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ABSTRACT: Background: The prevalence of allergic respiratory disease tends to increase in populations that adopt the so-called Westernized lifestyle. We investigated the association between atopy and several possible lifestyle-related factors in seven Danish population-based studies. Methods: A total of 20048 persons participated in the seven studies. We used logistic regression to analyse the associations between possible determinants and atopy defined as serum specific IgE or skin prick test positivity against inhalant allergens. Associations were expressed as odds ratios (ORs) with 95% confidence intervals (95% CIs). In addition, individual participant data meta-analyses were performed. Results: Atopy was significantly associated with younger age (OR per 1 year increase in age: 0.97; 95% CI: 0.97, 0.98); male sex (OR for males versus females: 1.34; 95% CI: 1.24, 1.45), heavy drinking (OR for heavy drinkers versus light drinkers: 1.15; 95% CI: 1.04, 1.27), never smoking (OR for current versus never smokers: 0.73; 95% CI: 0.67, 0.80), and higher educational level (OR for educated versus uneducated: 1.27; 95% CI: 1.15, 1.41). Atopy was not associated with blood pressure, serum total cholesterol, physical activity or body mass except in women only, where we found a positive association (OR for obese vs. normal weight: 1.18; 95% CI: 1.00, 1.39) with ptrend = 0.032. Conclusions: Of interest for preventive purposes, we found that atopy was associated with some of the reversible lifestyle-related factors that characterize a Westernized lifestyle.PLoS ONE 09/2015; 10(9):e0137406. DOI:10.1371/journal.pone.0137406
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ABSTRACT: Anti-CD52 therapy has been shown to be effective in the treatment of a number of B cell malignancies, hematopoietic disorders and autoimmune diseases (including rheumatoid arthritis and multiple sclerosis); however the current standard of treatment, the humanized monoclonal antibody alemtuzumab, is associated with the development of anti-drug anti-bodies in a high proportion of patients. In order to address this problem, we have identified a novel murine anti-CD52 antibody which has been humanized using a process that avoids the inclusion within the variable domains of non-human germline MHC class II binding pep-tides and known CD4+ T cell epitopes, thus reducing its potential for immunogenicity in the clinic. The resultant humanized antibody, ANT1034, was shown to have superior binding to CD52 expressing cells than alemtuzumab and was more effective at directing both antibody dependent and complement dependent cell cytotoxicity. Furthermore, when in the presence of a cross-linking antibody, ANT1034 was more effective at directly inducing apoptosis than alemtuzumab. ANT1034 also showed superior activity in a SCID mouse/human CD52 tumour xenograft model where a single 1 mg/Kg dose of ANT1034 led to increased mouse survival compared to a 10 mg/Kg dose of alemtuzumab. Finally, ANT1034 was compared to alemtuzumab in in vitro T cell assays in order to evaluate its potential to stimulate proliferation of T cells in peripheral blood mononuclear cells derived from a panel of human donors: whereas alemtuzumab stimulated proliferation in a high proportion of the donor cohort, ANT1034 did not stimulate proliferation in any of the donors. Therefore we have developed a candidate therapeutic humanized antibody, ANT1034, that may have the potential to be more efficacious and less immunogenic than the current standard anti-CD52 therapy.PLoS ONE 09/2015; 10(9). DOI:10.1371/journal.pone.0138123
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ABSTRACT: Atherosclerosis is a progressive disease characterized by inflammation, monocyte-macrophage migration, and lipid accumulation in the vascular wall. Atherosclerosis is initially characterized by endothelial dysfunction, which favors lipid and cell elements crossing inside blood vessel wall. In this study we investigated our three-dimensional computer model of plaque formation and development which we tested on experimental results obtained from rabbits and clinical study on human carotid and coronary arteries. Firstly, a model of plaque formation in the rabbit animal LDL transport model within simple experimental design is simulated numerically using animal data and histological recordings. Then some human patient data from carotid and coronary artery were used. The 3D blood flow is described by the Navier-Stokes equations, together with the continuity equation. Mass transfer within the blood lumen and through the arterial wall is coupled with the blood flow, and is modeled by a convection-diffusion equation. The LDL transports in lumen of the vessel and through the vessel tissue (which has a mass consumption term) are coupled by Kedem-Katchalsky equations. The inflammatory process is modeled using three additional reaction-diffusion partial differential equations. A full three-dimensional model was created. It includes blood flow and LDL concentration, as well as plaque formation and progression. From patient human carotid artery data we matched plaque volume progression using two and three time points for baseline, three and twelve months follow up. Also a group of patients with coronary artery disease (CAD) and intermediate lesions was evaluated by Computed Tomography Angiography (CTA), together with an innovative approach to simulate the WSS-related low density lipoprotein (LDL) transport across the endothelium and to identify LDL accumulation sites. The novelty of this work lies in the systematic verification of prediction of plaque progression by repeated CTA, six months after the baseline evaluation, and by patient-specific determinations of boundary conditions, including coronary vasodilating capability, known to affect local flow conditions. Our results for plaque localization correspond to low shear stress zone and we fitted parameters from our model using nonlinear least square method. Understanding and prediction of the evolution of N. Filipovic et al.: ARTREAT project: computer, experimental and clinical analysis of three-dimensional plaque… 130 atherosclerotic plaques either into vulnerable or stable plaques are major tasks for the medical community.
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