Archive for the ‘Scientific publication’ Category

CCL2 -2518 PROMOTER POLYMORPHISM AND A HIGH VASCULAR RISK SCORE ARE ASSOCIATED WITH IMPAIRED RENAL FUNCTION IN THE GENERAL POPULATION

donderdag, december 22nd, 2011
TitleCCL2 -2518 PROMOTER POLYMORPHISM AND A HIGH VASCULAR RISK SCORE ARE ASSOCIATED WITH IMPAIRED RENAL FUNCTION IN THE GENERAL POPULATION
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Year2005
Estimated date2005-06-30
CategoryScientific Publication
PlatformNone
DescriptionAbstract for the American Society of Nephrology, 2005.
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Influence of renal function on association of CCR2-64I with mortality in the general population

donderdag, december 22nd, 2011
TitleInfluence of renal function on association of CCR2-64I with mortality in the general population
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Year2005
Estimated date2005-01-12
CategoryScientific Publication
PlatformNone
DescriptionAbstract for the Dutch Nefrologie Dagen, 2005
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Conference report IBRO 2003

dinsdag, december 20th, 2011
TitleConference report IBRO 2003
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Year2003
Estimated date2003-07-30
CategoryScientific Publication
PlatformPC
DescriptionThis is my conference report I had to create to get travel funding for that particular conference when I was a PhD student.
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CYP3A5 GENOTYPE AFFECTS SYSTOLIC BLOOD PRESSURE IN THE GENERAL POPULATION

donderdag, december 15th, 2011
TitleCYP3A5 GENOTYPE AFFECTS SYSTOLIC BLOOD PRESSURE IN THE GENERAL POPULATION
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Year2004
Estimated date2004-10-07
CategoryScientific Publication
PlatformNone
DescriptionMy poster for the Dutch Nefrodagen 2004.
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HCR : A FUNCTIONAL ORPHAN CC CHEMOKINE RECEPTOR IN HUMAN ASTROCYTES

donderdag, december 15th, 2011
TitleHCR : A FUNCTIONAL ORPHAN CC CHEMOKINE RECEPTOR IN HUMAN ASTROCYTES
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Year2003
Estimated date2003-07-02
CategoryScientific Publication
PlatformPC
DescriptionMy poster for the International Brain Research Organisation conference in Prague, 2003.
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CC-Chemokine 5 receptor del32 polymorphism protects against the increased mortality rate seen in dialysis patients with systemic inflammation

donderdag, december 15th, 2011
TitleCC-Chemokine 5 receptor del32 polymorphism protects against the increased mortality rate seen in dialysis patients with systemic inflammation
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Year2006
Estimated date2006-10-10
CategoryScientific Publication
PlatformNone
DescriptionOur poster for the American Society of Nephrology conference in 2006.
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Induction of Glial L-CCR mRNA Expression in Spinal Cord and Brain in Experimental Autoimmune Encephalomyelitis

woensdag, december 7th, 2011
TitleInduction of Glial L-CCR mRNA Expression in Spinal Cord and Brain in Experimental Autoimmune Encephalomyelitis
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Year2004
Estimated date2003-06-01
CategoryScientific Publication
PlatformNone
DescriptionABSTRACT Chemokines and chemokine receptors are important regulators of leukocyte trafficking and immune response. It is well established that chemokines and their receptors are also expressed in the central nervous system (CNS), where their expression has been associated with various neuroinflammatory diseases, such as multiple sclerosis (MS). One of the most important chemokines involved in MS pathology is CCL2 (previously known as MCP-1). CCL2, released by glial cells, activates the chemokine receptor CCR2, causing the infiltration of blood monocytes in tissues affected by MS. There is evidence, however, that CCL2 also has local effects on CNS cells, including induction or modulation of cytokine release and synthesis of matrix metalloproteinases, that might contribute to CNS pathology. These effects are most likely independent of CCR2, since CCR2 expression in glial cells is rarely observed. We have recently provided evidence for the presence of an alternative CCL2 receptor in glial cells called L-CCR and have investigated the expression of L-CCR mRNA in a murine EAE model. It is shown that L-CCR mRNA is expressed in infiltrating macrophages during EAE, but not in infiltrating T cells. Prominent expression of L-CCR mRNA was detected in astrocytes and microglia already at early time points throughout the brain and spinal cord supporting the hypothesis that L-CCR expression in glial cells is related to CNS inflammation.
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Response to angiotensin-converting enzyme inhibition is selectively blunted by high sodium in angiotensin-converting enzyme DD genotype: evidence for gene–environment interaction in healthy volunteers

woensdag, december 7th, 2011
TitleResponse to angiotensin-converting enzyme inhibition is selectively blunted by high sodium in angiotensin-converting enzyme DD genotype: evidence for gene–environment interaction in healthy volunteers
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Year2010
Estimated date2010-04-01
CategoryScientific Publication
PlatformNone
DescriptionBackground Renin–angiotensin–aldosterone system blockade is a cornerstone in cardiovascular protection. Angiotensin-converting enzyme (ACE)-DD genotype has been associated with resistance to angiotensin-converting enzyme inhibition (ACEi), but data are conflicting. As sodium intake modifies the effect of ACEi as well as the genotype–phenotype relationship, we hypothesize gene– environment interaction between sodium-status, the response to ACEi, and ACE genotype. Method Thirty-five male volunteers (26W9 years; II nU6, ID nU18, DD nU11) were studied during placebo and ACEi (double blind, enalapril 20mg/day) on low [7 days 50mmol Naþ/day (lowsalt)]andhigh[7 days 200mmolNaþ/day (high salt)] sodium, with a washout of 6 weeks in-between. After each period mean arterial pressure (MAP) was measured before and during graded infusion of angiotensin II (Ang II). Results During high salt, ACEi reduced MAP in II and ID, but not in DD [II: 88 (78–94) versus 76 (72–88); ID: 87 (84–91) versus 83 (79–87); both P<0.05 and DD: 86 (82–96) versus 88 (80–90); ns, P<0.05 between genotypes]. However, during low salt, ACEi reduced MAP in all genotype groups [II: 83 (78–89) versus 77 (72–83); ID: 88 (84–91) versus 82 (78– 86); DD: 84 (80–91) versus 81 (75–85); all P<0.05]. During high saltRACEi, the Ang II response was blunted in DD, with an 18% rise in MAP during the highest dose versus 22 and 31% in ID and II (P<0.05). Low salt annihilated these differences. Conclusion In healthy participants, the MAP response to ACEi is selectively blunted in DD genotype during high salt, accompanied by blunted sensitivity to Ang II. Low salt corrects both abnormalities. Further analysis of this gene– environment interaction in patients may contribute to strategies for improvement of individual treatment efficacy. J Hypertens 28:2414–2421 Q 2010
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Low Levels of sRAGE Are Associated With Increased Risk for Mortality in Renal Transplant Recipients

woensdag, december 7th, 2011
TitleLow Levels of sRAGE Are Associated With Increased Risk for Mortality in Renal Transplant Recipients
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Year2007
Estimated date2007-05-01
CategoryScientific Publication
PlatformNone
DescriptionObjective. Infusion of the soluble form of the receptor for advanced glycation end-products (sRAGE) was protective against atherosclerosis and nephropathy in animal models. In this study we investigated determinants of endogenous sRAGE in renal transplant recipients and whether sRAGE was associated with mortality and graft loss. Methods and Results. A total of 591 patients participated at a median time of 6 years after transplantation. Independent determinants of sRAGE were mycophenolate mofetil medication (0.21, P0.001), creatinine clearance (0.15, P0.001), BMI (0.12, P0.003) and fasting insulin concentration (0.14, P0.001). Low sRAGE levels were associated with a 2–3 times higher risk for mortality especially after correction for creatinine clearance (P0.006). Conclusion. A lack of sRAGE is a risk factor for mortality in renal transplant recipients. The putatively protective role of sRAGE and in particular its association with mycophenolate mofetil usage needs further investigation. (Transplantation 2007;84: 659–663)
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Association Between Donor MBL Promoter Haplotype and Graft Survival and the Development of BOS After Lung Transplantation

woensdag, december 7th, 2011
TitleAssociation Between Donor MBL Promoter Haplotype and Graft Survival and the Development of BOS After Lung Transplantation
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Year2008
Estimated date2008-05-01
CategoryScientific Publication
PlatformNone
DescriptionBackground. Lung transplantation is a well accepted therapy for end-stage lung disease, despite high mortality rates. Mortality after transplantation is mainly caused by allograft failure in the first years after transplantation. Mannose binding lectin (MBL), a recognition molecule of innate immunity, has been associated with transplant outcome in other solid organ transplantation. In this study, the effect of donor- and recipient-MBL genotype on lung transplant outcome was investigated. Materials and Methods. All lung transplantations performed in our center, except from retransplantations and combined lung–liver or heart–lung transplantations, were included. Genotyping of theMBL2variants (promoter: L/H, Y/X, and P/Q allele and exon 1: A/D, A/B, and A/C allele) was performed in donor and recipient DNA. Analyses on graft survival and the development of bronchiolitis obliterans syndrome were performed with Kaplan-Meier (log rank) survival analysis. Results. Of the 277 included cases, DNA was available from 189 donors and 200 recipients and genotyping of the promoter single nucleotide polymorphisms was successful in 184 donors and 198 recipients and of the exon 1 single nucleotide polymorphisms in 181 donors and 193 recipients. Patients who received a graft from a donor with an X-allele had better graft survival (P0.007) and bronchiolitis obliterans syndrome free survival (P0.007). Recipient MBL genotype was not associated with transplant outcome. Conclusion. The donor X-allele, which corresponds to the LXPA haplotype is associated with superior lung transplant outcome. Our findings might prove to be important in finding ways to optimize outcome after lung transplantation. (Transplantation 2008;86: 1857–1863)
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