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Sievi N.A.,University of Zurich | Senn O.,University of Zurich | Brack T.,Cantonal Hospital of Glarus | Brutsche M.H.,Cantonal Hospital of St. Gallen | And 7 more authors.
Respirology | Year: 2015

Background and objective Both comorbidities and physical inactivity have been shown to impair quality of life and contribute to hospital admissions and mortality in chronic obstructive pulmonary disease (COPD) patients. We hypothesized that the comorbid status predicts the level of daily physical activity (PA) in COPD. Methods In 228 patients with COPD (76% men; median (quartiles) age: 64 (59/69) years; percentage of predicted forced expiratory volume in 1 s (FEV1% pred): 44 (31/63)), comorbidities were assessed by medical history, clinical interviews, examination and blood analysis. PA level (PAL) was measured by an activity monitor (SenseWear Pro, Bodymedia Inc., Pittsburgh, PA, USA). The association between PAL and comorbidities was investigated by univariate and multivariate regression analysis. Results Seventy-nine per cent of the COPD patients had at least one additional chronic comorbidity, 56% had two or more comorbidities and 35% had three or more comorbidities. In univariate analysis body mass index, the number of pack years and having at least one additional comorbidity was negatively associated with PAL while there was a positive nonlinear association between FEV1 and PAL. The presence of at least one additional comorbidity was independently associated with PAL irrespective of airflow limitation. Conclusions In this cohort, almost 80% of COPD patients had at least one additional chronic comorbidity. The level of daily PA seems to be significantly impaired by the presence of comorbidities irrespective of the type of comorbidity and independent of the degree of airflow limitation. copy; 2015 Asian Pacific Society of Respirology. Source


Malan N.T.,North West University South Africa | Smith W.,North West University South Africa | von Kanel R.,Clinic Barmelweid | Hamer M.,University College London | And 2 more authors.
VASA. Zeitschrift für Gefässkrankheiten | Year: 2015

BACKGROUND: Low levels of testosterone in men and changes in retinal microvascular calibre are both associated with hypertension and cardiovascular disease risk. Sex hormones are also associated with blood flow in microvascular beds which might be a key intermediate mechanism in the development of hypertension. Whether a direct association between endogenous testosterone and retinal microvascular calibre exists is currently unknown. We aimed to determine whether testosterone is independently associated with ocular perfusion via a possible association with retinal vascular calibre or whether it plays only a secondary role via its effect on blood pressure in a bi-ethnic male cohort.PROBANDS AND METHODS: A total of 72 black and 81 white men (28-68 years of age) from the follow-up phase of the Sympathetic activity and Ambulatory Blood Pressure in Africans (SABPA) study were included in this sub-study. Ambulatory pulse pressure and intraocular perfusion pressures were obtained, while metabolic variables and testosterone were measured from fasting venous blood samples. Retinal vascular calibre was quantified from digital photographs using standardised protocols.RESULTS: The black men revealed a poorer cardiometabolic profile and higher pulsatile pressure (>50 mm Hg), intraocular pressure and diastolic ocular perfusion pressure than the white men (p≤0.05). Only in the white men was free testosterone positively associated with retinal calibre, i.e. arterio-venular ratio and central retinal arterial calibre and inversely with central retinal venular calibre. These associations were not found in the black men, independent of whether pulse pressure and ocular perfusion pressure were part of the model.CONCLUSIONS: These results suggest an independent, protective effect of testosterone on the retinal vasculature where an apparent vasodilatory response in the retinal resistance microvessels was observed in white men. Source


Kuebler U.,University of Zurich | Zuccarella-Hackl C.,University of Bern | Arpagaus A.,University of Zurich | Wolf J.M.,Brandeis University | And 6 more authors.
Brain, Behavior, and Immunity | Year: 2015

Acute psychosocial stress stimulates transient increases in circulating pro-inflammatory plasma cytokines, but little is known about stress effects on anti-inflammatory cytokines or underlying mechanisms. We investigated the stress kinetics and interrelations of pro- and anti-inflammatory measures on the transcriptional and protein level. Forty-five healthy men were randomly assigned to either a stress or control group. While the stress group underwent an acute psychosocial stress task, the second group participated in a non-stress control condition. We repeatedly measured before and up to 120. min after stress DNA binding activity of the pro-inflammatory transcription factor NF-κB (NF-κB-BA) in peripheral blood mononuclear cells, whole-blood mRNA levels of NF-κB, its inhibitor IκBα, and of the pro-inflammatory cytokines interleukin (IL)-1ß and IL-6, and the anti-inflammatory cytokine IL-10. We also repeatedly measured plasma levels of IL-1ß, IL-6, and IL-10.Compared to non-stress, acute stress induced significant and rapid increases in NF-κB-BA and delayed increases in plasma IL-6 and mRNA of IL-1ß, IL-6, and IκBα (p's < .045). In the stress group, significant increases over time were also observed for NF-κB mRNA and plasma IL-1ß and IL-10 (p's < .055). NF-κB-BA correlated significantly with mRNA of IL-1β (r = .52, p = .002), NF-κB (r = .48, p = .004), and IκBα (r = .42, p = .013), and marginally with IL-6 mRNA (r = .31, p = .11). Plasma cytokines did not relate to NF-κB-BA or mRNA levels of the respective cytokines.Our data suggest that stress induces increases in NF-κB-BA that relate to subsequent mRNA expression of pro-inflammatory, but not anti-inflammatory cytokines, and of regulatory-cytoplasmic-proteins. The stress-induced increases in plasma cytokines do not seem to derive from de novo synthesis in circulating blood cells. © 2014 Elsevier Inc. Source


Scheepers J.D.W.,North West University South Africa | Malan L.,North West University South Africa | De Kock A.,North West University South Africa | Malan N.T.,North West University South Africa | And 2 more authors.
Physiology and Behavior | Year: 2015

Objectives: Defensive coping (DefS) in Blacks has been associated with greater cardiovascular risk than in their White counterparts. We examined associations between endothelial function mental stress responses and markers of vascular structure in a bi-ethnic cohort. Methods: We examined vascular function and structure in 368 Black (43.84. ±. 8.31. years) and White Africans (44.78. ±. 10.90. years). Fasting blood samples, 24. h blood pressure, left carotid intima-media thickness of the far wall (L-CIMTf), and left carotid cross-sectional wall area (L-CSWA) values were obtained. von Willebrand factor (VWF), endothelin-1 (ET-1) and nitric oxide metabolite (NOx) responses to the Stroop mental stress test were calculated to assess endothelial function. DefS was assessed using the Coping Strategy Indicator questionnaire. Interaction between main effects was demonstrated for 283 participants with DefS scores above the mean of 26 for L-CIMTf. Results: Blunted stress responses for VWF (men 16.71% vs. 51.10%; women 0.85% vs. 42.09%, respectively) and NOx (men -64.52% vs. 74.89%; women -76.16% vs. 113.29%, respectively) were evident in the DefS Blacks compared to the DefS Whites (p<0.001). ET-1 increased more in Blacks (men 150% and women 227%, p<0.001) compared to the Whites (men 61.25% and women 35.49%, p<0.001). Ambulatory pulse pressure, but not endothelial function markers, contributed to L-CIMTf (δR2=0.11 p<0.001), and L-CSWA (δR2=0.08, p<0.001) in DefS African men but not in any other group. Conclusions: Blunted stress-induced NOx and VWF responses and augmented ET-1 responses in DefS Blacks indicate endothelial dysfunction. DefS may facilitate disturbed endothelial responses and enforce vascular remodelling via compensatory increases in pulse pressure in Black men. These observations may indicate an increased risk of cardiovascular incidents via functional and structural changes of the vasculature in DefS Blacks. © 2015 Elsevier Inc. Source


Mensen A.,Clinic Barmelweid | Poryazova R.,University of Zurich | Schwartz S.,University of Geneva | Khatami R.,Clinic Barmelweid
PLoS ONE | Year: 2014

Humor processing involves distinct processing stages including incongruity detection, emotional response, and engagement of mesolimbic reward regions. Dysfunctional reward processing and clinical symptoms in response to humor have been previously described in both hypocretin deficient narcolepsy-cataplexy (NC) and in idiopathic Parkinson disease (PD). For NC patients, humor is the strongest trigger for cataplexy, a transient loss of muscle tone, whereas dopamine-deficient PD-patients show blunted emotional responses to humor. To better understand the role of reward system and the various contributions of hypocretinergic and dopaminergic mechanisms to different stages of humor processing we examined the electrophysiological response to humorous and neutral pictures when given as reward feedback in PD, NC and healthy controls. Humor compared to neutral feedback demonstrated modulation of early ERP amplitudes likely corresponding to visual processing stages, with no group differences. At 270 ms post-feedback, conditions showed topographical and amplitudinal differences for frontal and left posterior electrodes, in that humor feedback was absent in PD patients but increased in NC patients. We suggest that this effect relates to a relatively early affective response, reminiscent of increased amygdala response reported in NC patients. Later ERP differences, corresponding to the late positive potential, revealed a lack of sustained activation in PD, likely due to altered dopamine regulation in reward structures in these patients. This research provides new insights into the temporal dynamics and underlying mechanisms of humor detection and appreciation in health and disease. © 2014 Mensen et al. Source

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