University of Antwerp

About: University of Antwerp is a education organization based out in Antwerp, Belgium. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 16682 authors who have published 48837 publications receiving 1689748 citations. The organization is also known as: Universiteit Antwerpen & UAntwerp.

To NET or not to NET:current opinions and state of the science regarding the formation of neutrophil extracellular traps

Abstract: Since the discovery and definition of neutrophil extracellular traps (NETs) 14 years ago, numerous characteristics and physiological functions of NETs have been uncovered. Nowadays, the field continues to expand and novel mechanisms that orchestrate formation of NETs, their previously unknown properties, and novel implications in disease continue to emerge. The abundance of available data has also led to some confusion in the NET research community due to contradictory results and divergent scientific concepts, such as pro- and anti-inflammatory roles in pathologic conditions, demarcation from other forms of cell death, or the origin of the DNA that forms the NET scaffold. Here, we present prevailing concepts and state of the science in NET-related research and elaborate on open questions and areas of dispute.

Galaxies–intergalactic medium interaction calculation – I. Galaxy formation as a function of large-scale environment

Abstract: [Abridged] We present the first results of hydrodynamical simulations that follow the formation of galaxies to z=0 in spherical regions of radius ~20 Mpc/h drawn from the Millennium Simulation. The regions have overdensities that deviate by (-2, -1, 0, +1, +2)sigma from the cosmic mean, where sigma is the rms mass fluctuation on a scale of ~20Mpc/h at z=1.5. The simulations have mass resolution of up to 10^6 Msun/h, cover the entire range of large-scale environments and allow extrapolation of statistics to the entire 500 (Mpc/h)^3 Millennium volume. They include gas cooling, photoheating from an ionising background, SNe feedback and winds, but no AGN. We find that the specific SFR density at z <~ 10 varies systematically from region to region by up to an order of magnitude, but the global value, averaged over all volumes, reproduces observational data. Massive, compact galaxies, similar to those observed in the GOODS fields, form in the overdense regions as early as z=6, but do not appear in the underdense regions until z~3. These environmental variations are not caused by a dependence of the star formation properties on environment, but rather by a strong variation of the halo mass function from one environment to another, with more massive haloes forming preferentially in the denser regions. At all epochs, stars form most efficiently in haloes of circular velocity ~ 250 km/s. However, the star formation history exhibits a form of "downsizing" (even in the absence of AGN): the stars comprising massive galaxies at z=0 have mostly formed by z=1-2, whilst those comprising smaller galaxies typically form at later times. However, additional feedback is required to limit star formation in massive galaxies at late times.

Measurement and QCD analysis of the diffractive deep-inelastic scattering cross-section at HERA

Abstract: A detailed analysis is presented of the diffractive deep-inelastic scattering process $ep\to eXY$, where $Y$ is a proton or a low mass proton excitation carrying a fraction $1 - \xpom > 0.95$ of the incident proton longitudinal momentum and the squared four-momentum transfer at the proton vertex satisfies $|t|<1 {\rm GeV^2}$. Using data taken by the H1 experiment, the cross section is measured for photon virtualities in the range $3.5 \leq Q^2 \leq 1600 \rm GeV^2$, triple differentially in $\xpom$, $Q^2$ and $\beta = x / \xpom$, where $x$ is the Bjorken scaling variable. At low $\xpom$, the data are consistent with a factorisable $\xpom$ dependence, which can be described by the exchange of an effective pomeron trajectory with intercept $\alphapom(0)= 1.118 \pm 0.008 {\rm (exp.)} ^{+0.029}_{-0.010} {\rm (model)}$. Diffractive parton distribution functions and their uncertainties are determined from a next-to-leading order DGLAP QCD analysis of the $Q^2$ and $\beta$ dependences of the cross section. The resulting gluon distribution carries an integrated fraction of around 70% of the exchanged momentum in the $Q^2$ range studied. Total and differential cross sections are also measured for the diffractive charged current process $e^+ p \to \bar{ u}_e XY$ and are found to be well described by predictions based on the diffractive parton distributions. The ratio of the diffractive to the inclusive neutral current $ep$ cross sections is studied. Over most of the kinematic range, this ratio shows no significant dependence on $Q^2$ at fixed $\xpom$ and $x$ or on $x$ at fixed $Q^2$ and $\beta$.

Phagocytosis in atherosclerosis: Molecular mechanisms and implications for plaque progression and stability

Abstract: Macrophages play a key role in atherosclerotic plaque destabilization and rupture. In this light, selective removal of macrophages may be beneficial for plaque stability. However, macrophages are phagocytic cells and thus have an important additional role in scavenging of modified lipoproteins, unwanted or dead cells and cellular debris via phagocytosis. The concept of phagocytosis as well as the underlying mechanisms is well defined but the effect of phagocytosis in terms of plaque stability remains poorly understood. Recent findings point towards a complex role of macrophage phagocytosis in atherogenesis. Macrophages are necessary for removal of apoptotic cells from plaques, but exert strong proatherogenic properties upon phagocytosis of lipoproteins, erythrocytes and platelets. Apart from heterophagy, autophagocytosis better known as autophagy may occur in advanced atherosclerotic plaques. Several lines of evidence indicate that autophagy is initiated in plaque smooth muscle cells as a result of cellular distress. Since autophagy is well recognized as a survival mechanism, autophagic smooth muscle cells in the fibrous cap may reflect an important feature underlying plaque stability. All together, phagocytosis is a crucial process involved in atherogenesis that may significantly affect the stability of the atherosclerotic plaque.