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Search Results: 1 - 10 of 1457 matches for " Wim Vermeulen "
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Nucleotide Excision Repair in Caenorhabditis elegans
Hannes Lans,Wim Vermeulen
Molecular Biology International , 2011, DOI: 10.4061/2011/542795
Abstract: Nucleotide excision repair (NER) plays an essential role in many organisms across life domains to preserve and faithfully transmit DNA to the next generation. In humans, NER is essential to prevent DNA damage-induced mutation accumulation and cell death leading to cancer and aging. NER is a versatile DNA repair pathway that repairs many types of DNA damage which distort the DNA helix, such as those induced by solar UV light. A detailed molecular model of the NER pathway has emerged from in vitro and live cell experiments, particularly using model systems such as bacteria, yeast, and mammalian cell cultures. In recent years, the versatility of the nematode C. elegans to study DNA damage response (DDR) mechanisms including NER has become increasingly clear. In particular, C. elegans seems to be a convenient tool to study NER during the UV response in vivo, to analyze this process in the context of a developing and multicellular organism, and to perform genetic screening. Here, we will discuss current knowledge gained from the use of C. elegans to study NER and the response to UV-induced DNA damage. 1. DNA Damage Response Mechanisms To preserve and faithfully transmit DNA to the next generation, cells are equipped with a variety of DNA repair pathways and associated DNA damage responses, collectively referred to as the DNA damage response (DDR). DNA is continuously damaged by environmental and metabolism-derived genotoxic agents. It is vital for cells and organisms to properly cope with DNA damage, because unrepaired damage can give rise to mutation and cell death. The importance of the DDR is illustrated by several human cancer prone and/or progeroid hereditary diseases, which are based on defects in the DDR. Over the last decades, a wealth of information on the molecular mechanism of different repair pathways has been gathered from detailed in vitro and live cell studies. Currently, this acquired knowledge is being used to develop therapeutic strategies to treat patients suffering from the consequences of unrepaired DNA damage, such as cancer and aging [1]. Damage is repaired by different DNA repair pathways depending on the type of DNA lesion, genomic location, and the cell cycle phase (for reviews see [2–4]). Lesions originating from different genotoxic sources can range from small base modifications to double-strand breaks. Small base modifications, such as oxidative lesions which do not substantially distort the double helix, are repaired by base excision repair (BER). BER removes single or several bases and repairs the gap by DNA synthesis. Bigger
ATP-dependent chromatin remodeling in the DNA-damage response
Hannes Lans, Jurgen A Marteijn, Wim Vermeulen
Epigenetics & Chromatin , 2012, DOI: 10.1186/1756-8935-5-4
Abstract: All living organisms depend on faithful preservation and transmission of genetic information to the next generation. Genetic information is stored within DNA, which is embedded in a dynamic nucleoprotein complex, called chromatin. The integrity of DNA is inescapably and continuously threatened by spontaneous and induced alterations to its basic structure. DNA itself is unstable and undergoes hydrolysis, which creates abasic sites and causes deamination [1]. Furthermore, cellular metabolic processes such as oxidative respiration produce oxygen radicals and other reactive molecules, which damage DNA [2]. Finally, exposure to environmental sources such as solar UV irradiation, × radiation, and numerous chemicals induces DNA injuries.DNA damage interferes with vital processes such as transcription and replication, which may cause cells to die or senesce, thus contributing to aging [3]. Replication of damaged DNA templates severely affects the fidelity of the polymerases, and may result in permanent mutations or chromosomal aberrations, which are at the basis of malignant transformation. Genetic erosion and its consequences are neutralized by a variety of DNA repair and associated DNA-damage signaling pathways, collectively called the DNA-damage response (DDR) [3-6]. In this review, we will focus on three repair pathways which are among the best characterized with regard to their repair mechanisms and interactions with chromatin: nucleotide excision repair (NER), which removes helix-distorting intra-strand lesions, and homologous recombination (HR) and non-homologous end-joining (NHEJ), both of which repair double-strand breaks (DSBs).All DNA-associated processes, such as transcription, replication, recombination, and DNA repair, are for a large part regulated by the chromatin structure [7,8]. Because this nucleoprotein complex limits the ability of other proteins to interact with DNA, the chromatin structure needs to be modified to facilitate efficient access to DNA. In
Chromatin structure and DNA damage repair
Christoffel Dinant, Adriaan B Houtsmuller, Wim Vermeulen
Epigenetics & Chromatin , 2008, DOI: 10.1186/1756-8935-1-9
Abstract: Proper functioning of all living organisms depends on faithful maintenance of genomic information. Although it is generally believed that information stored is relatively safe and stable, the integrity of DNA is continuously challenged by numerous genotoxic agents and environmental stress. Essential cellular functions such as oxidative respiration and lipid peroxidation create reactive oxygen species that can damage DNA. In addition, spontaneous hydrolysis of nucleotides induces non-instructive abasic sites. Finally, environmental physical and chemical agents, such as ultraviolet (UV) and ionising radiation, as well as numerous genotoxic chemicals present in food or combustion products in the air, induce a wide variety of DNA lesions. It has been estimated that in an average mammalian cell ten to a hundred thousand DNA lesions are introduced each day [1].The consequences of DNA damage are diverse and adverse. Acute cellular effects arise from impeded gene transcription and DNA replication, causing cellular malfunctioning, irreversible cell cycle arrest (senescence) or cell death (apoptosis) which are important factors in (premature) aging [2,3]. DNA lesions interfere with proper chromosome segregation during cell division resulting in chromosome aberrations. In addition, replication errors due to DNA damage may introduce irreversible mutations. Chromosomal aberrations as well as mutations in coding genes may lead to carcinogenesis [3].To counteract the severe biological consequences of DNA lesions an intricate network of genome surveillance mechanisms or DNA damage response (DDR) processes has evolved. The heart of this defence system is formed by complementary DNA repair systems that cover most of the genetic insults. In addition to the direct removal of lesions, DNA injuries trigger a signalling cascade that results in a slowdown of cell cycle progression, providing cells more time to repair DNA damage prior to replication or cell division.The template for the DDR
Involvement of Global Genome Repair, Transcription Coupled Repair, and Chromatin Remodeling in UV DNA Damage Response Changes during Development
Hannes Lans ,Jurgen A. Marteijn,Bj?rn Schumacher,Jan H. J. Hoeijmakers,Gert Jansen,Wim Vermeulen
PLOS Genetics , 2010, DOI: 10.1371/journal.pgen.1000941
Abstract: Nucleotide Excision Repair (NER), which removes a variety of helix-distorting lesions from DNA, is initiated by two distinct DNA damage-sensing mechanisms. Transcription Coupled Repair (TCR) removes damage from the active strand of transcribed genes and depends on the SWI/SNF family protein CSB. Global Genome Repair (GGR) removes damage present elsewhere in the genome and depends on damage recognition by the XPC/RAD23/Centrin2 complex. Currently, it is not well understood to what extent both pathways contribute to genome maintenance and cell survival in a developing organism exposed to UV light. Here, we show that eukaryotic NER, initiated by two distinct subpathways, is well conserved in the nematode Caenorhabditis elegans. In C. elegans, involvement of TCR and GGR in the UV-induced DNA damage response changes during development. In germ cells and early embryos, we find that GGR is the major pathway contributing to normal development and survival after UV irradiation, whereas in later developmental stages TCR is predominantly engaged. Furthermore, we identify four ISWI/Cohesin and four SWI/SNF family chromatin remodeling factors that are implicated in the UV damage response in a developmental stage dependent manner. These in vivo studies strongly suggest that involvement of different repair pathways and chromatin remodeling proteins in UV-induced DNA repair depends on developmental stage of cells.
Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity
Ruud CW Vermeulen, Ruud M Kurk, Frans C Visser, Wim Sluiter, Hans R Scholte
Journal of Translational Medicine , 2010, DOI: 10.1186/1479-5876-8-93
Abstract: Female patients (n = 15) and controls (n = 15) performed a cardiopulmonary exercise test (CPET) by cycling at a continuously increased work rate till maximal exertion. The CPET was repeated 24 h later. Before the tests, blood was taken for the isolation of peripheral blood mononuclear cells (PBMC), which were processed in a special way to preserve their oxidative phosphorylation, which was tested later in the presence of ADP and phosphate in permeabilized cells with glutamate, malate and malonate plus or minus the complex I inhibitor rotenone, and succinate with rotenone plus or minus the complex II inhibitor malonate in order to measure the ATP production via Complex I and II, respectively. Plasma CK was determined as a surrogate measure of a decreased oxidative phosphorylation in muscle, since the previous finding that in a group of patients with external ophthalmoplegia the oxygen consumption by isolated muscle mitochondria correlated negatively with plasma creatine kinase, 24 h after exercise.At both exercise tests the patients reached the anaerobic threshold and the maximal exercise at a much lower oxygen consumption than the controls and this worsened in the second test. This implies an increase of lactate, the product of anaerobic glycolysis, and a decrease of the mitochondrial ATP production in the patients. In the past this was also found in patients with defects in the mitochondrial oxidative phosphorylation. However the oxidative phosphorylation in PBMC was similar in CFS/ME patients and controls. The plasma creatine kinase levels before and 24 h after exercise were low in patients and controls, suggesting normality of the muscular mitochondrial oxidative phosphorylation.The decrease in mitochondrial ATP synthesis in the CFS/ME patients is not caused by a defect in the enzyme complexes catalyzing oxidative phosphorylation, but in another factor.Clinical trials registration number: NL16031.040.07Chronic fatigue syndrome/myalgic encephalopathy (CFS/ME) as a
Incomplete quality of life data in lung transplant research: comparing cross sectional, repeated measures ANOVA, and multi-level analysis
Karin M Vermeulen, Wendy J Post, Mark M Span, Wim van der Bij, Gerard H Ko?ter, Elisabeth M TenVergert
Respiratory Research , 2005, DOI: 10.1186/1465-9921-6-101
Abstract: Results from cross-sectional analysis, repeated measures on complete cases (ANOVA), and a multi-level analysis were compared. The scores on the dimension 'energy' of the Nottingham Health Profile (NHP) after transplantation were used to illustrate the differences between methods.Compared to repeated measures ANOVA, the cross-sectional and multi-level analysis included more patients, and allowed for a longer period of follow-up. In contrast to the cross sectional analyses, in the complete case analysis, and the multi-level analysis, the correlation between different time points was taken into account. Patterns over time of the three methods were comparable. In general, results from repeated measures ANOVA showed the most favorable energy scores, and results from the multi-level analysis the least favorable. Due to the separate subgroups per time point in the cross-sectional analysis, and the relatively small number of patients in the repeated measures ANOVA, inclusion of predictors was only possible in the multi-level analysis.Results obtained with the various methods of analysis differed, indicating some reduction of bias took place. Multi-level analysis is a useful approach to study changes over time in a data set where missing data, to reduce bias, make efficient use of available data, and to include predictors, in studies concerning the effects of LgTX on HRQL.Lung transplantation has become an accepted treatment option for appropriately selected patients with end-stage lung disease. Besides clinical outcome measures such as survival, Health Related Quality of Life (HRQL) has become an increasingly important endpoint in studies regarding the effectiveness of lung transplantation. Studies in which HRQL was included as an outcome measure generally report improvements across many domains of HRQL after lung transplantation [1-7]. The aim of the present study was twofold. First, to address the problem of missing data in the field of HRQL and lung transplantation, and
Dynamic Interaction of TTDA with TFIIH Is Stabilized by Nucleotide Excision Repair in Living Cells
Giuseppina Giglia-Mari,Catherine Miquel,Arjan F. Theil,Pierre-Olivier Mari,Deborah Hoogstraten,Jessica M. Y. Ng,Christoffel Dinant,Jan H. J. Hoeijmakers,Wim Vermeulen
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0040156
Abstract: Transcription/repair factor IIH (TFIIH) is essential for RNA polymerase II transcription and nucleotide excision repair (NER). This multi-subunit complex consists of ten polypeptides, including the recently identified small 8-kDa trichothiodystrophy group A (TTDA)/ hTFB5 protein. Patients belonging to the rare neurodevelopmental repair syndrome TTD-A carry inactivating mutations in the TTDA/hTFB5 gene. One of these mutations completely inactivates the protein, whereas other TFIIH genes only tolerate point mutations that do not compromise the essential role in transcription. Nevertheless, the severe NER-deficiency in TTD-A suggests that the TTDA protein is critical for repair. Using a fluorescently tagged and biologically active version of TTDA, we have investigated the involvement of TTDA in repair and transcription in living cells. Under non-challenging conditions, TTDA is present in two distinct kinetic pools: one bound to TFIIH, and a free fraction that shuttles between the cytoplasm and nucleus. After induction of NER-specific DNA lesions, the equilibrium between these two pools dramatically shifts towards a more stable association of TTDA to TFIIH. Modulating transcriptional activity in cells did not induce a similar shift in this equilibrium. Surprisingly, DNA conformations that only provoke an abortive-type of NER reaction do not result into a more stable incorporation of TTDA into TFIIH. These findings identify TTDA as the first TFIIH subunit with a primarily NER-dedicated role in vivo and indicate that its interaction with TFIIH reflects productive NER.
Blood transfusions increase circulating plasma free hemoglobin levels and plasma nitric oxide consumption: a prospective observational pilot study
Iris C Vermeulen Windsant, Norbert CJ de Wit, Jonas TC Sertorio, Erik AM Beckers, Jose E Tanus-Santos, Michael J Jacobs, Wim A Buurman
Critical Care , 2012, DOI: 10.1186/cc11359
Abstract: Thirty patients electively received 1 stored packed RBC unit (n = 8) or 2 stored packed RBC units (n = 22). Blood samples were drawn to analyze plasma levels of fHb, haptoglobin, and NO consumption prior to transfusion, and 15, 30, 60 and 120 minutes and 24 hours after transfusion. Differences were compared using Pearson's chi-square test or Fisher's exact test for dichotomous variables, or an independent-sample t test or Mann-Whitney U test for continuous data. Continuous, multiple-timepoint data were analyzed using repeated one-way analysis of variance or the Kruskall-Wallis test. Correlations were analyzed using Spearman or Pearson correlation.Storage duration correlated significantly with fHb concentrations and NO consumption within the storage medium (r = 0.51, P < 0.001 and r = 0.62, P = 0.002). fHb also significantly correlated with NO consumption directly (r = 0.61, P = 0.002). Transfusion of 2 RBC units significantly increased circulating fHb and NO consumption in the recipient (P < 0.001 and P < 0.05, respectively), in contrast to transfusion of 1 stored RBC unit. Storage duration of the blood products did not correlate with changes in fHb and NO consumption in the recipient. In contrast, pre-transfusion recipient plasma haptoglobin levels inversely influenced post-transfusion fHb concentrations.These data suggest that RBC transfusion can significantly increase post-transfusion plasma fHb levels and plasma NO consumption in the recipient. This finding may contribute to the potential pathophysiological mechanism underlying the much-discussed adverse relation between blood transfusions and patient outcome. This observation may be of particular importance for patients with substantial transfusion requirements.Transfusion of stored red blood cells (RBCs) is a common medical procedure, particularly in the context of critical care [1]. Approximately 40% of patients admitted to the ICU receive packed red blood cell (pRBC) transfusion, with a mean of 5 units per p
A Case-Control Study of the Protective Effect of Alcohol, Coffee, and Cigarette Consumption on Parkinson Disease Risk: Time-Since-Cessation Modifies the Effect of Tobacco Smoking
Marianne van der Mark, Peter C. G. Nijssen, Jelle Vlaanderen, Anke Huss, Wim M. Mulleners, Antonetta M. G. Sas, Teus van Laar, Hans Kromhout, Roel Vermeulen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095297
Abstract: The aim of this study was to investigate the possible reduced risk of Parkinson Disease (PD) due to coffee, alcohol, and/or cigarette consumption. In addition, we explored the potential effect modification by intensity, duration and time-since-cessation of smoking on the association between cumulative pack-years of cigarette smoking (total smoking) and PD risk. Data of a hospital based case-control study was used including 444 PD patients, diagnosed between 2006 and 2011, and 876 matched controls from 5 hospitals in the Netherlands. A novel modeling method was applied to derive unbiased estimates of the potential modifying effects of smoking intensity, duration, and time-since-cessation by conditioning on total exposure. We observed no reduced risk of PD by alcohol consumption and only a weak inverse association between coffee consumption and PD risk. However, a strong inverse association of total smoking with PD risk was observed (OR = 0.27 (95%CI: 0.18–0.42) for never smokers versus highest quartile of tobacco use). The observed protective effect of total smoking was significantly modified by time-since-cessation with a diminishing protective effect after cessation of smoking. No effect modification by intensity or duration of smoking was observed indicating that both intensity and duration have an equal contribution to the reduced PD risk. Understanding the dynamics of the protective effect of smoking on PD risk aids in understanding PD etiology and may contribute to strategies for prevention and treatment.
Sharing Experiences: Establishing an Expertise Centre on the Protection of Dutch Cultural Heritage
Theo Vermeulen
Liber Quarterly : The Journal of European Research Libraries , 2008,
Abstract: In the Netherlands an Expertise Centre on the Protection of Dutch Cultural Heritage is being established to bring together scattered knowledge and expertise on collection safety and security issues. A website is being set up based on a broad, integrated security concept. The website will include the DICE database for incident registration. More specialised expertise will be made available on demand. The Centre has been funded for two years, whereupon its viability will be assessed. For the Centre to become a success, the entire cultural heritage field should overcome its reluctance to share sensitive information and commit itself to the Centre.
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