Endothelin-1 stimulates neutrophil adhesion to endothelial cells by an effect on the expression of adhesive molecules on the neutrophil surface. Endothelin-1 stimulates neutrophil accumulation in vivo and in vitro in the heart. Antibodies against the integrin complex block the endothelin-1-dependent neutrophil adhesion. These findings have potential importance in the pathophysiology of endothelin-1-increased states.

Poly(vinyl alcohol), PVA, is the most frequently used material in embolization of tumors, aneurisms and arteriovenous malformations due to its low toxicity, good biocompatibility and desirable physical properties. It is well known that PVA particles cannot be prepared by direct polymerization of vinyl alcohol. Its synthesis is typically performed by the suspension polymerization of vinyl acetate to produce poly(vinyl acetate), PVAc, followed by the saponification of the PVAc particles. This work shows that, using the suspension polymerization technique, it is possible to obtain spherical particles with a core‐shell structure of PVA/PVAc with regular morphology, instead of particles with irregular shapes and sizes, as usually found in many commercial embolization products. Therefore, this work presents the production of PVA/PVAc spherical particles that can be used to occlude blood vessels, eliminating the disadvantages of commercial PVA. In vivo clinical tests with white “New Zealand” rabbits undergoing kidney inflammation reaction have shown that these spherical particles are much more efficient for vascular embolization.

The aim of our study was to assess bone mineral density (BMD) in pre-menopausal women with systemic lupus erythematosus (SLE) and the influence of disease activity and use of corticosteroids. Lumbar and femoral BMD were measured in 43 patients with SLE (28 on regular steroid therapy, 15 with recent onset, non-treated) and compared with 43 healthy women matched for age. In addition, 21 SLE patients treated with corticosteroids were followed-up with a mean of 36.6 +/- 12.7 months. BMD was significantly lower in SLE patients with prednisone doses > or = 7.5 mg/day than those of recent onset (lumbar: 1.07 +/- 0.11 vs 1.15 +/- 0.13, P = 0.039; femur: 0.85 +/- 0.13 vs 0.98 +/- 0.21, P = 0.034) and the control group (lumbar: 1.07 +/- 0.11 vs 1.13 +/- 0.10, P = 0.040; femur: 0.85 +/- 0.13 vs 0.93 +/- 0.10, P = 0.028). In addition, 18% of SLE steroid users had osteoporosis. Lumbar and femoral BMD were inversely correlated with the time of treatment and the cumulative doses of prednisone. There were no significant BMD changes during the 3-yr follow-up period. In conclusion, in SLE pre-menopausal patients lumbar and femoral BMD is decreased and related to long-term corticosteroid therapy.

The present study addressed the effect of interventions aimed to increase NO in the setting of acute renal ischemia/reperfusion (I/R) in uninephrectomized rabbits. In the 60-minute post-I/R period, L-arginine+superoxide (O2.-) dismutase (SOD) synergistically improved the renal functional (69.4% versus 10.4% of the pre-I/R glomerular filtration rate with or without L-arginine+SOD, respectively; p < .01) and histological parameters (82.9% decrease of medullary congestion in L-arginine+SOD, P < .01 versus vehicle) and blocked the I/R-dependent neutrophil accumulation (89.3% reduction). In spite of these results over the short term, a second set of experiments disclosed that the protection by L-arginine+SOD was no longer present at 24 and 48 hours (plasma creatinine in vehicle-treated versus L-arginine+SOD-treated animals [mg/100 mL]: 24 hours after I/R, 9.4 +/- 1.9 versus 8.07 +/- 0.65; 48 hours after I/R, 11.6 +/- 3.6 versus 9.7 +/- 0.9; P = NS in all the cases). Additional experiments were conducted using a milder 30-minute ischemic model, which showed no significant functional or histological protection by using L-arginine+SOD. In conclusion, our experiments disclosed the following: (1) the critical importance of the interaction between NO and O2.- in the acute protective effect of L-arginine (this effect not only improved renal function and histology but also reduced neutrophil accumulation) and (2) the discordance existing between the immediate protection afforded by L-arginine+SOD and the lack of protection observed at 24 and 48 hours. This finding suggests that a punctual intervention on the NO system at the time of I/R is not sufficient to reduce renal damage over the long term.

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