Contribution of EDRF and EDHF to restoration of endothelial function following dietary restrictions in hypercholesterolemic rats.

The mechanisms underlying the impairment of endothelium-mediated vasorelaxation induced by dietary hypercholesterolemia and the mechanisms of restoration of endothelial function following reintroduction of low cholesterol diet were evaluated. Feeding rats with high cholesterol diet induced hypercholesterolemia and high blood pressure. This was associated with reduced vasorelaxation in response to acetylcholine, isoproterenol, and adenosine. At the same time, exaggerated contractile responses to serotonin and phenylephrine were observed. Reintroduction of a normal diet to cholesterol fed rats resulted in significant normalization of blood pressure, serum lipid profile, relaxation and contractile responses. The contributions of endothelial derived relaxing factors (EDRF), endothelial derived contractile factors (EDCFs)/prostanoids, and endothelial derived hyperpoalrising factor (EDHF) to the vasorelaxation in each group of animals were assessed. EDCFs constricting activity was increased in both cholesterol fed groups as compared to the control group. EDRF and EDHF were found to be the primary factors involved in the regulation of endothelium-mediated responsiveness. In control animals, EDRF was responsible for 70-90% of relaxation, depending on the agonist used. In cholesterol fed animals, EDRF was significantly reduced while EDHF was maintained or enhanced showing that EDHF had a significant role in maintaining the endothelial responses. Importantly, the restoration of vasorelaxation following reintroduction of normal diet was mediated not only by improvement of EDRF-dependent relaxation, but also to a significant extent by a further increase in EDHF-mediated relaxation. Taken together, the data showed that EDRF was attenuated during hypercholesterolemia and dietary interventions with low fat content restored these responses. However, EDHF-mediated responses were not reduced by hypercholesterolemia and subsequently improved their function after application of low cholesterol diet. The results implicate EDHF-mediated relaxation is also an important mechanism for restoration of endothelial function upon application of dietary restrictions for reduction of serum cholesterol level.

Factors affecting language improvement in children with autism

Autism is a controversy disease, it is difficult to diagnose and treat. In children with Autism, the acquisition of language has been found to be a predictor of long-term outcome. Delineation of factors that are associated with the development of language may have practical as well as conceptual implications. This study was conducted on twenty children who received language intervention sessions in phoniatric unit at Ain Shams University Hospitals. The aim was to investigate the factors affecting the language improvement in those children. The results showed significant correlation between language improvement and mental age, social age, the child's attention, the severity of autism and the age of starting therapy. The presence of echolalia, mother's education level and working of the mother showed non- significant correlation

Estudos microbiológicos e químicos do fungo marinho Scolecobasidium arenarium / Microbiological and chemical studies of the marine fungus Scolecobasidium arenarium

A micologia marinha e uma fonte promissora para a descoberta de novas moleculas bioativas, so que muito pouco explorada. Por este motivo nos incentivamos a dar inicio ao primeiro projeto no Brasil no estudo de um fungo marinho, frente a descoberta de novos produtos naturais provenientes de fungos marinhos. Uma linhagem desconhecida de um fungo marinho, denominado SS99F-6, foi isolada de sedimentos marinhos coletados no litoral norte do Estado de Sao Paulo; Posteriormente foi identificada como sendo o fungo marinho Scolecobasidium arenarium. O fungo foi submetido a fermentacao de pequena escala, objetivando a producao de metabolitos secundarios. Os metabolitos secundarios. Os metabolitos secundarios produzidos foram isolados atraves de varias tecnicas cromatograficas, resultando em 5 moleculas. Tres moleculas foram identificadas como dicetopiperazinas, sendo: a conhecida ciclo [Pro-Val] e duas novas na literatura, a ciclo [Phe-Leu] e a ciclo [Ile-Val]. As outras duas moleculas contem compostos aromaticos, no entanto nao puderam ser caracterizadas totalmente.

The involvement of K+ channels and the possible pathway of EDHF in the rabbit femoral artery

Experiments were designed to characterize the cellular mechanisms of action of endothelium-derived vasodilator substances in the rabbit femoral artery. Acetylcholine (ACh, 10(-8)-10(-5) M) induced a concentration-dependent relaxation of isolated endothelium-intact arterial rings precontracted with norepinephrine (NE, 10(-6) M). The ACh-induced response was abolished by the removal of endothelium. NG-nitro-L-arginine (L-NAME, 10(-4) M), an inhibitor of NO synthase, partially inhibited ACh-induced endothelium-dependent relaxation, whereas indomethacin (10(-5) M) showed no effect on ACh-induced relaxation. 25 mM KCl partially inhibited ACh-induced relaxation by shifting the concentration-response curve and abolished the response when combined with L-NAME and NE. In the presence of L-NAME, ACh-induced relaxation was unaffected by glibenclamide (10(-5) M) but significantly reduced by apamin (10(-6) M), and almost completely blocked by tetraethylammonium (TEA, 10(-3) M), iberiotoxin (10(-7) M) and 4-aminopyridine (4-AP, 5 x 10(-3) M). The cytochrome P450 inhibitors, 7-ethoxyresorufin (7-ER, 10(-5) M) and miconazole (10(-5) M) also significantly inhibited ACh-induced relaxation. Ouabain (10(-6) M), an inhibitor of Na+, K(+)-ATPase, or K(+)-free solution, also significantly inhibited ACh-induced relaxation. ACh-induced relaxation was not significantly inhibited by 18-alpha-glycyrrhetinic acid (18 alpha-GA, 10(-4) M). These results of this study indicate that ACh-induced endothelium-dependent relaxation of the rabbit femoral artery occurs via a mechanism that involves activation of Na+, K(+)-ATPase and/or activation of both the voltage-gated K+ channel (Kv) and the large-conductance, Ca(2+)-activated K+ channel (BKCa). The results further suggest that EDHF released by ACh may be a cytochrome P450 product.