehring*, Stephan B. Felix, Marcus Dörr† and Martin Bahls† <br
Astonishing comics: a disability studies perspective on x-men comics
No full textDissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Comunicação e Expressão, Programa de Pós-Graduação em Letras/Inglês e Literatura Correspondente, Florianópolis, 2013Stan Lee co-created in 1963 the X-Men; comics characters who in consequence of developing super-powers at puberty due to natural genetic evolution suffer society?s prejudice. In their analysis of the X-Men Trilogy X-Men (Bryan Singer 2000); X2: X-Men United (Bryan Singer 2003); and X-Men: the Last Stand (Brett Ratner 2006); through a Disability Studies perspective Michael M. Chemers (2004), Ramona Ilea (2009), Martin Mantle (2007), and Jennifer Rinaldi (2008) argue that mutants can be understood as social characterizations of disability. This investigation studies whether this affirmation also holds true for mutants depicted in X-Men comics. I will analyze the comics storylines God Loves, Man Kills (Marvel Graphic Novel # 05) and Gifted (Astonishing X-Men # 01 - 06) ? on which X2: X-Men United and X-Men: the Last Stand were based respectively. Stan Lee foi o co-criador, em 1964, dos X-Men, personagens de histórias em quadrinhos os quais, em conseqüência de desenvolverem super-poderes na puberdade, são alvos do preconceito da sociedade. Ao analisar a Trilogia dos filmes dos X-Men - X-Men (Bryan Singer 2000); X2: X-Men United (Bryan Singer 2003); e X-Men: The Last Stand (Brett Ratner 2006); a partir de uma perspective de Estudos sobre Deficiência. Michael M. Chemers (2004), Ramona Ilea (2009), Martin Mantle (2007), e Jennifer Rinaldi (2008) argumentam que os mutantes podem ser compreendidos como caracterizações sociais de deficiência. Este estudo investiga se esta afirmação também é válida para os mutantes presentes nas histórias em quadrinhos dos X-Men. As linhas narrativas a serem analisadas são: God Loves, Man Kills (Marvel Graphic Novel 05) e Gifted (Astonishing X-Men # 01 - 06); nas quais foram baseados X2: X-Men United e X-Men: the Last Stand respectivamente
Association of Asymmetric and Symmetric Dimethylarginine with Inflammation in the Population-Based Study of Health in Pomerania
No full textThe amino acids arginine (Arg), asymmetric (ADMA) and symmetric dimethylarginine (SDMA) are related to nitric oxide (NO) metabolism and potential markers of two different disease entities: cardiovascular disease such as atherosclerosis and systemic inflammation in critically ill patients with sepsis. Although very different in their pathophysiological genesis, both entities involve the functional integrity of blood vessels. In this context, large population-based data associating NO metabolites with proinflammatory markers, e.g., white blood cell count (WBC), high-sensitivity C-reactive protein (hsCRP), and fibrinogen, or cytokines are sparse. We investigated the association of Arg, ADMA and SDMA with WBC, hsCRP, and fibrinogen in 3556 participants of the Study of Health in Pomerania (SHIP)-TREND study. Furthermore, in a subcohort of 456 subjects, 31 inflammatory markers and cytokines were analyzed. We identified Arg and SDMA to be positively associated with hsCRP (β coefficient 0.010, standard error (SE) 0.002 and 0.298, 0.137, respectively) as well as fibrinogen (β 5.23 × 10−3, SE 4.75 × 10−4 and 0.083, 0.031, respectively). ADMA was not associated with WBC, hsCRP, or fibrinogen. Furthermore, in the subcohort, Arg was inversely related to a proliferation-inducing ligand (APRIL). SDMA was positively associated with osteocalcin, tumor necrosis factor receptor 1 and 2, and soluble cluster of differentiation 30. Our findings provide new insights into the involvement of Arg, ADMA, and SDMA in subclinical inflammation in the general population
Exercise training to reduce cardiovascular risk in patients with metabolic syndrome and type 2 diabetes mellitus: How does it work?
No full textMetabolic syndrome (MetS) – a clustering of pathological conditions, including abdominal obesity, hypertension, dyslipidemia and hyperglycaemia – is closely associated with the development of type 2 diabetes mellitus (T2DM) and a high risk of cardiovascular disease.
A combination of multigenetic predisposition and lifestyle choices accounts for the varying inter-individual risk to develop MetS and T2DM, as well as for the individual amount of the increase in cardiovascular risk in those patients. A physically active lifestyle can offset about half of the genetically mediated cardiovascular risk. Yet, the extent to which standardized exercise programmes can reduce cardiovascular risk differs between patients. Exercise parameters, such as frequency, intensity, type and duration or number of repetitions, differentially target metabolic function, vascular health and physical fitness. In addition, exercise-induced molecular mechanisms are modulated by other patient-specific variables, such as age, diet and medication.
This review discusses the molecular and cellular mechanisms underlying the effects of exercise training on cardiovascular risk specifically in patients with MetS and T2DM.The author(s) disclosed receipt of the following financial support for the research, authorship and/or publication of this article: NK, MB and MD are supported by the German Centre for Cardiovascular Research (DZHK, partner sites Berlin (NK) and Greifswald (MB, MD)). EMVC is supported by the Fund for Scientific Research Flanders
Heterogeneous Metabolic Response to Exercise Training in Heart Failure with Preserved Ejection Fraction
No full textThe prevalence of heart failure with preserved ejection fraction (HFpEF) is constantly increasing and no evidence-based pharmacological treatment option is available. While exercise training (ET) improves diastolic function, its metabolic mechanisms in HFpEF are unclear. We assessed the metabolic response to 12 weeks of ET in patients with HFpEF by performing a post hoc analysis of the EX-DHF-P trial (ISRCTN42524037). Plasma concentrations of 188 endogenous metabolites were measured in 44 ET and 20 usual care (UC) patients at baseline and 3-months follow-up. Metabolic differences between ET and UC from baseline to follow-up were compared and differential responses to ET were examined by random forest feature selection. ET prevented the increase of acetylornithine and carnitine as well as the decrease of three glycerophospholipids. After ET, two opposite metabolic response clusters were identified. Cluster belonging was associated with perceived well-being at baseline and changes in low-density lipoprotein but not with cardiorespiratory, ventilatory or echocardiographic parameters. These two ET-induced metabolic response patterns illustrate the heterogeneity of the HFpEF patient population. Our results suggest that other biological parameters might be helpful besides clinical variables to improve HFpEF patient stratification. Whether this approach improves response prediction regarding ET and other treatments should be explored
Impact of COVID-19 on young healthcare professionals
No full textThe ongoing new coronavirus pandemic has impacted and continues to impact daily life and work worldwide. In this context, young health care professionals face a number of unique challenges: they are often at early and vulnerable stages of their clinical and scientific careers, they are frequently intensively involved in the care of patients with COVID-19, and they have yet to establish international networks within their fields of expertise. The European Association of Preventive Cardiology (EAPC) Young Community therefore performed a survey to assess the influence of the pandemic on the daily life and ambitions of early career clinicians and researchers in preventive cardiology. Between June and August 2021, an online survey with a total of 26 questions was distributed to individuals aged ≤40 years via ESC Communication channels. Questions comprised multiple-choice questions and statements with a Likert scale. Our primary aim was to assess the present career status as well as future career plans of young professionals in preventive cardiology, in the context of the coronavirus pandemic. The questions furthermore Graphical Abstract * Corresponding author.The authors would like to thank the study participants for taking the time to answer the survey
Influence of gene expression on the development and progression of atherosclerosis
No full textThis investigation aimed to compare gene expression differences between atheroresistant (brachial) and atherosusceptible (femoral) arteries in 13day old Rapacz HC swine, as well as identify gene expression associated with the initiation and progression of peripheral atherosclerosis in the same arteries of one and two year old Rapacz HC swine. Methods: A paired t-test was used to compare gene expression of healthy brachial and femoral arteries in the 13day old Rapacz HC swine. A 2x2 ANOVA was used to analyze the arteries from one and two year old Rapacz HC swine. Disease phenotype was quantified using Sudan IV, H/E, and VVG staining. Hypotheses: We hypothesized that gene expression differences between healthy brachial and femoral arteries in the 13day old Rapacz HC swine will contribute to the uneven atherosclerotic disease distribution later in the animal’s life. In addition, we hypothesized that gene expression differences will diverge in one and two year old animals due to an increase in disease in the femoral but no lesion formation in the brachial artery. Results: Healthy arteries from the 13day old Rapacz HC swine showed a total of 366 significantly different expressed probe sets between the atheroprotected and atherosusceptible artery. Analysis of these probe sets is the first evidence that gene expression differences could contribute to the uneven disease distribution later in life. A total of 184 probe sets were identified by the ANOVA as having a significant age*artery interaction. In addition BLAST identified that these probe sets are very similar to genes involved in known atherogenic pathways. Interestingly, contrary to our hypothesis the number of differently expressed genes decreased with increasing disease in the femoral artery
The effect of maternal exercise during pregnancy on offspring vascular function in swine
No full textMaternal behavior influences the intrauterine environment and programs lifelong atherosclerotic disease susceptibility in offspring. An increased atherosclerotic disease risk has previously been reported for adult progeny exposed to an adverse in utero environment. Very few studies have investigated whether positive maternal health behaviors during pregnancy reduce atherosclerotic disease risk in offspring. The purpose of this investigation was to test the hypothesis that maternal exercise during pregnancy improves endothelial function in offspring. Six months old swine were randomly assigned to an exercise (n = 7) or sedentary (n = 8) group throughout pregnancy. Exercise consisted of treadmill running for 20-45 min, five times per week, for all but the last week of gestation. Vascular reactivity was measured using dose-dependent endothelium-dependent (bradykinin (BK); 10-11 -10-6 M) and -independent (sodium nitroprusside (SNP); 10-10 - 10-4 M) vasorelaxation in femoral arteries from offspring at 3, 5, and 9 months of age using in vitro wire-myography. L-Name (300 μM) was used to block nitric oxide (NO) signaling in BK-induced relaxation. Quantitative PCR and Western blotting were used to assess transcript and protein abundance, respectively, of eNOS, GUCY1A2, GUCY1A3, GUCY1B3, PRKG1, MYPT1, PPP1R14A, and SERCA2. Exercise had no effect on BK relaxation with and without L-Name. A main effect on SNP relaxation (P \u3c 0.01) was observed. Furthermore, a significant age x treatment interaction for SNP (P \u3c 0.05) manifested by a reduced SNP relaxation response in offspring of exercised trained compared to sedentary swine at 3 (P \u3c 0.01), 5 (P \u3c 0.05), and 9 months (P \u3c 0.05) of age was identified. A significant main effect was observed for PPP14R1 (P \u3c 0.05) and differential regulation of its protein product CPI-17. Contrary to our hypothesis, exercise during pregnancy does not alter BK-induced endothelial function via NO signaling. However, programming of NO-induced cGMP-dependent vascular smooth relaxation may contribute to a reduced vasorelaxation response in offspring from exercise trained compared to sedentary swine
Towards a personalised approach in exercise-based cardiovascular rehabilitation: How can translational research help? A ‘call to action’ from the Section on Secondary Prevention and Cardiac Rehabilitation of the European Association of Preventive Cardiology
No full textThe benefit of regular physical activity and exercise training for the prevention of cardiovascular and metabolic diseases is undisputed. Many molecular mechanisms mediating exercise effects have been deciphered. Personalised exercise prescription can help patients in achieving their individual greatest benefit from an exercise-based cardiovascular rehabilitation programme. Yet, we still struggle to provide truly personalised exercise prescriptions to our patients. In this position paper, we address novel basic and translational research concepts that can help us understand the principles underlying the inter-individual differences in the response to exercise, and identify early on who would most likely benefit from which exercise intervention. This includes hereditary, non-hereditary and sex-specific concepts. Recent insights have helped us to take on a more holistic view, integrating exercise-mediated molecular mechanisms with those influenced by metabolism and immunity. Unfortunately, while the outline is recognisable, many details are still lacking to turn the understanding of a concept into a roadmap ready to be used in clinical routine. This position paper therefore also investigates perspectives on how the advent of ‘big data’ and the use of animal models could help unravel inter-individual responses to exercise parameters and thus influence hypothesis-building for translational research in exercise-based cardiovascular rehabilitation
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