Archive for the ‘Scientific publication’ Category
woensdag, december 7th, 2011
| Title | Induction of Glial L-CCR mRNA Expression in Spinal Cord and Brain in Experimental Autoimmune Encephalomyelitis |
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| Year | 2004 |
| Estimated date | 2003-06-01 |
| Category | Scientific Publication |
| Platform | None |
| Description | ABSTRACT 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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Tags: 2004, Induction of Glial L-CCR mRNA Expression in Spinal Cord and Brain in Experimental Autoimmune Encephalomyelitis, None, Scientific Publication
Posted in Scientific publication | Reacties uitgeschakeld
woensdag, december 7th, 2011
| Title | 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 |
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| Year | 2010 |
| Estimated date | 2010-04-01 |
| Category | Scientific Publication |
| Platform | None |
| Description | Background 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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Tags: 2010, None, 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, Scientific Publication
Posted in Scientific publication | Reacties uitgeschakeld
woensdag, december 7th, 2011
| Title | Low Levels of sRAGE Are Associated With Increased Risk for Mortality in Renal Transplant Recipients |
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| Year | 2007 |
| Estimated date | 2007-05-01 |
| Category | Scientific Publication |
| Platform | None |
| Description | Objective. 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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Tags: 2007, Low Levels of sRAGE Are Associated With Increased Risk for Mortality in Renal Transplant Recipients, None, Scientific Publication
Posted in Scientific publication | Reacties uitgeschakeld
woensdag, december 7th, 2011
| Title | Association Between Donor MBL Promoter Haplotype and Graft Survival and the Development of BOS After Lung Transplantation |
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| Year | 2008 |
| Estimated date | 2008-05-01 |
| Category | Scientific Publication |
| Platform | None |
| Description | Background. 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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Tags: 2008, Association Between Donor MBL Promoter Haplotype and Graft Survival and the Development of BOS After Lung Transplantation, None, Scientific Publication
Posted in Scientific publication | Reacties uitgeschakeld
