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- Dahlöf, Björn, 1953, et al.
(författare)
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Perindopril/indapamide combination more effective than enalapril in reducing blood pressure and left ventricular mass: the PICXEL study
- 2005
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Ingår i: J Hypertens. - 0263-6352. ; 23:11, s. 2063-70
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Few data are available comparing the effects of monotherapy and combination therapy on target organ damage. The PICXEL study compared the efficacy of a strategy based on first-line combination with perindopril/indapamide versus monotherapy with enalapril in reducing left ventricular hypertrophy (LVH) in hypertensive patients. METHODS: In this 1-year multicentre randomized double-blind study, patients received an increasing dosage of perindopril/indapamide (n = 284) or enalapril (n = 272). Changes in blood pressure and echocardiographic measures of LVH were assessed from baseline to the end of treatment. Reading of the echocardiograms was central and blinded for therapy, patient and sequence. RESULTS: Systolic and diastolic blood pressure decreased significantly more in the perindopril/indapamide than in the enalapril group (P < 0.0001 and P = 0.003). The left ventricular mass index decreased by 13.6 +/- 23.9 g/m(2) (mean +/- SD) with perindopril/indapamide (P < 0.0001) and 3.9 +/- 23.9 g/m(2) with enalapril (P < 0.005); these decreases were significantly different (P < 0.0001). The left ventricular internal diameter, posterior and interventricular septal wall thickness decreased significantly with perindopril/indapamide (P < or = 0.0001); the interventricular septal wall thickness decreased significantly with enalapril (P < 0.001). Both treatments were well tolerated. CONCLUSION: A strategy based on first-line combination with perindopril/indapamide achieved better blood pressure decrease with a significantly greater degree of LVH reduction than a strategy based on monotherapy with enalapril in hypertensive patients with LVH.
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| 2. |
- Gosse, L., et al.
(författare)
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Finite moment problems and applications to multiphase computations in geometric optics
- 2005
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Ingår i: Communications in Mathematical Sciences. - 1539-6746 .- 1945-0796. ; 3:3, s. 373-392
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Tidskriftsartikel (refereegranskat)abstract
- Recovering a function out of a finite number of moments is generally an ill-posed inverse problem. We focus on two special cases arising from applications to multiphase geometric optics computations where this problem can be carried out in a restricted class of given densities. More precisely, we present a simple algorithm for the inversion of Markov's moment problem which appears in the treatment of Brenier and Corrias' K-multibranch solutions and study Stieltje's algorithm in order to process moment systems arising from a Wigner analysis. Numerical results are provided for moderately intricate wave-fields.
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| 3. |
- Gosse, L., et al.
(författare)
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Resolution of the finite Markov moment problem
- 2005
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Ingår i: Comptes rendus. Mathematique. - : Elsevier BV. - 1631-073X .- 1778-3569. ; 341:12, s. 775-780
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Tidskriftsartikel (refereegranskat)abstract
- We expose in full detail a constructive procedure to invert the so-called 'finite Markov moment problem'. The proofs rely on the general theory of Toeplitz matrices together with the classical Newton's relations.
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| 5. |
- Wenink, Mark H., et al.
(författare)
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The inhibitory Fc gamma IIb receptor dampens TLR4-mediated immune responses and is selectively up-regulated on dendritic cells from rheumatoid arthritis patients with quiescent disease
- 2009
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Ingår i: Journal of Immunology. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 183:7, s. 4509-4520
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Tidskriftsartikel (refereegranskat)abstract
- Rheumatoid arthritis (RA) is a common autoimmune disease leading to profound disability and premature death. Although a role for FcgammaRs and TLRs is accepted, their precise involvement remains to be elucidated. FcgammaRIIb is an inhibitory FcR important in the maintenance of tolerance. We hypothesized that the inhibitory FcgammaRIIb inhibits TLR responses on monocyte-derived dendritic cells (DC) and serves as a counterregulatory mechanism to dampen inflammation, and we surmised that this mechanism might be defective in RA. The expression of the inhibitory FcgammaRIIb was found to be significantly higher on DCs from RA patients having low RA disease activity in the absence of treatment with antirheumatic drugs. The expression of activating FcgammaRs was similarly distributed among all RA patients and healthy controls. Intriguingly, only DCs with a high expression of FcgammaRIIb were able to inhibit TLR4-mediated secretion of proinflammatory cytokines when stimulated with immune complexes. In addition, when these DCs were coincubated with the combination of a TLR4 agonist and immune complexes, a markedly inhibited T cell proliferation was apparent, regulatory T cell development was promoted, and T cells were primed to produce high levels of IL-13 compared with stimulation of the DCs with the TLR4 agonist alone. Blocking FcgammaRIIb with specific Abs fully abrogated these effects demonstrating the full dependence on the inhibitory FcgammaRIIb in the induction of these phenomena. This TLR4-FcgammaRIIb interaction was shown to dependent on the PI3K and Akt pathway.
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