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Search Results: 1 - 10 of 64171 matches for " Peter Van Loo "
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Evidence for Co-Evolution between Human MicroRNAs and Alu-Repeats
Stefan Lehnert, Peter Van Loo, Pushpike J. Thilakarathne, Peter Marynen, Geert Verbeke, Frans C. Schuit
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004456
Abstract: This paper connects Alu repeats, the most abundant repetitive elements in the human genome and microRNAs, small RNAs that alter gene expression at the post-transcriptional level. Base-pair complementarity could be demonstrated between the seed sequence of a subset of human microRNAs and Alu repeats that are integrated parallel (sense) in mRNAs. The most common target site coincides with the evolutionary most conserved part of Alu. A primate-specific gene cluster on chromosome 19 encodes the majority of miRNAs that target the most conserved sense Alu site. The individual miRNA genes within this cluster are flanked by an Alu-LINE signature, which has been duplicated with the clustered miRNA genes. Gene duplication events in this locus are supported by comparing repeat length variations of the LINE elements within the cluster with those in the rest of the chromosome. Thus, a dual relationship exists between an evolutionary young miRNA cluster and their Alu targets that may have evolved in the same time window. One hypothesis for this dual relationship is that these miRNAs could protect against too high rates of duplicative transposition, which would destroy the genome.
ModuleMiner - improved computational detection of cis-regulatory modules: are there different modes of gene regulation in embryonic development and adult tissues?
Peter Van Loo, Stein Aerts, Bernard Thienpont, Bart De Moor, Yves Moreau, Peter Marynen
Genome Biology , 2008, DOI: 10.1186/gb-2008-9-4-r66
Abstract: The identification and functional annotation of transcriptional regulatory sequences in the human genome is lagging far behind the rapidly increasing knowledge of protein-encoding genes. These transcriptional regulatory sequences are often build up in a modular manner and exert their function in cis through the concerted binding of multiple transcription factors (and co-factors), resulting in the formation of protein complexes that interact with RNA polymerase II [1,2]. These sequences are called cis-regulatory modules (CRMs). In theory, these CRMs can be detected by the presence of multiple transcription factor binding sites (TFBSs). In practice, however, reliable detection of functional TFBSs is difficult and results in many false positives, partly because these binding sites are too short and too degenerate [3]. Hence, the computational detection of functional regulatory sequences in the human genome remains a formidable challenge.Multiple methods have been developed that aim to detect regulatory sequences computationally [4-8]. Promising and validated results have been delivered mostly in model organisms with relatively compact genomes (for example, Drosophila melanogaster) [9-11]. In the larger human genome, deep sequence conservation (for instance, up to zebrafish) or extreme sequence conservation (for example, perfect conservation in mouse over 200 base pairs), irrespective of TFBS detection, remains the method of choice for approaches validating regulatory sequences in vitro or in vivo [12-14]. Although these conservation approaches are quite successful in predicting which regions have a regulatory function, they provide no information regarding what expression pattern these regions produce and by which transcription factors they are targeted.When several similar CRMs have been characterized, and the regulatory factors and binding sites have been elucidated, one can use this knowledge to find new examples of similar CRMs that direct the transcription of othe
Copynumber: Efficient algorithms for single- and multi-track copy number segmentation
Nilsen Gro,Liest?l Knut,Loo Peter Van,Moen Vollan Hans Kristian
BMC Genomics , 2012, DOI: 10.1186/1471-2164-13-591
Abstract: Background Cancer progression is associated with genomic instability and an accumulation of gains and losses of DNA. The growing variety of tools for measuring genomic copy numbers, including various types of array-CGH, SNP arrays and high-throughput sequencing, calls for a coherent framework offering unified and consistent handling of single- and multi-track segmentation problems. In addition, there is a demand for highly computationally efficient segmentation algorithms, due to the emergence of very high density scans of copy number. Results A comprehensive Bioconductor package for copy number analysis is presented. The package offers a unified framework for single sample, multi-sample and multi-track segmentation and is based on statistically sound penalized least squares principles. Conditional on the number of breakpoints, the estimates are optimal in the least squares sense. A novel and computationally highly efficient algorithm is proposed that utilizes vector-based operations in R. Three case studies are presented. Conclusions The R package copynumber is a software suite for segmentation of single- and multi-track copy number data using algorithms based on coherent least squares principles.
Data-driven subtypes of major depressive disorder: a systematic review
van Loo Hanna M,de Jonge Peter,Romeijn Jan-Willem,Kessler Ronald C
BMC Medicine , 2012, DOI: 10.1186/1741-7015-10-156
Abstract: Background According to current classification systems, patients with major depressive disorder (MDD) may have very different combinations of symptoms. This symptomatic diversity hinders the progress of research into the causal mechanisms and treatment allocation. Theoretically founded subtypes of depression such as atypical, psychotic, and melancholic depression have limited clinical applicability. Data-driven analyses of symptom dimensions or subtypes of depression are scarce. In this systematic review, we examine the evidence for the existence of data-driven symptomatic subtypes of depression. Methods We undertook a systematic literature search of MEDLINE, PsycINFO and Embase in May 2012. We included studies analyzing the depression criteria of the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) of adults with MDD in latent variable analyses. Results In total, 1176 articles were retrieved, of which 20 satisfied the inclusion criteria. These reports described a total of 34 latent variable analyses: 6 confirmatory factor analyses, 6 exploratory factor analyses, 12 principal component analyses, and 10 latent class analyses. The latent class techniques distinguished 2 to 5 classes, which mainly reflected subgroups with different overall severity: 62 of 71 significant differences on symptom level were congruent with a latent class solution reflecting severity. The latent class techniques did not consistently identify specific symptom clusters. Latent factor techniques mostly found a factor explaining the variance in the symptoms depressed mood and interest loss (11 of 13 analyses), often complemented by psychomotor retardation or fatigue (8 of 11 analyses). However, differences in found factors and classes were substantial. Conclusions The studies performed to date do not provide conclusive evidence for the existence of depressive symptom dimensions or symptomatic subtypes. The wide diversity of identified factors and classes might result either from the absence of patterns to be found, or from the theoretical and modeling choices preceding analysis.
Elevated extracellular matrix production and degradation upon bone morphogenetic protein-2 (BMP-2) stimulation point toward a role for BMP-2 in cartilage repair and remodeling
Esmeralda N Blaney Davidson, Elly L Vitters, Peter LEM van Lent, Fons AJ van de Loo, Wim B van den Berg, Peter M van der Kraan
Arthritis Research & Therapy , 2007, DOI: 10.1186/ar2305
Abstract: Cartilage damage is a major problem in joint diseases like osteoarthritis (OA) and rheumatoid arthritis. As a response to cartilage injury, chondrocytes display a reparative response [1,2]. Unfortunately, this response is very limited, resulting in suboptimal repair [3]. Until now, reparative responses that have been induced by drilling and microfractures have been unable to overcome this problem [4]. They yield a new tissue, often fibrocartilage that does not compare to original cartilage in structural, biomechanical, and biochemical aspects [5]. Currently, in experimental settings, growth factors are used to promote chondrogenic differentiation in vitro. This has the potential to eventually produce cartilage that can overcome the current problems.Bone morphogenetic protein-2 (BMP-2) is one of the candidate growth factors with good potential in cartilage tissue engineering as well as cartilage repair. BMP-2 belongs to the transforming growth factor-beta (TGF-β) superfamily, consisting of TGF-βs, growth differentiation factors, BMPs, activins, inhibins, and glial cell line-derived neurotrophic factor [6]. BMPs have been identified as very potent inducers of bone, but since then it has become evident that their function is not limited to skeletal development [7]. BMP-2 expression is found in mesenchymal condensation in embryonic development [8]. BMP-2 is able to induce chondrogenesis in human mesenchymal stem cells in culture [9]. For cartilage reparative reasons, BMP-2 can be used to induce chondrogenesis by coating a scaffold with BMP-2 before implantation [10]. Thereby, the scaffold itself can be replaced by the original tissue. This can be combined with culturing mesenchymal stem cells or tissue-specific cells on the coated scaffold to gain de novo tissue formation in the scaffold [11]. Although BMP-2 is able to induce cartilage formation, we found that the expression of BMP-2 in healthy cartilage was low but that its expression was elevated in areas surrounding
Studies on Prn Variation in the Mouse Model and Comparison with Epidemiological Data
Marjolein van Gent,Inge H. M. van Loo,Kees J. Heuvelman,Albert J. de Neeling,Peter Teunis,Frits R. Mooi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018014
Abstract: The virulence factor pertactin (Prn) is a component of pertussis vaccines and one of the most polymorphic Bordetella pertussis antigens. After the introduction of vaccination shifts in predominant Prn types were observed and strains with the Prn vaccine type (Prn1) were replaced by strains carrying non-vaccine types (Prn2 and Prn3), suggesting vaccine-driven selection. The aim of this study was to elucidate the shifts observed in Prn variants. We show that, although Prn2 and Prn3 circulated in similar frequencies in the 1970s and 1980s, in the 1990s Prn2 strains expanded and Prn3 strains disappeared, suggesting that in vaccinated populations Prn2 strains are fitter than Prn3 strains. We established a role for Prn in the mouse model by showing that a Prn knock-out (Prn-ko) mutation reduced colonization in trachea and lungs. Restoration of the mutation resulted in a significant increase in colonization compared to the knock-out mutant. The ability of clinical isolates with different Prn variants to colonize the mouse lung was compared. Although these isolates were also polymorphic at other loci, only variation in the promoter for pertussis toxin (ptxP) and Prn were found to contribute significantly to differences in colonization. Analysis of a subset of strains with the same ptxP allele revealed that the ability to colonize mice decreased in the order Prn1>Prn2 and Prn3. Our results are consistent with the predominance of Prn1 strains in unvaccinated populations. Our results show that ability to colonize mice is practically the same for Prn2 and Prn3. Therefore other factors may have contributed to the predominance of Prn2 in vaccinated populations. The mouse model may be useful to assess and predict changes in the B. pertussis population due to vaccination.
Non-Thermal Radio Emission from Single Hot Stars
S. Van Loo
Revista mexicana de astronomía y astrofísica , 2003,
Collaboratively charting the gene-to-phenotype network of human congenital heart defects
Roland Barriot, Jeroen Breckpot, Bernard Thienpont, Sylvain Brohée, Steven Van Vooren, Bert Coessens, Leon-Charles Tranchevent, Peter Van Loo, Marc Gewillig, Koenraad Devriendt, Yves Moreau
Genome Medicine , 2010, DOI: 10.1186/gm137
Abstract: We built on the recent advances in Wiki-based technologies to develop a collaborative knowledge base and gene prioritization portal aimed at mapping genes and genomic regions, and untangling their relations with corresponding human phenotypes, congenital heart defects (CHDs). This portal is not only an evolving community repository of current knowledge on the genetic basis of CHDs, but also a collaborative environment for the study of candidate genes potentially implicated in CHDs - in particular by integrating recent strategies for the statistical prioritization of candidate genes. It thus serves and connects the broad community that is facing CHDs, ranging from the pediatric cardiologist and clinical geneticist to the basic investigator of cardiogenesis.This study describes the first specialized portal to collaboratively annotate and analyze gene-phenotype networks. Of broad interest to the biological community, we argue that such portals will play a significant role in systems biology studies of numerous complex biological processes.CHDWiki is accessible at http://www.esat.kuleuven.be/~bioiuser/chdwiki webciteRecently, Wiki technology - inspired by the well-known Wikipedia encyclopedia - has been proposed as a potential strategy for the collaborative development of biological knowledge bases [1-6]. Although a 'Wikipedia for Genes' is likely to emerge, a number of challenges remain. First, classical Wiki technology in itself (based on free text) is unsuitable for developing genetic knowledge bases because of the imperative need for structured information. Hence, Wiki platforms for genetic knowledge bases need to provide a strong framework for integration with classical database technology. Wikiproteins already implements this need at a high level by abstractly linking concepts, such as proteins and biological processes [1]. Second, and probably foremost, each community uses specific terminology, has specific goals, and uses specific data and tools. Such specificit
EGFR Gene Variants Are Associated with Specific Somatic Aberrations in Glioma
Carl Wibom, Soma Ghasimi, Peter Van Loo, Thomas Br?nnstr?m, Johan Trygg, Ching Lau, Roger Henriksson, Tommy Bergenheim, Ulrika Andersson, Patrik Rydén, Beatrice Melin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047929
Abstract: A number of gene variants have been associated with an increased risk of developing glioma. We hypothesized that the reported risk variants may be associated with tumor genomic instability. To explore potential correlations between germline risk variants and somatic genetic events, we analyzed matched tumor and blood samples from 95 glioma patients by means of SNP genotyping. The generated genotype data was used to calculate genome-wide allele-specific copy number profiles of the tumor samples. We compared the copy number profiles across samples and found two EGFR gene variants (rs17172430 and rs11979158) that were associated with homozygous deletion at the CDKN2A/B locus. One of the EGFR variants (rs17172430) was also associated with loss of heterozygosity at the EGFR locus. Our findings were confirmed in a separate dataset consisting of matched blood and tumor samples from 300 glioblastoma patients, compiled from publically available TCGA data. These results imply there is a functional effect of germline EGFR variants on tumor progression.
NADPH-oxidase-driven oxygen radical production determines chondrocyte death and partly regulates metalloproteinase-mediated cartilage matrix degradation during interferon-γ-stimulated immune complex arthritis
Peter LEM van Lent, Karin CAM Nabbe, Arjen B Blom, Annet Sloetjes, Astrid EM Holthuysen, Jay Kolls, Fons AJ Van De Loo, Steven M Holland, Wim B Van Den Berg
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1760
Abstract: During rheumatoid arthritis (RA), large numbers of inflammatory cells, mainly macrophages, migrate into the synovial layer [1]. Many of these macrophages become activated by mechanisms that are as yet unknown. Activated macrophages produce cytokines such as tumour necrosis factor-α (TNFα) and interleukin-1 (IL-1) and enzymes such as the metalloproteinase family, which can mediate severe cartilage destruction. A strong correlation was found between the number of activated macrophages and cartilage erosion [2]. Important triggers of macrophages are IgG-containing immune complexes, which are found in large amounts in the joints of many RA patients [3]. In previous studies we have found, by comparing various experimental arthritis models, that severe cartilage destruction developed mainly when immune complexes were present [4]. Severe cartilage destruction is thereby defined as chondrocyte death and cartilage matrix destruction. The latter is induced predominantly by metalloproteinases (MMPs), which are released in a latent form. Upon activation these enzymes degrade the collagen type II network in the cartilage resulting in irreversible erosion [5]. During immune complex (IC)-mediated arthritides, synovial macrophages seemed to be dominant factors in the induction of severe cartilage destruction [6].IgG-containing ICs communicate with macrophages with FcγR. Three classes have been described, and previous studies in our laboratory showed that absence of the activating FcγRI and FcγRIII completely abrogated severe cartilage destruction [7-9].The mechanism of FcγR-mediated chondrocyte death and MMP-mediated cartilage destruction is not known. However, we found recently that FcγRI is the dominant activating FcγR causing cartilage destruction [10,11]. In T cell-driven immune complex arthritis (ICA), chondrocyte death in FcγRI-/- was completely abrogated, whereas MMP-mediated cartilage destruction was significantly diminished [12]. Moreover, ICA stimulated by local overexpre
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