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    <title>Dagnelie, P.C.</title>
    <link>http://repub.eur.nl/res/aut/7014/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Biomarker Evaluation Does Not Confirm Efficacy of Computer-tailored Nutrition Education (Article)</title>
      <link>http://repub.eur.nl/res/pub/31047/</link>
      <pubDate>2011-09-01T00:00:00Z</pubDate>
      <description>Objective: To evaluate the efficacy of computer-tailored nutrition education with objective outcome measures. Design: A 3-group randomized, controlled trial with posttests at 1 and 6 months post-intervention. Setting: Worksites and 2 neighborhoods in the urban area of Rotterdam. Participants: A convenience sample of healthy Dutch adults (n = 442). Interventions: A computer-tailored intervention delivered on CD-ROM; a computer-tailored intervention delivered in print; and a generic information condition. Main Outcome Measures: Blood lipids (total, high-density lipoprotein, and low-density lipoprotein cholesterol, and triacylglycerol) were measured by analyzing venous blood samples. Analysis: Linear mixed model procedure. Results: There were no significant differences among the 3 intervention groups in total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triacylglycerol. Conclusions and Implications: Contrary to results based on self-report data, no effects of the computer-tailored interventions were found based on objective outcomes. This contradiction calls for a critical reflection on the use of computer-tailored nutrition education interventions and the need to improve those interventions. Furthermore, this study indicates that feasible methods are needed to objectively assess the impact of computer-tailored nutrition education interventions in free-living subjects. </description>
    </item> <item>
      <title>Mortality in inflammatory bowel disease in the Netherlands 1991-2002: Results of a population-based study: The IBD South-Limburg cohort (Article)</title>
      <link>http://repub.eur.nl/res/pub/20941/</link>
      <pubDate>2010-08-24T00:00:00Z</pubDate>
      <description>Background: The aim was to evaluate overall and disease-specific mortality in a population-based inflammatory bowel disease (IBD) cohort in the Netherlands, as well as risk factors for mortality. Methods: IBD patients diagnosed between 1 January 1991 and 1 January 2003 were included. Standardized mortality ratios (SMRs) were calculated overall and with regard to causes of death, gender, as well as age, phenotype, smoking status at diagnosis, and medication use. Results: At the censoring date, 72 out of 1187 patients had died (21 Crohn's disease [CD], 47 ulcerative colitis [UC], and 4 indeterminate colitis [IC] patients). The SMR (95% confidence interval [CI]) was 1.1 (0.7-1.6) for CD, 0.9 (0.7-1.2) for UC and 0.7 (0.2-1.7) for IC. Disease-specific mortality risk was significantly increased for gastrointestinal (GI) causes of death both in CD (SMR 7.5, 95% CI: 2.8-16.4) and UC (SMR 3.4, 95% CI: 1.4-7.0); in CD patients, especially in patients &lt;40 years of age at diagnosis. For UC, an increased SMR was noted in female patients and in patients &lt;19 years and &gt;80 years at diagnosis. In contrast, UC patients had a decreased mortality risk from cancer (SMR 0.5, 95% CI; 0.2-0.9). Conclusions: In this population-based IBD study, mortality in CD, UC, and IC was comparable to the background population. The increased mortality risk for GI causes might reflect complicated disease course, with young and elderly patients at diagnosis needing intensive follow-up. Caution in interpreting the finding on mortality risk from cancer is needed as follow-up was probably to short to observe IBD-related cancers.</description>
    </item> <item>
      <title>Examining the minimal required elements of a computer-tailored intervention aimed at dietary fat reduction: Results of a randomized controlled dismantling study (Article)</title>
      <link>http://repub.eur.nl/res/pub/14790/</link>
      <pubDate>2008-10-01T00:00:00Z</pubDate>
      <description>This study investigated the minimally required feedback elements of a computer-tailored dietary fat reduction intervention to be effective in improving fat intake. In all 588 Healthy Dutch adults were randomly allocated to one of four conditions in an randomized controlled trial: (i) feedback on dietary fat intake [personal feedback (P feedback)], (ii) P feedback and feedback on one's own behavior relative to that of peers [personal-normative feedback (PN feedback)], (iii) PN feedback and practical suggestions on how to change fat intake [personal - normative - action feedback (PNA feedback)] and (iv) generic information. Data on fat intake, awareness of one's own fat intake and intention to change were collected 1 and 6 months post-intervention. Between-group differences were tested with analysis of variance. Among respondents with high fat intakes at baseline (risk consumers) and those who underestimated their fat intake at baseline (underestimators), differences in awareness and (saturated) fat intake were found between the generic and PNA feedback conditions. Compared with generic information P feedback was more effective in changing awareness and intention among the underestimators, and PN feedback was more effective in changing intention among both risk consumers and underestimators. In conclusion, the combination of personal, normative and action feedback is required for inducing change in fat intake and improving awareness of fat intake.</description>
    </item> <item>
      <title>Weight loss and elevated gluconeogenesis from alanine in lung cancer patients (Article)</title>
      <link>http://repub.eur.nl/res/pub/9236/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>BACKGROUND: The role of gluconeogenesis from protein in the pathogenesis
          of weight loss in lung cancer is unclear. OBJECTIVE: Our aim was to study
          gluconeogenesis from alanine in lung cancer patients and to analyze its
          relation to the degree of weight loss. DESIGN: In this cross-sectional
          study, we used primed-constant infusions of [6,6-(2)H(2)]-D-glucose and
          [3-(13)C]-L-alanine to assess whole-body glucose and alanine turnover and
          gluconeogenesis from alanine in weight-losing (WL, n = 9) and
          weight-stable (WS, n = 10) lung cancer patients and healthy control (n =
          15) subjects. RESULTS: Energy intake and plasma alanine concentrations did
          not differ significantly among the subject groups. Mean (+/-SEM)
          whole-body glucose production was significantly higher in WL than in WS
          and control subjects (0.74 +/- 0.06 compared with 0.55 +/- 0.04 and 0.51
          +/- 0.04 mmol*kg(-)(1)*h(-)(1), respectively, P &lt; 0.01). Alanine turnover
          was significantly elevated in WL compared with WS and control subjects
          (0.57 +/- 0.04 compared with 0.42 +/- 0.05 and 0.40 +/- 0.03
          mmol*kg(-)(1)*h(-)(1), respectively, P &lt; 0.01). Gluconeogenesis from
          alanine was significantly higher in WL than in WS and control subjects
          (0.47 +/- 0.04 compared with 0.31 +/- 0.04 and 0.29 +/- 0.04
          mmol*kg(-)(1)*h(-)(1), respectively, P &lt; 0.01). The degree of weight loss
          was positively correlated with glucose and alanine turnover and with
          gluconeogenesis from alanine (r = 0.45 for all, P &lt; 0.01). CONCLUSIONS:
          Aberrant glucose and alanine metabolism occurred in WL lung cancer
          patients. These changes were related to the degree of weight loss and not
          to the presence of lung cancer per se.</description>
    </item> <item>
      <title>Randomized clinical trial of adenosine 5'-triphosphate in patients with advanced non-small-cell lung cancer (Article)</title>
      <link>http://repub.eur.nl/res/pub/9253/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>BACKGROUND: Extracellular adenosine 5'-triphosphate (ATP) is involved in
          the regulation of a variety of biologic processes, including
          neurotransmission, muscle contraction, and liver glucose metabolism, via
          purinergic receptors. In nonrandomized studies involving patients with
          different tumor types including non-small-cell lung cancer (NSCLC), ATP
          infusion appeared to inhibit loss of weight and deterioration of quality
          of life (QOL) and performance status. We conducted a randomized clinical
          trial to evaluate the effects of ATP in patients with advanced NSCLC
          (stage IIIB or IV). METHODS: Fifty-eight patients were randomly assigned
          to receive either 10 intravenous 30-hour ATP infusions, with the infusions
          given at 2- to 4-week intervals, or no ATP. Outcome parameters were
          assessed every 4 weeks until 28 weeks. Between-group differences were
          tested for statistical significance by use of repeated-measures analysis,
          and reported P values are two-sided. RESULTS: Twenty-eight patients were
          allocated to receive ATP treatment and 30 received no ATP. Mean weight
          changes per 4-week period were -1.0 kg (95% confidence interval [CI] =
          -1.5 to -0.5) in the control group and 0.2 kg (95% CI = -0.2 to +0.6) in
          the ATP group (P =.002). Serum albumin concentration declined by -1.2 g/L
          (95% CI= -2.0 to -0.4) per 4 weeks in the control group but remained
          stable (0.0 g/L; 95% CI = -0.3 to +0.3) in the ATP group (P =.006). Elbow
          flexor muscle strength declined by -5.5% (95% CI = -9.6% to -1. 4%) per 4
          weeks in the control group but remained stable (0.0%; 95% CI= -1.4% to
          +1.4%) in the ATP group (P =.01). A similar pattern was observed for knee
          extensor muscles (P =.02). The effects of ATP on body weight, muscle
          strength, and albumin concentration were especially marked in cachectic
          patients (P =.0002, P =.0001, and P =. 0001, respectively, for ATP versus
          no ATP). QOL score changes per 4-week period in the ATP group showed
          overall less deterioration than in the control group-physical scores
          (-0.2% versus -2.4%; P =. 0002); functional scores (+0.4% versus -5.5%; P
          =.02); psychologic scores (-0.7% versus -2.4%; P =.11); overall QOL score
          (+0.1% versus -3.5%; P =.0001). CONCLUSIONS: This randomized trial
          demonstrates that ATP has beneficial effects on weight, muscle strength,
          and QOL in patients with advanced NSCLC.</description>
    </item> <item>
      <title>Altered hepatic gluconeogenesis during L-alanine infusion in weight-losing lung cancer patients as observed by phosphorus magnetic resonance spectroscopy and turnover measurements (Article)</title>
      <link>http://repub.eur.nl/res/pub/9254/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>Profound alterations in host metabolism in lung cancer patients with
          weight loss have been reported, including elevated phosphomonoesters
          (PMEs) as detected by 31P magnetic resonance spectroscopy (MRS). In
          healthy subjects, infusion of L-alanine induced significant increases in
          hepatic PMEs and phosphodiesters (PDEs) due to rising concentrations of
          3-phosphoglycerate and phosphoenolpyruvate, respectively. The aim of the
          present study was to monitor these changes in the tumor-free liver of lung
          cancer patients during L-alanine infusion by means of simultaneous 31P MRS
          and turnover measurements. Twenty-one lung cancer patients without liver
          metastases with (CaWL) or without weight loss (CaWS), and 12 healthy
          control subjects were studied during an i.v. L-alanine challenge of
          1.4-2.8 mmol/kg followed by 2.8 mmol/kg/h for 90 min. Plasma L-alanine
          concentrations increased during alanine infusion, from 0.35-0.37 mM at
          baseline to 5.37 +/- 0.14 mM in the CaWL patients, 6.67 +/- 0.51 mM in the
          CaWS patients, and 8.47 +/- 0.88 mM in the controls (difference from
          baseline and between groups during alanine infusion, all P &lt; 0.001).
          Glucose turnover and liver PME levels at baseline were significantly
          elevated in the CaWL patients. Alanine infusion increased whole-body
          glucose turnover by 8 +/- 3% in the CaWS patients (P = 0.03), whereas no
          significant change occurred in the CaWL and controls. PME levels increased
          by 50 +/- 16% in controls (area under the curve, P &lt; 0.01) and by 87 +/-
          31% in the CaWS patients (P &lt; 0.05) after 45-90 min. In contrast, no
          significant changes in PME levels were observed in the CaWL patients.
          Plasma insulin concentrations increased during L-alanine infusion in all
          groups to levels that were lower in the CaWL patients than in the CaWS
          patients and controls (P &lt; 0.05). In lung cancer patients, but not in
          controls, changes in PME and PDE levels during alanine infusion were
          inversely correlated with their respective baseline levels (r = -0.82 and
          -0.86, respectively; P &lt; 0.001). In addition, changes in PMEs during
          alanine infusion in lung cancer patients were inversely correlated with
          the degree of weight loss (r = -0.54; P &lt; 0.05). This study demonstrates
          the presence of major alterations in the pathway of hepatic
          gluconeogenesis in weight-losing lung cancer patients, as shown by
          elevated glucose flux before and during L-alanine infusion, and by the
          increased PME and PDE levels, which reflect accumulation of gluconeogenic
          intermediates in these patients. Weight-stable lung cancer patients show
          accelerated increases in PME and PDE levels during L-alanine infusion,
          suggesting enhanced induction of the gluconeogenic pathway. Our results
          suggest altered gluconeogenic enzyme activities and elevated alanine
          uptake within the livers of weight-losing/weight-stable lung cancer
          patients.</description>
    </item> <item>
      <title>Dietary exposure to polychlorinated biphenyls and dioxins from infancy until adulthood: A comparison between breast-feeding, toddler, and long-term exposure (Article)</title>
      <link>http://repub.eur.nl/res/pub/8983/</link>
      <pubDate>1999-01-01T00:00:00Z</pubDate>
      <description>Food is the major source for polychlorinated biphenyl (PCB) and dioxin
          accumulation in the human body. Therefore, investigating food habits from
          early ages until reproductive age (25 years) is important in order to
          assess exposure risk for the next generation. The objective of this study
          was to assess the PCB/dioxin exposure and the relative contribution of
          different foods to total exposure during preschool age. Particularly, the
          importance of lactational PCB/dioxin exposure vs. dietary exposure until
          adulthood was investigated. A cohort of 207 children was studied from
          birth until preschool age. Based on 3 planar PCBs and 17
          2,3,7,8-substituted dibenzo-para-dioxins (PCDDs) and dibenzofurans (PCDFs)
          measured in breast milk, a model was developed to calculate the cumulative
          toxic equivalent (TEQ) intake during breast-feeding (0-1 year). In 3.
          5-year-old children, daily dietary intake of planar PCB-TEQ and dioxin-TEQ
          was measured with a validated food questionnaire. Cumulative TEQ intake
          from 1 to 5 years was estimated using the PCB- and dioxin-TEQ intake
          measured with the food questionnaire. Cumulative TEQ intake from 6 to 25
          years was estimated using national food consumption and contamination data
          of PCB- and dioxin-TEQ intake. In toddlers, dairy products contributed 43%
          to PCB-TEQ and 50% to dioxin-TEQ intake. Meat and meat products
          contributed 14% and 19%, respectively, and processed foods 23% and 15%,
          respectively. Breast-feeding for 6 months contributed to the cumulative
          PCB/dioxin TEQ intake until 25 years of age, 12% in boys and 14% in girls.
          The daily TEQ intake per kilogram body weight is 50 times higher in
          breast-fed infants and three times higher in toddlers than in adults.
          Long-term dietary exposure to PCBs and dioxins in men and women is partly
          due to breast-feeding (12 and 14%, respectively). After weaning, dairy
          products, processed foods, and meat are major contributors of PCB and
          dioxin accumulation until reproductive age. Instead of discouraging
          breast-feeding, maternal transfer of PCBs and dioxins to the next
          generation must be avoided by enforcement of strict regulations for PCB
          and dioxin discharge and by reducing consumption of animal products and
          processed foods in all ages.</description>
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