Tech United Eindhoven RoboCup adult size humanoid team description 2012

This document presents the 2012 Tech United Eindhoven adult size humanoid robot team from The Netherlands. The team contributes the adult-size humanoid robot TUlip. Here we present the mechanical design and kinematic structure of the robot. We introduce the walking gait and contribute a controller structure including gravity compensation. Finally, we describe the vision system, self localization and world model, which are used for the attacker and defender strategy in the humanoid robot soccer game

Acute-Phase-HDL Remodeling by Heparan Sulfate Generates a Novel Lipoprotein with Exceptional Cholesterol Efflux Activity from Macrophages

During episodes of acute-inflammation high-density lipoproteins (HDL), the carrier of so-called good cholesterol, experiences a major change in apolipoprotein composition and becomes acute-phase HDL (AP-HDL). This altered, but physiologically important, HDL has an increased binding affinity for macrophages that is dependent on cell surface heparan sulfate (HS). While exploring the properties of AP-HDL∶HS interactions we discovered that HS caused significant remodeling of AP-HDL. The physical nature of this change in structure and its potential importance for cholesterol efflux from cholesterol-loaded macrophages was therefore investigated. In the presence of heparin, or HS, AP-HDL solutions at pH 5.2 became turbid within minutes. Analysis by centrifugation and gel electrophoresis indicated that AP-HDL was remodeled generating novel lipid poor particles composed only of apolipoprotein AI, which we designate β2. This remodeling is dependent on pH, glycosaminoglycan type, is promoted by Ca2+ and is independent of protease or lipase activity. Compared to HDL and AP-HDL, remodeled AP-HDL (S-HDL-SAA), containing β2 particles, demonstrated a 3-fold greater cholesterol efflux activity from cholesterol-loaded macrophage. Because the identified conditions causing this change in AP-HDL structure and function can exist physiologically at the surface of the macrophage, or in its endosomes, we postulate that AP-HDL contains latent functionalities that become apparent and active when it associates with macrophage cell surface/endosomal HS. In this way initial steps in the reverse cholesterol transport pathway are focused at sites of injury to mobilize cholesterol from macrophages that are actively participating in the phagocytosis of damaged membranes rich in cholesterol. The mechanism may also be of relevance to aspects of atherogenesis

RAS gene polymorphisms, classical risk factors and the advent of coronary artery disease in the Portuguese population

<p>Abstract</p> <p>Background</p> <p>Several polymorphisms within the renin-angiotensin system cluster of genes have been associated with the advent of coronary artery disease (CAD) or related pathologies. We investigated the distribution of 5 of these polymorphisms in order to find any association with CAD development and distinguish if any of the biochemical and behavioural factors interact with genetic polymorphisms in the advent of the disease.</p> <p>Methods</p> <p><it>ACE </it>I/D (rs4340), <it>ACE </it>A11860G (rs4343), <it>AT1R </it>A1166C (rs5186), <it>AGT </it>T174M (rs4762) and <it>AGT </it>M235T (rs699) gene polymorphisms were PCR-RFLP analysed in 298 CAD patients and 510 controls from Portugal. Several biochemical and behavioural markers were obtained.</p> <p>Results</p> <p><it>ACE </it>I/D DD and <it>ACE</it>11860 GG genotypes are risk factors for CAD in this population. The simultaneous presence of <it>ACE </it>I/D I and <it>ACE</it>11860 A alleles corresponds to a significant trend towards a decrease in CAD incidence. We found several synergistic effects between the studied polymorphisms and classical risk factors such as hypertension, obesity, diabetes and dyslipidaemia: the presence of the DD genotype of <it>ACE </it>I/D (and also <it>ACE</it>11860 GG) increases the odds of developing CAD when associated to each one of these classical risk factors, particularly when considering the male and early onset CAD subgroup analysis; <it>AGT</it>235 TT also increases the CAD risk in the presence of hypertension and dyslipidaemia, and <it>AT1R</it>1166 interacts positively with hypertension, smoking and obesity.</p> <p>Conclusion</p> <p><it>ACE </it>polymorphisms were shown to play a major role in individual susceptibility to develop CAD. There is also a clear interaction between RAS predisposing genes and some biochemical/environmental risk factors in CAD onset, demonstrating a significant enhancement of classical markers particularly by <it>ACE </it>I/D and <it>ACE</it>11860.</p

Transient expression of M-cell phenotype by enterocyte-like cells of the follicle-associated epithelium of mouse Peyer's patches

BACKGROUND &amp; AIMS: The follicle-associated epithelium (FAE) over mucosa-associated lymphoid tissues consists of distinct enterocytes and M cells concentrated at its periphery. The basement membrane composition was analyzed to test whether differences account for the distinct differentiation programs along the crypt-villus and crypt-FAE axes. To determine whether the decreased number of M cells in the FAE apex is caused by premature extrusion, we mapped the site where they undergo apoptosis. METHODS: The FAE basal lamina of Peyer's patches from BALB/c mice was analyzed by immunochemistry. M cells were identified using the Ulex europaeus agglutinin lectin. The cell proliferation and apoptotic compartments were characterized using bromodeoxyuridine incorporation and the TUNEL assay. RESULTS: The perlecan and laminin 2 stainings were different in FAE and villi. Myofibroblasts were absent beneath the FAE. The migration kinetics of cells along the FAE was similar to that along the villi. Apoptotic cells were detected exclusively at the apex of the FAE. CONCLUSIONS: FAE and M-cell differentiation is associated with a distinct basal lamina composition. FAE enterocytes express transient M-cell features as they move from the crypts toward the apoptotic compartment. M cells have a highly plastic phenotype that raises interesting questions about the control of intestinal epithelial cell differentiation