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Search Results: 1 - 10 of 220054 matches for " Frans C. Schuit "
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Modeling the asymmetric evolution of a mouse and rat-specific microRNA gene cluster intron 10 of the Sfmbt2 gene
Stefan Lehnert, Vladimir Kapitonov, Pushpike J Thilakarathne, Frans C Schuit
BMC Genomics , 2011, DOI: 10.1186/1471-2164-12-257
Abstract: We studied a large miRNA gene cluster in intron 10 of the mouse Sfmbt2 gene using bioinformatic tools.Mice and rats are unique to harbor a 55-65 Kb DNA sequence in intron 10 of the Sfmbt2 gene. This intronic region is rich in regularly repeated B1 retrotransposons together with inverted self-complementary CA/TG microsatellites. The smallest repeats unit, called MSHORT1 in the mouse, was duplicated 9 times in a tandem head-to-tail array to form 2.5 Kb MLONG1 units. The center of the mouse miRNA gene cluster consists of 13 copies of MLONG1. BLAST analysis of MSHORT1 in the mouse shows that the repeat unit is unique for intron 10 of the Sfmbt2 gene and suggest a dual phase model for growth of the miRNA gene cluster: arrangment of 10 MSHORT1 units into MLONG1 and further duplication of 13 head-to-tail MLONG1 units in the center of the miRNA gene cluster. Rats have a similar arrangment of repeat units in intron 10 of the Sfmbt2 gene. The discrepancy between 65 miRNA genes in the mouse cluster as compared to only 1 miRNA gene in the corresponding rat repeat cluster is ascribed to sequence differences between MSHORT1 and RSHORT1 that result in lateral-shifted, less-stable miRNA precursor hairpins for RSHORT1.Our data provides new evidence for the emerging concept that lineage-specific retroposons have played an important role in the birth of new miRNA genes during evolution. The large difference in the number of miRNA genes in two closely related species (65 versus 1, mice versus rats) indicates that this species-specific evolution can be a rapid process.Micro RNAs (miRNA's) are 19 to 22 nt long, non-coding, single-stranded RNAs that can fine-tune the expression of protein-encoding genes [1,2]. One example is the post-transcriptional repression of mRNA targets involving the so called miRNA "seed" which is nt 2-8 of the mature miRNA which recognizes complementary bases in the 3'untranslated region of the mRNA target [3]. miRNA genes form primary transcripts that are convert
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.
COUP-TFII Controls Mouse Pancreatic β-Cell Mass through GLP-1-β-Catenin Signaling Pathways
Marie Boutant, Oscar Henrique Pereira Ramos, Cécile Tourrel-Cuzin, Jamileh Movassat, Anissa Ilias, David Vallois, Julien Planchais, Jean-Paul Pégorier, Frans Schuit, Patrice X. Petit, Pascale Bossard, Kathrin Maedler, Anne Grapin-Botton, Mireille Vasseur-Cognet
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030847
Abstract: Background The control of the functional pancreatic β-cell mass serves the key homeostatic function of releasing the right amount of insulin to keep blood sugar in the normal range. It is not fully understood though how β-cell mass is determined. Methodology/Principal Findings Conditional chicken ovalbumin upstream promoter transcription factor II (COUP-TFII)-deficient mice were generated and crossed with mice expressing Cre under the control of pancreatic duodenal homeobox 1 (pdx1) gene promoter. Ablation of COUP-TFII in pancreas resulted in glucose intolerance. Beta-cell number was reduced at 1 day and 3 weeks postnatal. Together with a reduced number of insulin-containing cells in the ductal epithelium and normal β-cell proliferation and apoptosis, this suggests decreased β-cell differentiation in the neonatal period. By testing islets isolated from these mice and cultured β-cells with loss and gain of COUP-TFII function, we found that COUP-TFII induces the expression of the β-catenin gene and its target genes such as cyclin D1 and axin 2. Moreover, induction of these genes by glucagon-like peptide 1 (GLP-1) via β-catenin was impaired in absence of COUP-TFII. The expression of two other target genes of GLP-1 signaling, GLP-1R and PDX-1 was significantly lower in mutant islets compared to control islets, possibly contributing to reduced β-cell mass. Finally, we demonstrated that COUP-TFII expression was activated by the Wnt signaling-associated transcription factor TCF7L2 (T-cell factor 7-like 2) in human islets and rat β-cells providing a feedback loop. Conclusions/Significance Our findings show that COUP-TFII is a novel component of the GLP-1 signaling cascade that increases β-cell number during the neonatal period. COUP-TFII is required for GLP-1 activation of the β-catenin-dependent pathway and its expression is under the control of TCF7L2.
Detection of novel 3' untranslated region extensions with 3' expression microarrays
Lieven Thorrez, Leon-Charles Tranchevent, Hui Chang, Yves Moreau, Frans Schuit
BMC Genomics , 2010, DOI: 10.1186/1471-2164-11-205
Abstract: Based on our dataset encompassing expression in 22 different murine tissues, we identified 845 genes with predicted 3'UTR extensions. These extensions have a similar conservation as known 3'UTRs, which is distinctly higher than intergenic regions. We verified 8 of the predictions by PCR and found all of the predicted regions to be expressed. The method can be extended to other 3' expression microarray platforms as we demonstrate with human data. Additional confirming evidence was obtained from public paired end read data.We show that many genes have 3'UTR regions extending beyond currently known gene regions and provide a method to identify such regions based on microarray expression data. Since 3' UTR contain microRNA binding sites and other stability determining regions, identification of the full length 3' UTR is important to elucidate posttranscriptional regulation.The 3' untranslated region (3'UTR) of a gene does not belong to the protein coding sequence, however it plays an important role in posttranscriptional regulation [1]. This region of the transcript typically contains binding sites for proteins and microRNAs which influence the stability, localization and translation of the messenger RNA [2]. Not only the presence of microRNAs and RNA binding proteins themselves determines the mRNA fate, but also the presence of their binding sites on the transcript is critical for the specific regulation to occur. Therefore it is important to identify the 3' ends of the transcript.Delineation of the 3' end of a transcript so far relied on ESTs or high-throughput sequencing of full-length cDNAs in various cell lines or in one specific tissue [3,4]. Paired-End diTag (PET) analysis, during which short fragments from both transcript ends are extracted, concatenated and sequenced, possesses a unique capability to accurately and efficiently characterize transcript boundaries. This approach was demonstrated on 2 human cancer cell lines [5]. However it has recently been shown
Modulation of Protein Fermentation Does Not Affect Fecal Water Toxicity: A Randomized Cross-Over Study in Healthy Subjects
Karen Windey, Vicky De Preter, Thierry Louat, Frans Schuit, Jean Herman, Greet Vansant, Kristin Verbeke
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0052387
Abstract: Objective Protein fermentation results in production of metabolites such as ammonia, amines and indolic, phenolic and sulfur-containing compounds. In vitro studies suggest that these metabolites might be toxic. However, human and animal studies do not consistently support these findings. We modified protein fermentation in healthy subjects to assess the effects on colonic metabolism and parameters of gut health, and to identify metabolites associated with toxicity. Design After a 2-week run-in period with normal protein intake (NP), 20 healthy subjects followed an isocaloric high protein (HP) and low protein (LP) diet for 2 weeks in a cross-over design. Protein fermentation was estimated from urinary p-cresol excretion. Fecal metabolite profiles were analyzed using GC-MS and compared using cluster analysis. DGGE was used to analyze microbiota composition. Fecal water genotoxicity and cytotoxicity were determined using the Comet assay and the WST-1-assay, respectively, and were related to the metabolite profiles. Results Dietary protein intake was significantly higher during the HP diet compared to the NP and LP diet. Urinary p-cresol excretion correlated positively with protein intake. Fecal water cytotoxicity correlated negatively with protein fermentation, while fecal water genotoxicity was not correlated with protein fermentation. Heptanal, 3-methyl-2-butanone, dimethyl disulfide and 2-propenyl ester of acetic acid are associated with genotoxicity and indole, 1-octanol, heptanal, 2,4-dithiapentane, allyl-isothiocyanate, 1-methyl-4-(1-methylethenyl)-benzene, propionic acid, octanoic acid, nonanoic acid and decanoic acid with cytotoxicity. Conclusion This study does not support a role of protein fermentation in gut toxicity. The identified metabolites can provide new insight into colonic health. Trial Registration ClinicalTrial.gov NCT01280513
Blood Volume Status in Patients with Chronic Fatigue Syndrome: Relation to Complaints  [PDF]
C. (Linda) M. C. van Campen, Frans C. Visser
International Journal of Clinical Medicine (IJCM) , 2018, DOI: 10.4236/ijcm.2018.911067
Abstract: Four studies have compared a possible decrease in circulating blood volume in Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) patients when compared to a healthy population. A more recent study has proven a correlation between RBC volume and OI in chronic OI patients without being diagnosed ME/CFS. The aim of the present study was to relate measured blood, RBC and plasma volumes (absolute and percent normalized) with the orthostatic intolerance complaints in ME/CFS patients. In the included 11 female ME/CFS patients, percentage decrease in normalized blood, RBC and plasma volume was similar for all three components: 83% ± 12%, 83% ± 12% and 83% ± 11%, respectively. In patients with a clinical suspicion of OI (n = 7) all 3 volume components were significantly lower compared to patients without clinical suspicion of OI (n = 4). The difference percentage to normalized Blood volume was 77(7) vs 94(10) (p-value < 0.02), difference percentage to normalized RBC volume was 76(7) vs 96(10) (p-value < 0.01) and difference percentage to normalized plasma volume was 77(7) vs 93(10) (p-value < 0.05) in OI present versus absent. Plasma volumes were plotted against RBC volumes: the relation found was RBC volume = 0.99* Plasma volume + 1.55; p < 0.001; r = 0.90. In line with literature data, this pilot study shows that total blood volume and its components: RBC and plasma volume may be reduced in ME/CFS patients, especially in the presence of a clinical suspicion of OI.
Effect of an individually tailored one-year energy balance programme on body weight, body composition and lifestyle in recent retirees: a cluster randomised controlled trial
Andrea Werkman, Paul JM Hulshof, Annette Stafleu, Stef PJ Kremers, Frans J Kok, Evert G Schouten, Albertine J Schuit
BMC Public Health , 2010, DOI: 10.1186/1471-2458-10-110
Abstract: A randomised controlled trial was conducted among recent retirees (N = 413; mean age 59.5 years). Outcome measures were assessed using anthropometry, bio-impedance, blood pressure measurement and questionnaires.Waist circumference, body weight and blood pressure decreased significantly in men of the intervention and control group, but no significant between-group-differences were observed at 12 or at 24-months follow-up. A significant effect of the programme was only observed on waist circumference (-1.56 cm (95%CI: -2.91 to -0.21)) at 12 month follow up among men with low education (n = 85). Physical activity and dietary behaviours improved in both the intervention and control group during the intervention period. Although, these behaviours changed more favourably in the intervention group, these between-group-differences were not statistically significant.The multifaceted computer-tailored programme for recent retirees did not appear to be effective. Apparently the transition to occupational retirement and/or participation in the study had a greater impact than the intervention programme.Clinical Trials NCT00122213.The increasing prevalence of overweight and obesity also affects the older population [1] and prevention of weight gain is also important in this population [2,3]. Weight gain is more common during transitional stages [3], such as occupational retirement at the sixth decade. Changes in physical activity and dietary behaviour, possibly induced by the retirement, contribute to this phenomenon. Moreover, with biological ageing, fat mass (mostly abdominal fat mass) increases and fat-free mass (mostly muscle mass) decreases. However, the extent differs between men and women and does not necessarily coincide with weight gain [1,4,5]. Abdominal obesity is associated with increased risk for cardiovascular diseases, diabetes mellitus type II and other chronic diseases [6]. Hence, the period of occupational retirement is a good moment to intervene, because it may
Study protocol of a cluster randomised controlled trial investigating the effectiveness of a tailored energy balance programme for recent retirees
Andrea Werkman, Albertine J Schuit, Lydia Kwak, Stef PJ Kremers, Tommy LS Visscher, Frans J Kok, Evert G Schouten
BMC Public Health , 2006, DOI: 10.1186/1471-2458-6-293
Abstract: A systematic and stepwise approach (Intervention Mapping) is used to develop a low-intensity energy balance intervention programme for recent retirees. This one-year, low-intensity multifaceted programme aims to prevent accumulation of abdominal fat mass and general weight gain by increasing awareness of energy balance and influencing related behaviours of participants' preference. These behaviours are physical activity, fibre intake, portion size and fat consumption. The effectiveness of the intervention programme is tested in a cluster randomised controlled trial. Measurements of anthropometry, physical activity, energy intake, and related psychosocial determinants are performed at baseline and repeated at 6 months for intermediate effect, at 12 months to evaluate short-term intervention effects and at 24 months to test the sustainability of the effects.This intervention programme is unique in its focus on retirees and energy balance. It aims at increasing awareness and takes into account personal preferences of the users by offering several options for behaviour change. Moreover, the intervention programme is evaluated at short-term and long-term and includes consecutive outcome measures (determinants, behaviour and body composition).This study is performed as part of the Netherlands Heart Foundation 'Netherlands Research programme for weight Gain prevention' (NHF-NRG). This multidisciplinary programme aims to gain insight into behavioural determinants of weight gain and to identify potentially effective methods and strategies for the prevention of weight gain in distinct target groups: adolescents, young adults and recent retirees [1].Overweight and obesity are associated with chronic conditions such as diabetes, hypertension, cardiovascular diseases and certain types of cancer, and thus considered a major public health concern [2]. Many attempts have been made to treat overweight and obesity and although these attempts show short term weight loss in most subjec
Gene Expression Profiling of Early Hepatic Stellate Cell Activation Reveals a Role for Igfbp3 in Cell Migration
Inge Mannaerts, Ben Schroyen, Stefaan Verhulst, Leentje Van Lommel, Frans Schuit, Marc Nyssen, Leo A. van Grunsven
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0084071
Abstract: Background Scarring of the liver is the result of prolonged exposure to exogenous or endogenous stimuli. At the onset of fibrosis, quiescent hepatic stellate cells (HSCs) activate and transdifferentiate into matrix producing, myofibroblast-like cells. Aim and methods To identify key players during early HSC activation, gene expression profiling was performed on primary mouse HSCs cultured for 4, 16 and 64 hours. Since valproic acid (VPA) can partly inhibit HSC activation, we included VPA-treated cells in the profiling experiments to facilitate this search. Results Gene expression profiling confirmed early changes for known genes related to HSC activation such as alpha smooth muscle actin (Acta2), lysyl oxidase (Lox) and collagen, type I, alpha 1 (Col1a1). In addition we noticed that, although genes which are related to fibrosis change between 4 and 16 hours in culture, most gene expression changes occur between 16 and 64 hours. Insulin-like growth factor binding protein 3 (Igfbp3) was identified as a gene strongly affected by VPA treatment. During normal HSC activation Igfbp3 is up regulated and this can thus be prevented by VPA treatment in vitro and in vivo. siRNA-mediated silencing of Igfbp3 in primary mouse HSCs induced matrix metalloproteinase (Mmp) 9 mRNA expression and strongly reduced cell migration. The reduced cell migration after Igfbp3 knock-down could be overcome by tissue inhibitor of metalloproteinase (TIMP) 1 treatment. Conclusion Igfbp3 is a marker for culture-activated HSCs and plays a role in HSC migration. VPA treatment prevents Igfbp3 transcription during activation of HSCs in vitro and in vivo.
A comment on Thomas K. Burch’s paper “Does demography need differential equations?”
Frans J.C. Willekens
Canadian Studies in Population , 2011,
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