Emiel F M Wouters

Maastricht Universitair Medisch Centrum, Maestricht, Limburg, Netherlands

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Publications (673)3114.29 Total impact

  • American Journal of Respiratory and Critical Care Medicine 05/2015; 191(9):1081-1082. DOI:10.1164/rccm.201412-2296RR · 11.99 Impact Factor
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    ABSTRACT: Decreased physical performance due to loss of muscle mass (i.e. sarcopenia) is prevalent in ageing and appears more pronounced in chronic disease. A comprehensive profile of the sarcopenic phenotype in chronic obstructive pulmonary disease (COPD) is not yet available. The aim of the present study was to characterise prevalence, functional implications and predictive value of sarcopenia with or without abdominal obesity in Dutch COPD patients eligible for pulmonary rehabilitation. 505 COPD patients (aged 37-87 years; 57% male) underwent assessment of lung function, body composition and physical functioning, before entering pulmonary rehabilitation. Sarcopenia was assessed by appendicular skeletal muscle index (ASMI) and abdominal obesity by android/gynoid percentage fat mass (A/G%FM) using dual energy X-ray absorptiometry (DEXA). 86.5% of patients were sarcopenic and showed lower physical functioning, while coexistent abdominal obesity (78.0%) resulted in higher physical functioning. Implications on endurance were less pronounced in women. The predictive value for physical functioning was higher for the "three-compartment" model (ASMI, bone mineral content and A/G%FM) than the "two-compartment" model (fat-free mass index and fat mass index) or "one-compartment" model (body mass index). In patients eligible for pulmonary rehabilitation, sarcopenia is highly prevalent in all BMI-categories and associated with impaired strength, and in men also with decreased endurance. Abdominal obesity seems to have protective effects on physical functioning. ASMI is a better predictor for physical functioning than FFMI. Copyright ©ERS 2015.
    European Respiratory Journal 04/2015; DOI:10.1183/09031936.00197314 · 7.13 Impact Factor
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity, mortality, and resource use worldwide. The goal of this official American Thoracic Society (ATS)/European Respiratory Society (ERS) research statement is to describe evidence related to diagnosis, assessment and management; identify gaps in knowledge; and make recommendations for future research. It is not intended to provide clinical practice recommendations on COPD diagnosis and management. Clinicians, researchers, and patient advocates with expertise in COPD were invited to participate. A literature search of Medline was performed, and studies deemed relevant were selected. The search was not a systematic review of the evidence. Existing evidence was appraised and summarised, and then salient knowledge gaps were identified. Recommendations for research that addresses important gaps in the evidence in all areas of COPD were formulated via discussion and consensus. Great strides have been made in the diagnosis, assessment and management of COPD, as well as understanding its pathogenesis. Despite this, many important questions remain unanswered. This ATS/ERS research statement highlights the types of research that leading clinicians, researchers, and patient advocates believe will have the greatest impact on patient-centred outcomes. Copyright ©ATS/ERS 2015.
    European Respiratory Journal 04/2015; 45(4):879-905. DOI:10.1183/09031936.00009015 · 7.13 Impact Factor
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity, mortality, and resource use worldwide. The goal of this Official American Thoracic Society (ATS)/European Respiratory Society (ERS) Research Statement is to describe evidence related to diagnosis, assessment, and management; identify gaps in knowledge; and make recommendations for future research. It is not intended to provide clinical practice recommendations on COPD diagnosis and management. Clinicians, researchers, and patient advocates with expertise in COPD were invited to participate. A literature search of Medline was performed, and studies deemed relevant were selected. The search was not a systematic review of the evidence. Existing evidence was appraised and summarized, and then salient knowledge gaps were identified. Recommendations for research that addresses important gaps in the evidence in all areas of COPD were formulated via discussion and consensus. Great strides have been made in the diagnosis, assessment, and management of COPD as well as understanding its pathogenesis. Despite this, many important questions remain unanswered. This ATS/ERS Research Statement highlights the types of research that leading clinicians, researchers, and patient advocates believe will have the greatest impact on patient-centered outcomes.
    American Journal of Respiratory and Critical Care Medicine 04/2015; 191(7):e4-e27. DOI:10.1164/rccm.201501-0044ST · 11.99 Impact Factor
  • Pneumologie 02/2015; 69(S 01). DOI:10.1055/s-0035-1544631
  • Pneumologie 02/2015; 69(S 01). DOI:10.1055/s-0035-1544632
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    ABSTRACT: Family caregivers already have a paramount role in daily care for patients with chronic obstructive pulmonary disease (COPD), chronic heart failure (CHF), or chronic renal failure (CRF). To date, it remains unknown whether and to what extent the experience of caregiving changes over time. To examine changes in caregiver burden and positive aspects of caregiving during 1-year follow-up in patients with advanced COPD, CHF or CRF and to study determinants of changes in caregiver burden and positive aspects of caregiving. In this longitudinal observational study, patients and their family caregivers who had complete data at baseline and 12 months (n = 104) and family caregivers of patients who died during 1-year follow-up (n = 15) were included. Caregiver burden and positive aspects of caregiving were assessed using the Family Appraisal of Caregiving Questionnaire for Palliative Care (FACQ-PC). Domain scores were classified into three categories, and baseline characteristics were compared between these categories. A majority of the individuals showed 1-year changes in FACQ-PC domain scores. These individual changes were not explained by demographic or clinical patient characteristics at baseline or changes in patient characteristics during 1-year follow-up. Furthermore, caregiver burden was higher for caregivers of patients who died during 1-year follow-up compared to caregivers whose relative completed 1-year follow-up. This study showed that caregiver burden and positive aspects of caregiving can change over time, and these changes are highly individual. Therefore, healthcare providers should regularly pay attention to family caregivers, regardless the patients' characteristics. © 2015 Nordic College of Caring Science.
    Scandinavian Journal of Caring Sciences 02/2015; DOI:10.1111/scs.12204 · 0.89 Impact Factor
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    ABSTRACT: Rationale: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease that likely includes clinically relevant subgroups. Objectives: To identify subgroups of COPD in ECLIPSE subjects using unsupervised cluster analysis and to assess clinically meaningful outcomes of the clusters during 3 years of longitudinal follow-up. Methods: Factor analysis was used to reduce 41 variables determined at recruitment in 2,164 COPD patients to 13 main factors, and the variables with the highest loading were used for unsupervised cluster analysis. Clusters were then evaluated for their relationship with clinically meaningful outcomes during 3 years of follow-up. The relationships among clinical parameters were evaluated within clusters. Measurements and Main Results: Five subgroups were distinguished using cross-sectional clinical features. Importantly, these groups differed with regard to outcomes. Cluster A included milder patients and had fewer deaths and hospitalizations. Cluster B had less systemic inflammation at baseline but had notable changes in health status and emphysema extent. Cluster C had many comorbidities, evidence of systemic inflammation and the highest mortality. Cluster D had low FEV1, severe emphysema and the highest exacerbation and COPD hospitalization rate. Cluster E was intermediate for most variables and may represent a mixed group that includes further clusters. The relationships among clinical variables within clusters differed from that in the entire COPD population. Conclusions: Unsupervised cluster analysis using baseline data in ECLIPSE identified five COPD subgroups that differ in outcomes and inflammatory biomarkers and show different relationships between clinical parameters, suggesting the clusters represent clinically and biologically different subtypes of COPD.
    02/2015; DOI:10.1513/AnnalsATS.201403-125OC
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    ABSTRACT: Patient-clinician communication is an important prerequisite to delivering high-quality end-of-life care. However, discussions about end-of-life care are uncommon in patients with advanced chronic organ failure. To examine the quality of end-of-life care communication during one-year follow-up of patients with advanced chronic organ failure. In addition, we aimed to explore whether and to what extent quality of communication about end-of-life care changes towards the end of life and whether end-of-life care communication is related to patient-perceived quality of medical care. Clinically stable outpatients (n=265) with advanced chronic obstructive pulmonary disease, chronic heart failure, or chronic renal failure were visited at home at baseline and four, eight, and 12 months after baseline to assess quality of end-of-life care communication (Quality of Communication Questionnaire, QOC). Two years after baseline, survival status was assessed and if patients died during the study period, a bereavement interview was done with the closest relative. One-year follow-up was completed by 77.7% of the patients. Quality of end-of-life care communication was rated low at baseline and did not change over one year. Quality of end-of-life care communication was comparable for patients who completed two-year follow-up and patients who died during the study. The correlation between quality of end-of-life care communication and satisfaction with medical treatment was weak. End-of-life care communication is poor in patients with chronic organ failure and does not change towards the end of life. Future studies should develop an intervention aiming at initiating high-quality end-of-life care communication between patients with advanced chronic organ failure and their clinicians. Copyright © 2015 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.
    Journal of Pain and Symptom Management 01/2015; DOI:10.1016/j.jpainsymman.2014.12.008 · 2.74 Impact Factor
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    ABSTRACT: Note: MACVIALR (contre les maladies chroniques pour un vieillissement actif en Languedoc Roussillon), reference Site of the European Innovation Parternship on Active and Healthy Ageing (EIP on AHA), EIP on AHA Reference Site Network, European Union Geriatric Medicine Society (EUGMS), International Association of Gerontology and Geriatrics (IAGG), Groupe de recherche (GDR) français sur la longévité et le vieillissement, ECHAlliance, Healthy Ageing Research Center (HARC). Abstract: The broad concept of Active and Healthy Ageing was proposed by WHO as the process of optimizing opportunities for health to enhance quality of life as people age. It applies to both individuals and population groups. A universal active and healthy ageing definition is not available and may differ depending on the purpose of the definition and/or the questions raised. The European Innovation Partnership on Active and Healthy Ageing (EIP on AHA) has had a major impact but a definition of Active and Healthy Ageing is urgently needed. A meeting was organised in Montpellier October 2021, 2014 as the annual conference of the EIP on AHA Reference Site MACVIALR (contre les maladies chroniques pour un vieillissement actif en Languedoc Roussillon). The goal of the meeting was to propose an operational definition of Active and Healthy Ageing and tools that may be used for this definition. The current paper gives a summary of the plenary presentations that were given during the meeting.
    European geriatric medicine 12/2014; 5(6):406-415. DOI:10.1016/j.eurger.2014.12.006 · 0.55 Impact Factor
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    ABSTRACT: Background Acute respiratory distress syndrome (ARDS) is a life-threating condition with high morbidity and mortality. Inflammation is the main factor in the pathogenesis of ARDS. Therefore systemic corticosteroids are a rational therapeutic approach, but the effect of corticosteroids is still unclear. In this study, we looked at the effects of corticosteroids in ventilated sheep with ARDS, induced by lung lavage. Methods We performed a prospective, randomised study in 64 ventilated sheep with ARDS, to evaluate the effect of corticosteroids and oxygen concentration on gas exchange and lung injury. Oxygenation index (OI) and ventilation efficacy index (VEI) were calculated to evaluate gas exchange. Lung injury was assessed by inflammatory response in broncho-alveolar lavage fluid (BALF) and plasma and histology of the lung. Results OI, VEI, lung inflammation, surfactant production, or lung histology was not influenced by corticosteroids. In the 100 % oxygen groups, OI was higher and total number of cells and disaturated phospholipids were lower in BALF. Conclusion Our study showed that corticosteroids did not influence inflammation in early phase ARDS and that hyperoxia aggravated lung injury which could not be modulated by dexamethasone in early phase ARDS.
    Beiträge zur Klinik der Tuberkulose 12/2014; 193(1). DOI:10.1007/s00408-014-9670-x · 2.17 Impact Factor
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    ABSTRACT: RationaleMineral particles in the lung cause inflammation and silicosis. In myeloid and bronchial epithelial cells the inflammasome plays a role in responses to crystalline silica. Thioredoxin (TRX) and its inhibitory protein TRX-interacting protein link oxidative stress with inflammasome activation. We investigated inflammasome activation by crystalline silica polymorphs and modulation by TRX in vitro, as well as its localization and the importance of silica surface reactivity in rats.Methods We exposed bronchial epithelial cells and differentiated macrophages to silica polymorphs quartz and cristobalite and measured caspase-1 activity as well as the release of IL-1beta, bFGF and HMGB1; including after TRX overexpression or treatment with recombinant TRX. Rats were intratracheally instilled with vehicle control, Dörentruper quartz (DQ12) or DQ12 coated with polyvinylpyridine N-oxide. At days 3, 7, 28, 90, 180 and 360 five animals per treatment group were sacrificed. Hallmarks of silicosis were assessed with Haematoxylin-eosin and Sirius Red stainings. Caspase-1 activity in the bronchoalveolar lavage and caspase-1 and IL-1ß localization in lung tissue were determined using Western blot and immunohistochemistry (IHC).ResultsSilica polymorphs triggered secretion of IL-1ß, bFGF and HMGB1 in a surface reactivity dependent manner. Inflammasome readouts linked with caspase-1 enzymatic activity were attenuated by TRX overexpression or treatment. At day 3 and 7 increased caspase-1 activity was detected in BALF of the DQ12 group and increased levels of caspase-1 and IL-1ß were observed with IHC in the DQ12 group compared to controls. DQ12 exposure revealed silicotic nodules at 180 and 360 days. Particle surface modification markedly attenuated the grade of inflammation and lymphocyte influx and attenuated the level of inflammasome activation, indicating that the development of silicosis and inflammasome activation is determined by crystalline silica surface reactivity.Conclusion Our novel data indicate the pivotal role of surface reactivity of crystalline silica to activate the inflammasome in cultures of both epithelial cells and macrophages. Inhibitory capacity of the antioxidant TRX to inflammasome activation was evidenced. DQ12 quartz exposure induced acute and chronic functional activation of the inflammasome in the heterogeneous cell populations of the lung in associated with its crystalline surface reactivity.
    Particle and Fibre Toxicology 11/2014; 11(1):58. DOI:10.1186/s12989-014-0058-0 · 6.99 Impact Factor
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    ABSTRACT: This European Respiratory Society (ERS) statement provides a comprehensive overview on physical activity in patients with chronic obstructive pulmonary disease (COPD). A multidisciplinary Task Force of experts representing the ERS Scientific Group 01.02 "Rehabilitation and Chronic Care" determined the overall scope of this statement through consensus. Focused literature reviews were conducted in key topic areas and the final content of this Statement was agreed upon by all members. The current knowledge regarding physical activity in COPD is presented, including the definition of physical activity, the consequences of physical inactivity on lung function decline and COPD incidence, physical activity assessment, prevalence of physical inactivity in COPD, clinical correlates of physical activity, effects of physical inactivity on hospitalisations and mortality, and treatment strategies to improve physical activity in patients with COPD. This Task Force identified multiple major areas of research that need to be addressed further in the coming years. These include, but are not limited to, the disease-modifying potential of increased physical activity, and to further understand how improvements in exercise capacity, dyspnoea and self-efficacy following interventions may translate into increased physical activity. The Task Force recommends that this ERS statement should be reviewed periodically (e.g. every 5-8 years).
    European Respiratory Journal 10/2014; DOI:10.1183/09031936.00046814 · 7.13 Impact Factor
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    ABSTRACT: Occupational and environmental exposures to airborne asbestos and silica are associated with the development of lung fibrosis in the forms of asbestosis and silicosis, respectively. However, both diseases display distinct pathological presentations, likely associated with differences in gene expression induced by different mineral structures, composition and bio-persistent properties. We hypothesized that effects of mineral exposure in the airway epithelium may dictate deviating molecular events that may explain the different pathologies of asbestosis vs. silicosis. Using robust gene expression-profiling in conjunction with in-depth pathway analysis, we assessed early (24 h) alterations in gene expression associated with crocidolite asbestos or cristobalite silica exposures in primary human bronchial epithelial cells (NHBE). Observations were confirmed in an immortal human bronchial epithelial cell line (BEAS-2B) by QRT-PCR and protein assays. Utilization of overall gene expression, unsupervised hierarchical cluster analysis and integrated pathway analysis revealed gene alterations that were common to both minerals or unique to either mineral. Our findings reveal that both minerals had potent effects on genes governing cell adhesion/migration, inflammation, and cellular stress, key features of fibrosis. Asbestos exposure was most specifically associated with aberrant cell proliferation and carcinogenesis, whereas silica exposure was highly associated with additional inflammatory responses, as well as pattern recognition, and fibrogenesis. These findings illustrate the use of gene-profiling as a means to determine early molecular events that may dictate pathological processes induced by exogenous cellular insults. In addition, it is a useful approach for predicting the pathogenicity of potentially harmful materials.
    Human Molecular Genetics 10/2014; 24(5). DOI:10.1093/hmg/ddu551 · 6.68 Impact Factor
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    ABSTRACT: In COPD, matrix remodeling contributes to airflow limitation. Recent evidence suggests that next to fibroblasts, the process of epithelial-mesenchymal transition can contribute to matrix remodeling. CSE has been shown to induce EMT in lung epithelial cells, but the signaling mechanisms involved are largely unknown and subject of this study. EMT was assessed in A549 and BEAS2B cells stimulated with CSE by qPCR, Western blotting and immunofluorescence for epithelial and mesenchymal markers, as were collagen production, cell adhesion and barrier integrity as functional endpoints. Involvement of TGF-β and HIF1α signaling pathways were investigated. In addition, mouse models were used to examine the effects of CS on hypoxia signaling and of hypoxia per se on mesenchymal expression. CSE induced EMT characteristics in A549 and BEAS2B cells, evidenced by decreased expression of epithelial markers and a concomitant increase in mesenchymal marker expression after CSE exposure. Furthermore cells that underwent EMT showed increased production of collagen, decreased adhesion and disrupted barrier integrity. The induction of EMT was found to be independent of TGF-β signaling. On the contrary, CS was able to induce hypoxic signaling in A549 and BEAS2B cells as well as in mice lung tissue. Importantly, HIF1α knock-down prevented induction of mesenchymal markers, increased collagen production and decreased adhesion after CSE exposure, data that are in line with the observed induction of mesenchymal marker expression by hypoxia in vitro and in vivo. Together these data provide evidence that both bronchial and alveolar epithelial cells undergo a functional phenotypic shift in response to CSE exposure which can contribute to increased collagen deposition in COPD lungs. Moreover, HIF1α signaling appears to play an important role in this process.
    PLoS ONE 10/2014; 9(10):e107757. DOI:10.1371/journal.pone.0107757 · 3.53 Impact Factor
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    ABSTRACT: Background Respiratory infections are a major cause of morbidity and mortality worldwide. A high percentage of all respiratory tract infections are caused by RNA viruses. Real-time PCR is a highly sensitive method for the detection of respiratory viruses in clinical samples. A good RNA isolation protocol is of high importance, since RNA is more unstable than DNA and many clinical samples contain RNAses. Objectives To evaluate the performance of three different RNA extraction protocols for the extraction of respiratory viral RNA from sputum samples obtained from patients with the suspicion of a viral respiratory tract infection. Study design A total of 50 sputum samples, PCR positive for a respiratory RNA virus, were used for viral RNA isolation with the phenol/chloroform method, RTP®DNA/RNA virus mini kit and the automated MagNa Pure LC (MPLC) extraction system. After isolation, real-time PCR was performed for the detection of viral RNA in the sputum samples. Results The MPLC extraction increased the detection probability from 82% (phenol/chloroform) and 86% (RTP®DNA/RNA virus mini kit) to 94%. In 16% the RTP®DNA/RNA virus mini kit resulted in lower Ct values compared to the phenol/chloroform method, while in 32% the phenol/chloroform resulted in lower Ct values. Conclusions The extraction of viral RNA performed with the MPLC extraction method was superior to the extraction with the RTP®DNA/RNA virus mini kit and to the extraction with phenol/chloroform. In general, there was no difference in the detection of viral RNA between the phenol/chloroform extraction method and the RTP®DNA/RNA virus mini kit.
    Journal of Clinical Virology 10/2014; 61(2). DOI:10.1016/j.jcv.2014.07.012 · 3.47 Impact Factor
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    ABSTRACT: Remodeling in COPD has at least two dimensions: small airway wall thickening and destruction of alveolar walls. The aim of this study was to characterize and assess similarities in alveolar and small airway wall matrix remodeling in chronic COPD models. From this comparative characterization of matrix remodeling we derived and elaborated underlying mechanisms to the matrix changes reported in COPD. Lung tissue sections of chronic models for COPD, either induced by exposure to cigarette smoke, chronic intratracheal LPS instillation or local TNF expression (SPC-TNFα mice), were stained for elastin, collagen and hyaluronan. Furthermore TNFα, MMP2, 9 and 12 mRNA expression was analyzed using qPCR and localized using immunohistochemistry. Both collagen and hyaluronan were increased in alveolar and small airway walls of all three models. Interestingly, elastin contents were differentially affected, with a decrease in both alveolar and airway walls in SPC-TNFα mice. Furthermore TNFα, and MMP2 and 9 mRNA and protein levels were found to be increased in alveolar walls and around airway walls only in SPC-TNFα mice. We show that only SPC-TNFα mice show changes in elastin remodeling which are comparable to what has been observed in COPD patients. This reveals that the SPC-TNFα model is a suitable model to study processes underlying matrix remodeling and in particular elastin breakdown as seen in COPD. Furthermore we indicate a possible role for MMP2 and MMP9 in the breakdown of elastin in airways and alveoli of SPC-TNFα mice.
    AJP Lung Cellular and Molecular Physiology 08/2014; 307(7). DOI:10.1152/ajplung.00116.2014 · 4.04 Impact Factor
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    ABSTRACT: Depression is highly prevalent among patients with Chronic Obstructive Pulmonary Disease (COPD). The relationship of depression with systemic inflammation in COPD remains unknown. The objective of this observational study was to compare depression scores at baseline and after 36 months follow-up between COPD patients with persistent systemic inflammation (PSI) and never inflamed patients (NI) in the ECLIPSE cohort.
    Respiratory Medicine 08/2014; DOI:10.1016/j.rmed.2014.07.013 · 2.92 Impact Factor
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    ABSTRACT: Rationale and Objectives: Computed tomography (CT) of the chest can be used to assess pectoralis muscle area (PMA) and subcutaneous adipose tissue (SAT) area. Adipose tissue content is associated with inflammatory mediators in chronic obstructive pulmonary disease (COPD) subjects. Based on gender differences in body composition, we aimed to assess the hypothesis that in subjects with COPD, the relationships between PMA, SAT, and blood biomarkers of inflammation differ by gender. Materials and Methods: We compared chest CT measures of PMA and SAT on a single slice at aortic arch and supraesternal notch levels from 73 subjects (28 women) with COPD between genders. The relationships of PMA and SAT area to biomarkers were assessed using within-gender regression models. Results: Women had a lesser PMA and a greater SAT area than men (difference-range for PMA, 13.3-22.8 cm(2); for SAT, 11.8-12.4 cm(2); P < .05 for all comparisons) at both anatomic levels. These differences in PMA and SAT remained significant after adjustment for age and body mass index. Within-gender regression models adjusted for age showed that SAT was directly associated with C-reactive protein (for aortic arch level, P = .04) and fibrinogen (for both anatomic locations, P = .003) only in women, whereas PMA was not associated with any biomarkers in either gender. Conclusions: It appears that in subjects with COPD, there are gender-based differences in the relationships between subcutaneous adipose tissue and inflammatory biomarkers.
    Academic Radiology 08/2014; 21(10). DOI:10.1016/j.acra.2014.05.013 · 2.08 Impact Factor

Publication Stats

20k Citations
3,114.29 Total Impact Points

Institutions

  • 1988–2015
    • Maastricht Universitair Medisch Centrum
      • Central Diagnostic Laboratory
      Maestricht, Limburg, Netherlands
  • 2011–2014
    • CIRO
      • Program Development Centre
      Roermond, Limburg, Netherlands
    • Philipps University of Marburg
      Marburg, Hesse, Germany
  • 1986–2014
    • Maastricht University
      • • Department of Respiratory Medicine
      • • Department of Respiratory Medicine
      • • Humane Biologie
      Maestricht, Limburg, Netherlands
  • 2012
    • Biometrics
      Saint-Clair, Île-de-France, France
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2010
    • Ghent University
      • VIB Department of Medical Protein Research
      Gand, Flemish, Belgium
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2009
    • Universitair Ziekenhuis Ghent
      Gand, Flanders, Belgium
    • Catharina Hospital
      Eindhoven, North Brabant, Netherlands
  • 2006–2008
    • Academic Medical Center (AMC)
      Amsterdamo, North Holland, Netherlands
  • 2007
    • Cardiff University
      Cardiff, Wales, United Kingdom
  • 2005
    • Leiden University
      Leyden, South Holland, Netherlands
    • University of Groningen
      Groningen, Groningen, Netherlands
    • University of Vermont
      • Department of Pathology
      Burlington, VT, United States
  • 2000–2001
    • Zeeuws Radiotherapeutisch Instituut
      Flushing, Zeeland, Netherlands
  • 1997
    • Open Universiteit Nederland
      Heerlen, Limburg, Netherlands
  • 1989–1996
    • Landesklinikum Horn
      Horn, Lower Austria, Austria
  • 1995
    • Wageningen University
      Wageningen, Gelderland, Netherlands
    • Transnationale Universiteit Limburg
      Mississippi, United States