Endothelin 1 levels in relation to clinical presentation and outcome of Henoch Schonlein purpura

<p>Abstract</p> <p>Background</p> <p>Henoch Schonlein purpura (HSP) is a common vasculitis of small vessels whereas endothelin-1 (ET-1) is usually reported elevated in vasculities and systematic inflammation. The aim of the present study was to investigate whether ET-1 levels are correlated with the clinical presentation and the outcome of HSP.</p> <p>Methods</p> <p>The study sample consisted of thirty consecutive patients with HSP. An equal number of healthy patients of similar age and the same gender were served as controls. The patients' age range was 2–12.6 years with a mean ± SD = 6.3 ± 3 years. All patients had a physical examination with a renal, and an overall clinical score. Blood and urinary biochemistry, immunology investigation, a skin biopsy and ET-1 measurements in blood and urine samples were made at presentation, 1 month later and 1 year after the appearance of HSP. The controls underwent the same investigation with the exception of skin biopsy.</p> <p>Results</p> <p>ET-1 levels in plasma and urine did not differ between patients and controls at three distinct time points. Furthermore the ET-1 were not correlated with the clinical score and renal involvement was independent from the ET-1 measurements. However, the urinary ET-1 levels were a significant predictor of the duration of the acute phase of HSP (HR = 0.98, p = 0.032, CI0.96–0.99). The ET-1 levels did not correlate with the duration of renal involvement.</p> <p>Conclusion</p> <p>Urinary ET-1 levels are a useful marker for the duration of the acute phase of HSP but not for the length of renal involvement.</p

Losartan Decreases p42/44 MAPK Signaling and Preserves LZ+ MYPT1 Expression

Heart failure is associated with impairment in nitric oxide (NO) mediated vasodilatation, which has been demonstrated to result from a reduction in the relative expression of the leucine zipper positive (LZ+) isoform of the myosin targeting subunit (MYPT1) of myosin light chain phosphatase. Further, captopril preserves normal LZ+ MYPT1 expression, the sensitivity to cGMP-mediated vasodilatation and modulates the expression of genes in the p42/44 MAPK and p38 MAPK signaling cascades. This study tests whether angiotensin receptor blockade (ARB) with losartan decreases p42/44 MAPK or p38 MAPK signaling and preserves LZ+ MYPT1 expression in a rat infarct model of heart failure. In aortic smooth muscle, p42/44 MAPK activation increases and LZ+ MYPT1 expression falls after LAD ligation. Losartan treatment decreases the activation of p42/44 MAPK to the uninfarcted control level and preserves normal LZ+ MYPT1 expression. The expression and activation of p38 MAPK, however, is low and does not change following LAD ligation or with losartan therapy. These data suggest that either reducing or blocking the effects of circulating angiotensin II, both decreases the activation of the p42/44 MAPK signaling cascade and preserves LZ+ MYPT1 expression. Thus, the ability of ACE-inhibitors and ARBs to modulate the vascular phenotype, to preserve normal flow mediated vasodilatation may explain the beneficial effects of these drugs compared to other forms of afterload reduction in the treatment of heart failure

Electrical transport and giant magnetoresistance in La 0.62 Er 0.05 Ba 0.33 Fe x Mn 1− x O 3 ( x = 0.00, and 0.15) manganites

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Short-range ferromagnetic order in perovskite manganite La 0.62 Er 0.05 Ba 0.33 Mn 0.95 Fe 0.05 O 3

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Theoretical investigations on the magnetocaloric and electrical properties of a perovskite manganite La 0.67 Ba 0.1 Ca 0.23 MnO 3

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Structural and Static Magnetic Behavior of Antiferromagnetic Compounds La0.67Sr0.33−x Ca x Mn0.75Fe0.25 O 3 (x = 0.00 and 0.17)

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Structural, magnetocaloric, electrical properties and theoretical investigations in manganite La 0.67 Sr 0.1 Ca 0.23 MnO 3 type perovskite

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Cooperative role of ETA and ETB receptors in mediating the diuretic response to intramedullary hyperosmotic NaCl infusion

Acute intramedullary infusion of hyperosmotic NaCl, used to simulate a high-salt diet-induced increase of medullary osmolality, increases urine production and endothelin release from the kidney. To determine whether endothelin mediates this diuretic and natriuretic response, urine flow and Na+ excretion rate were measured during acute intramedullary infusion of hyperosmotic NaCl in anesthetized rats, with or without endothelin receptor antagonism. Isosmotic NaCl was infused into the left renal medulla during an equilibration period and 30-min baseline period, followed by hyperosmotic NaCl for two additional 30-min periods. Hyperosmotic NaCl infusion significantly increased urine flow of vehicle-treated rats (from 5.9 ± 0.9 to 11.1 ± 1.8 μl/min). Systemic ETB receptor blockade enhanced this effect (A-192621; from 7.7 ± 1.1 to 18.7 ± 2.9 μl/min; P < 0.05), ETA receptor blockade (ABT-627) had no significant effect alone, but the diuresis was markedly attenuated by combined ABT-627 and A-192621 administration (from 4.4 ± 0.7 to 5.4 ± 0.9 μl/min). Mean arterial pressures overall were not significantly different between groups. Surprisingly, the natriuretic response to hyperosmotic NaCl infusion was not significantly altered by systemic endothelin receptor blockade, and furthermore, intramedullary ETB receptor blockade enhanced the diuretic and natriuretic response to hyperosmotic NaCl infusion. ETA receptor blockade significantly attenuated both the diuretic and natriuretic responses to hyperosmotic NaCl infusion in ETB receptor-deficient sl/sl rats. These results demonstrate an important role of endothelin in mediating diuretic responses to intramedullary infusion of hyperosmotic NaCl. Moreover, these data suggest ETA and ETB receptors are both required for the full diuretic and natriuretic actions of endothelin