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Search Results: 1 - 10 of 174359 matches for " Gert De Hertogh "
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Evidence for the involvement of infectious agents in the pathogenesis of Crohns disease
Gert De Hertogh, Jeroen Aerssens, Karen P Geboes, Karel Geboes
World Journal of Gastroenterology , 2008,
Abstract: Many advances have been made in the understanding of Crohn’s disease (CD) pathogenesis during the last decade. CD is currently seen as a predominantly T-lymphocyte-driven disease characterized by the presence of a complex cocktail of interacting cytokines, chemokines and other mediators produced by a variety of cell types. Prevailing theories of CD pathogenesis suggest that patients’ T-lymphocytes are inappropriately activated in the setting of an immune imbalance, which is itself caused by an unfortunate confluence of genetic and environmental factors. The T-cell response then leads to the chronic inflammation characteristic for the disease. Various environmental factors may play a role in the development of CD, but microbes are most consistently implied. This theory is based on epidemiological, clinicopathological, genetic and experimental evidence. Despite the abundance of arguments for the implication of bacteria in the etiopathogenesis of CD, the precise role of bacteria in this disease still remains elusive. Three not necessarily mutually exclusive theories have been proposed: (1) an unidentified persistent pathogen; (2) an abnormally permeable mucosal barrier leading to excessive bacterial translocation; and (3) a breakdown in the balance between putative “protective” versus “harmful” intestinal bacteria (“dysbiosis”). At present, one cannot exclude with certainty any of these three proposed hypotheses; they may all apply to CD to a certain extent.
Assessment of the Microbiota in Microdissected Tissues of Crohn's Disease Patients
Gert De Hertogh,Bart Lemmens,Peter Verhasselt,Ronald de Hoogt,Xavier Sagaert,Marie Joossens,Gert Van Assche,Paul Rutgeerts,Severine Vermeire,Jeroen Aerssens
International Journal of Inflammation , 2012, DOI: 10.1155/2012/505674
Abstract: The microbiota of the gastrointestinal tract is frequently mentioned as one of the key players in the etiopathogenesis of Crohn's disease (CD). Four hypotheses have been suggested: the single, still unknown bacterial pathogen, an abnormal overall composition of the bowel microbiota (“dysbiosis”), an abnormal immunological reaction to an essentially normally composed microbiota, and increased bacterial translocation. We propose that laser capture microdissection of selected microscopic structures, followed by broad-range 16S rRNA gene sequencing, is an excellent method to assess spatiotemporal alterations in the composition of the bowel microbiota in CD. Using this approach, we demonstrated significant changes of the composition, abundance, and location of the gut microbiome in this disease. Some of these abnormal findings persisted even after macroscopic mucosal healing. Further investigations along these lines may lead to a better understanding of the possible involvement of the bowel bacteria in the development of clinical Crohn's disease. 1. Introduction Crohn’s disease (CD) is characterized by chronic, segmental, transmural inflammation of the entire gastrointestinal tract. Although the exact etiology of the disease is still unclear, it is generally assumed to originate from immunologic changes induced by environmental influences in a genetically suspectible host. The first discovered CD susceptibility gene was the Caspase Recruitment Domain 15 (CARD15) on chromosome 16q [1, 2]. The protein product of this gene is present in monocytes, dentritic cells, Paneth cells, and intestinal epithelial cells. It recognizes a breakdown product of the bacterial cell wall, muramyl dipeptide, via its carboxyterminal leucine rich repeat region (LRR). Subsequently, it activates NFκB. Three single nucleotide polymorphisms (SNPs) of the CARD15 gene (Arg702Trp-SNP8, Gly908Arg-SNP12 and Leu1007fsinsC-SNP13) are associated with CD in the Caucasian population [3–7]. These 3 SNPs may interfere with the function of the LRR, potentially leading to a disturbance of the normal relationship between the human host and their bowel microbiota. Bacteria have indeed been suggested as one of the most important environmental factors in the pathogenesis of CD. Currently, four hypotheses are proposed. First, the disease may be caused by a single, still unidentified bacterial pathogen (Mycobacterium avium subsp. paratuberculosis (MAP) and adherent-invasive Escherichia coli are possible candidates) [8–11]. Second, the normal balance between beneficial and harmful bacterial species in the
Relationship between Vitreous Levels of Matrix Metalloproteinases and Vascular Endothelial Growth Factor in Proliferative Diabetic Retinopathy
Ahmed M. Abu El-Asrar, Ghulam Mohammad, Mohd. Imtiaz Nawaz, Mohammad Mairaj Siddiquei, Kathleen Van den Eynde, Ahmed Mousa, Gert De Hertogh, Ghislain Opdenakker
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0085857
Abstract: To investigate which matrix metalloproteinases (MMPs) are more likely to be involved in the angiogenic process in proliferative diabetic retinopathy (PDR), we measured the levels of MMPs in the vitreous fluid from patients with PDR and controls and correlated these levels with the levels of vascular endothelial growth factor (VEGF). Vitreous samples from 32 PDR and 24 nondiabetic patients were studied by mosaic multiplex MMPs enzyme-linked immunosorbent assay (ELISA), single ELISA, Western blot and zymography analysis. Epiretinal membranes from 11 patients with PDR were studied by immunohistochemistry. MMP-8 and MMP-13 were not detected. ELISA, Western blot and gelatin ymography assays revealed significant increases in the expression levels of MMP-1, MMP-7, MMP-9 and VEGF in vitreous samples from PDR patients compared to nondiabetic controls, whereas MMP-2 and MMP-3 were not upregulated in vitreous samples from PDR patients. Significant correlations existed between ELISA and zymography assays for the quantitation of MMP-2 (r=0.407; p=0.039) and MMP-9 (r=0.711; p<0.001). Significant correlations were observed between levels of VEGF and levels of MMP-1 (r=0.845; P<0.001) and MMP-9 (r=0.775; p<0.001), and between levels of MMP-1 and MMP-9 (r=0.857; p<0.001). In epiretinal membranes, cytoplasmic immunoreactivity for MMP-9 was present in vascular endothelial cells and stromal monocytes/macrophages and neutrophils. Our findings suggest that among the MMPs measured, MMP-1 and MMP-9 may contribute to the angiogenic switch in PDR.
A Spontaneous Animal Model of Intestinal Dysmotility Evoked by Inflammatory Nitrergic Dysfunction
Tatsuhiro Masaoka, Tim Vanuytsel, Christophe Vanormelingen, Sebastien Kindt, Shadea Salim Rasoel, Werend Boesmans, Gert De Hertogh, Ricard Farré, Pieter Vanden Berghe, Jan Tack
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095879
Abstract: Background and Aims Recent reports indicate the presence of low grade inflammation in functional gastrointestinal disorders (FGID), in these cases often called “post-inflammatory” FGIDs. However, suitable animal models to study these disorders are not available. The Biobreeding (BB) rat consists of a diabetes-resistant (BBDR) and a diabetes-prone (BBDP) strain. In the diabetes-prone strain, 40–60% of the animals develop diabetes and concomitant nitrergic dysfunction. Our aim was to investigate the occurrence of intestinal inflammation, nitrergic dysfunction and intestinal dysmotility in non-diabetic animals. Methods Jejunal inflammation (MPO assay, Hematoxylin&Eosin staining and inducible nitric oxide synthase (iNOS) mRNA expression), in vitro jejunal motility (video analysis) and myenteric neuronal numbers (immunohistochemistry) were assessed in control, normoglycaemic BBDP and diabetic BBDP rats. To study the impact of iNOS inhibition on these parameters, normoglycaemic BBDP rats were treated with aminoguanidine. Results Compared to control, significant polymorphonuclear (PMN) cell infiltration, enhanced MPO activity, increased iNOS mRNA expression and a decreased ratio of nNOS to Hu-C/D positive neurons were observed in both normoglycaemic and diabetic BBDP rats. Aminoguanidine treatment decreased PMN infiltration, iNOS mRNA expression and MPO activity. Moreover, it restored the ratio of nNOS to Hu-C/D positive nerves in the myenteric plexus and decreased the abnormal jejunal elongation and dilation observed in normoglycaemic BBDP rats. Conclusions Aminoguanidine treatment counteracts the inflammation-induced nitrergic dysfunction and prevents dysmotility, both of which are independent of hyperglycaemia in BB rats. Nitrergic dysfunction may contribute to the pathophysiology of “low-grade inflammatory” FGIDs. Normoglycaemic BBDP rats may be considered a suitable animal model to study the pathogenesis of FGIDs.
Mucosal Gene Expression of Antimicrobial Peptides in Inflammatory Bowel Disease Before and After First Infliximab Treatment
Ingrid Arijs,Gert De Hertogh,Katleen Lemaire,Roel Quintens,Leentje Van Lommel,Kristel Van Steen,Peter Leemans,Isabelle Cleynen,Gert Van Assche,Séverine Vermeire,Karel Geboes,Frans Schuit,Paul Rutgeerts
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0007984
Abstract: Antimicrobial peptides (AMPs) protect the host intestinal mucosa against microorganisms. Abnormal expression of defensins was shown in inflammatory bowel disease (IBD), but it is not clear whether this is a primary defect. We investigated the impact of anti-inflammatory therapy with infliximab on the mucosal gene expression of AMPs in IBD.
Atonal homolog 1 Is a Tumor Suppressor Gene
Wouter Bossuyt,Avedis Kazanjian,Natalie De Geest,Sofie Van Kelst,Gert De Hertogh,Karel Geboes,Greg P. Boivin,Judith Luciani,Francois Fuks,Marinee Chuah,Thierry VandenDriessche,Peter Marynen,Jan Cools,Noah F. Shroyer,Bassem A. Hassan
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000039
Abstract: Colon cancer accounts for more than 10% of all cancer deaths annually. Our genetic evidence from Drosophila and previous in vitro studies of mammalian Atonal homolog 1 (Atoh1, also called Math1 or Hath1) suggest an anti-oncogenic function for the Atonal group of proneural basic helix-loop-helix transcription factors. We asked whether mouse Atoh1 and human ATOH1 act as tumor suppressor genes in vivo. Genetic knockouts in mouse and molecular analyses in the mouse and in human cancer cell lines support a tumor suppressor function for ATOH1. ATOH1 antagonizes tumor formation and growth by regulating proliferation and apoptosis, likely via activation of the Jun N-terminal kinase signaling pathway. Furthermore, colorectal cancer and Merkel cell carcinoma patients show genetic and epigenetic ATOH1 loss-of-function mutations. Our data indicate that ATOH1 may be an early target for oncogenic mutations in tissues where it instructs cellular differentiation.
Atonal homolog 1 Is a Tumor Suppressor Gene
Wouter Bossuyt equal contributor,Avedis Kazanjian equal contributor,Natalie De Geest,Sofie Van Kelst,Gert De Hertogh,Karel Geboes,Greg P Boivin,Judith Luciani,Francois Fuks,Marinee Chuah,Thierry VandenDriessche,Peter Marynen,Jan Cools,Noah F Shroyer ,Bassem A Hassan
PLOS Biology , 2009, DOI: 10.1371/journal.pbio.1000039
Abstract: Colon cancer accounts for more than 10% of all cancer deaths annually. Our genetic evidence from Drosophila and previous in vitro studies of mammalian Atonal homolog 1 (Atoh1, also called Math1 or Hath1) suggest an anti-oncogenic function for the Atonal group of proneural basic helix-loop-helix transcription factors. We asked whether mouse Atoh1 and human ATOH1 act as tumor suppressor genes in vivo. Genetic knockouts in mouse and molecular analyses in the mouse and in human cancer cell lines support a tumor suppressor function for ATOH1. ATOH1 antagonizes tumor formation and growth by regulating proliferation and apoptosis, likely via activation of the Jun N-terminal kinase signaling pathway. Furthermore, colorectal cancer and Merkel cell carcinoma patients show genetic and epigenetic ATOH1 loss-of-function mutations. Our data indicate that ATOH1 may be an early target for oncogenic mutations in tissues where it instructs cellular differentiation.
Spoken in de dwaaltuin. Lucebert en de verleidingen van de intertekstualiteit.
Jager, Gert de
Neerlandistiek.nl , 2001,
Abstract: The complexity of Lucebert's work has generated a type of criticism which attempts to elucidate poetry through intertextuality. In this line of research it is generally assumed that the straightforward location of congruities between texts by Lucebert and external sources can guide the reading process and justify a particular interpretation. Consequently, Lucebert's poems are often fitted into an intertextual mould with great ingenuity. In doing so, however, the consistency of individual poems and collections of poems is ignored; the passionate quest for possible connections with texts that are unrelated to the poet's work trivializes the types of consistency to be found within his work. Intertexts are not always suitable as frames of reference by which to interpret the work of poets such as Lucebert. Lucebert employed existing texts and traditions of ideas in an unsystematic and opportunistic manner and considered cohesion of both his poems and collections most important. As such, interpretations that fail to do justice to or even deny particular principles of form and organization have little to offer. In interpreting Lucebert's poems, it is above all relevant to recognize the poet's tendency to think in images. His work, therefore, does not in the first place appeal to the erudition of readers, but, rather, to their imaginative faculty.
Management of headache disorders: design of a randomised clinical trial screening for prognostic patient characteristics
Willem J De Hertogh, Peter H Vaes, Dirk Devroey, Steven Truijen, William Duquet, Rob Oostendorp
BMC Musculoskeletal Disorders , 2007, DOI: 10.1186/1471-2474-8-38
Abstract: The coexistence of headache and neck pain can lead to the referral to a musculoskeletal physiotherapist. This treatment can only be successful if an underlying cervical segmental dysfunction is present. In such cases a physical treatment can be a valuable option that should be considered.The aim of this study is to identify prognostic therapeutic patient characteristics and to increase the number of correct physiotherapy referrals.This trial is designed to identify patient characteristics which can influence the prognosis of the patient. Patients with recurrent headache and co-existent neck pain are recruited via a multicenter setup. After screening for eligibility, subjects are tested at baseline and randomly allocated to one of two treatment groups. Testing includes the administering of questionnaires (a Headache Diagnosis Questionnaire, Headache Inventory List and the Headache Impact Test (HIT-6)) and physical tests (Thermal Stimuli, Manual Cervical Spine Examination and Pressure Algometry). Treatment groups are a usual care group (UC) administered by the General Practitioner (GP) and a usual care plus musculoskeletal physiotherapy treatment group (UCMT). UC is based on the Dutch GP Guideline for Headache. UCMT consists of the UC plus a combination of exercises and spinal cervical mobilisations. Follow-up measurements consist of the completion of the Headache Inventory List, the HIT-6 and scoring of the global perceived effect (GPE). The latter allowing the distinction between responders (positive effect) and non-responders (no effect or worse). Logistic regression analysis will be used to identify the specific patient characteristics of the responders and the non-responders. The additional value of the musculoskeletal physiotherapy will be examined. Follow-up measurements up to 52 weeks are scheduled.This trial aims to identify prognostic patient characteristics, in order to supply a useful diagnostic tool for all health care workers, dealing with headache suffe
Effect of TENS on pain in relation to central sensitization in patients with osteoarthritis of the knee: study protocol of a randomized controlled trial
David Beckwée, Willem De Hertogh, Pierre Lievens, Ivan Bautmans, Peter Vaes
Trials , 2012, DOI: 10.1186/1745-6215-13-21
Abstract: Patients with knee pain due to OAk will be recruited through advertisements in local media. Temporal summation, before and after a heterotopic noxious conditioning stimulation, will be measured. In addition, pain on a numeric rating score, WOMAC subscores for pain and function and global perceived effect will be assessed. Patients will be randomly allocated to one of two treatment groups (tens, sham tens). Follow-up measurements will be scheduled after a period of 6 and 12 weeks.Tens influences pain through the electrical stimulation of low-threshold A-beta cutaneous fibers. The responsiveness of central pain-signaling neurons of centrally sensitized OAk patients may be augmented to the input of these electrical stimuli. This would encompass an adverse therapy effect of tens. To increase treatment effectiveness it might be interesting to identify a subgroup of symptomatic OAk patients, i.e., non-sensitized patients, who are likely to benefit from burst tens.ClinicalTrials.gov: NCT01390285Osteoarthritis (OA) is characterized by damaged articular cartilage of synovial joints. About 17% of people aged over 45 years suffer from pain and loss of function due to symptomatic knee osteoarthritis (OAk) [1] and 40% of people aged over 65 years have symptomatic OA of the knee or hip [2,3]. The prevalence of arthritis and more especially OA increases with age [4]. Therefore, the direct health care costs associated with this disease will become a major burden in the near future as the proportion of elderly people in the population increases [5]. Because there is no cure for OA, the treatment is focused on reducing physical disability and impairment and controlling pain while minimizing the potentially harmful side effects of medications [6].Transcutaneous electrical nerve stimulation (tens) is a non-pharmacological, inexpensive and safe form of analgesia [7]. The pain modulating effect of tens is assigned to peripheral components which may be regulated by central mechanisms [8].
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