University of Duisburg-Essen

About: University of Duisburg-Essen is a education organization based out in Essen, Nordrhein-Westfalen, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 16072 authors who have published 39972 publications receiving 1109199 citations.

The Mechanism of CO and CO2 Hydrogenation to Methanol over Cu-Based Catalysts

Abstract: Methanol, an important chemical, fuel additive, and precursor for clean fuels, is produced by hydrogenation of carbon oxides over Cu-based catalysts. Despite the technological maturity of this process, the understanding of this apparently simple reaction is still incomplete with regard to the reaction mechanism and the active sites. Regarding the latter, recent progress has shown that stepped and ZnOx-decorated Cu surfaces are crucial for the performance of industrial catalysts. Herein, we integrate this insight with additional experiments into a full microkinetic description of methanol synthesis. In particular, we show how the presence or absence of the Zn promoter dramatically changes not only the activity, but unexpectedly the reaction mechanism itself. The Janus-faced character of Cu with two different sites for methanol synthesis, Zn-promoted and unpromoted, resolves the long-standing controversy regarding the Cu/Zn synergy and adds methanol synthesis to the few major industrial catalytic processes that are described on an atomic level.

Common variants at ten loci modulate the QT interval duration in the QTSCD Study

Abstract: The QT interval, a measure of cardiac repolarization, predisposes to ventricular arrhythmias and sudden cardiac death (SCD) when prolonged or shortened. A common variant in NOS1AP is known to influence repolarization. We analyze genome-wide data from five population-based cohorts (ARIC, KORA, SardiNIA, GenNOVA and HNR) with a total of 15,842 individuals of European ancestry, to confirm the NOS1AP association and identify nine additional loci at P < 5 x 10(-8). Four loci map near the monogenic long-QT syndrome genes KCNQ1, KCNH2, SCN5A and KCNJ2. Two other loci include ATP1B1 and PLN, genes with established electrophysiological function, whereas three map to RNF207, near LITAF and within NDRG4-GINS3-SETD6-CNOT1, respectively, all of which have not previously been implicated in cardiac electrophysiology. These results, together with an accompanying paper from the QTGEN consortium, identify new candidate genes for ventricular arrhythmias and SCD.

Mechanisms of DNA double strand break repair and chromosome aberration formation.

Abstract: It is widely accepted that unrepaired or misrepaired DNA double strand breaks (DSBs) lead to the formation of chromosome aberrations. DSBs induced in the DNA of higher eukaryotes by endogenous processes or exogenous agents can in principle be repaired either by non-homologous endjoining (NHEJ), or homology directed repair (HDR). The basis on which the selection of the DSB repair pathway is made remains unknown but may depend on the inducing agent, or process. Evaluation of the relative contribution of NHEJ and HDR specifically to the repair of ionizing radiation (IR) induced DSBs is important for our understanding of the mechanisms leading to chromosome aberration formation. Here, we review recent work from our laboratories contributing to this line of inquiry. Analysis of DSB rejoining in irradiated cells using pulsed-field gel electrophoresis reveals a fast component operating with half times of 10-30 min. This component of DSB rejoining is severely compromised in cells with mutations in DNA-PKcs, Ku, DNA ligase IV, or XRCC4, as well as after chemical inhibition of DNA-PK, indicating that it reflects classical NHEJ; we termed this form of DSB rejoining D-NHEJ to signify its dependence on DNA-PK. Although chemical inhibition, or mutation, in any of these factors delays processing, cells ultimately remove the majority of DSBs using an alternative pathway operating with slower kinetics (half time 2-10 h). This alternative, slow pathway of DSB rejoining remains unaffected in mutants deficient in several genes of the RAD52 epistasis group, suggesting that it may not reflect HDR. We proposed that it reflects an alternative form of NHEJ that operates as a backup (B-NHEJ) to the DNA-PK-dependent (D-NHEJ) pathway. Biochemical studies confirm the presence in cell extracts of DNA end joining activities operating in the absence of DNA-PK and indicate the dominant role for D-NHEJ, when active. These observations in aggregate suggest that NHEJ, operating via two complementary pathways, B-NHEJ and D-NHEJ, is the main mechanism through which IR-induced DSBs are removed from the DNA of higher eukaryotes. HDR is considered to either act on a small fraction of IR induced DSBs, or to engage in the repair process at a step after the initial end joining. We propose that high speed D-NHEJ is an evolutionary development in higher eukaryotes orchestrated around the newly evolved DNA-PKcs and pre-existing factors. It achieves within a few minutes restoration of chromosome integrity through an optimized synapsis mechanism operating by a sequence of protein-protein interactions in the context of chromatin and the nuclear matrix. As a consequence D-NHEJ mostly joins the correct DNA ends and suppresses the formation of chromosome aberrations, albeit, without ensuring restoration of DNA sequence around the break. B-NHEJ is likely to be an evolutionarily older pathway with less optimized synapsis mechanisms that rejoins DNA ends with kinetics of several hours. The slow kinetics and suboptimal synapsis mechanisms of B-NHEJ allow more time for exchanges through the joining of incorrect ends and cause the formation of chromosome aberrations in wild type and D-NHEJ mutant cells.

Prefrontal control and Internet addiction: a theoretical model and review of neuropsychological and neuroimaging findings

Abstract: Most people use the Internet as a functional tool to perform their personal goals in everyday-life such as making airline or hotel reservations. However, some individuals suffer from a loss of control over their Internet use resulting in personal distress, symptoms of psychological dependence, and diverse negative consequences. This phenomenon is often referred to as Internet addiction. Only Internet Gaming Disorder has been included in the appendix of the DSM-5, but it has already been argued that Internet addiction could also comprise problematic use of other applications with cybersex, online relations, shopping, and information search being Internet facets at risk for developing an addictive behavior. Neuropsychological investigations have pointed out that certain prefrontal functions in particular executive control functions are related to symptoms of Internet addiction, which is in line with recent theoretical models on the development and maintenance of the addictive use of the Internet. Control processes are particularly reduced when individuals with Internet addiction are confronted with Internet-related cues representing their first choice use. For example, processing Internet-related cues interferes with working memory performance and decision making. Consistent with this, results from functional neuroimaging and other neuropsychological studies demonstrate that cue-reactivity, craving, and decision making are important concepts for understanding Internet addiction. The findings on reductions in executive control are consistent with other behavioral addictions, such as pathological gambling. They also emphasize the classification of the phenomenon as an addiction, because there are also several similarities with findings in substance dependency. The neuropsychological and neuroimaging results have important clinical impact, as one therapy goal should enhance control over the Internet use by modifying specific cognitions and Internet use expectancies.