4,237 research outputs found

    Effect of some products of protein catabolism on the endothelium-dependent and -independent relaxation of rabbit thoracic aorta rings.

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    We have investigated the effect that some products of protein catabolism have on endothelium-dependent and -independent relaxation of rabbit aorta rings precontracted with phenylephrine (PE). All the products tested, i.e., creatinine (CRT), guanidinosuccinic acid (GSA), urea (UR), guanidine (GND) and methylguanidine (MG), are structurally related to L-arginine (L-ARG), the substrate for nitric oxide (NO) biosynthesis which accounts for the biological properties of endothelium-derived relaxing factor (EDRF). Endothelium-derived NO (EDNO) release was induced by agents acting via a receptor- [acetylcholine (ACh)] or a nonreceptor-mediated mechanism (calcium ionophore A23187), and the endothelial-independent relaxation was induced by the NO donor glyceryl trinitrate (GTN). CRT (0.1-10 mM) did not modify the endothelium-dependent relaxation caused by ACh or A23187 but produced a small increase in the response to the endothelium-independent vasorelaxant GTN. Concentrations of GSA up to 1 mM did not affect the relaxation of rabbit aortic rings induced by either ACh or A23187, but at 10 mM, GSA enhanced the relaxation produced by these agents. UR (1-100 mM) inhibited, in a concentration-dependent manner, the relaxation induced by ACh, but not that caused by A23187 or GTN. By comparison, GND and MG (0.1-10 mM) produced a concentration-related inhibition of both ACh- and A23187-induced relaxation. The inhibition by these compounds was either completely or partially reversed by L-ARG. In contrast, the relaxation induced by GTN was inhibited only by higher concentrations (10 mM) of GND or MG. These results indicate that some products of protein catabolism can reduce EDNO formation in vitro

    Levamisole inhibits in vivo rat platelet aggregation by a release of prostacyclin-like factor.

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    1. The anti-thrombotic effect of levamisole (LMS) and acetylsalicylic acid (ASA) were examined in vitro and in vivo models. 2. LMS inhibits rat platelet aggregation induced by either adenosine 5'-diphosphate (ADP) or collagen (CLG) in vitro and in vivo. 3. LMS is more active in vivo than in vitro while acetylsalicylic acid (ASA) is more active in vitro than in vivo. It seems that in vivo LMS does not act by blocking thromboxane A2 formation only, but via participation of an endogenous factor. 4. The release of LMS-induced anti-thrombotic factor is inhibited by ASA pretreatment, indicating to be a cyclooxygenase metabolite of arachidonic acid. 5. The LMS-induced anti-thrombotic factor has a t1/2 of 3.6 +/- 0.8 min that is similar to the t1/2 of synthetic prostacyclin (PGI2) tested in our system (3.9 +/- 0.5 min; P = NS). 6. The release of PGI2-like substance from vascular tissue is LMS dose-dependent

    Human recombinant platelet phospholipase A2 exacerbates poly-L-arginine induced rat paw edema.

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    In this study by using the human recombinant non-pancreatic-secreted platelet PLA2 (r-hnps-PLA2) and rabbit polyclonal antibodies directed against either the human (group II) or the porcine enzyme (group I), we have shown a possible involvement of platelet PLA2 in poly-L-arginine (25 kDa)-induced rat paw edema. Local treatment of rats with the anti-platelet-PLA2 antibody (anti-hnps-PLA2) but not with anti-porcine-PLA2 antibody (anti-porc-PLA2) significantly reduced the edema induced by a maximal dose of poly-L-arginine (1 mg/paw). Furthermore when r-hnps-PLA2 (1-10 micrograms) was injected together with a subliminal dose of poly-L-arginine (50 micrograms/paw), a dose-dependent increase in both edema and protein leakage was observed. This effect was selectively inhibited by the anti-hnps-PLA2 (10-100 micrograms/paw) but not anti-porc-PLA2 (10-100 micrograms paw). Thus, platelets seem to be involved in both vascular and cellular components of the inflammatory response by contributing, most likely in the early phase, to the edema formation through secretion of PLA2

    Dynamic filtering of static dipoles in magnetoencephalography

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    We consider the problem of estimating neural activity from measurements of the magnetic fields recorded by magnetoencephalography. We exploit the temporal structure of the problem and model the neural current as a collection of evolving current dipoles, which appear and disappear, but whose locations are constant throughout their lifetime. This fully reflects the physiological interpretation of the model. In order to conduct inference under this proposed model, it was necessary to develop an algorithm based around state-of-the-art sequential Monte Carlo methods employing carefully designed importance distributions. Previous work employed a bootstrap filter and an artificial dynamic structure where dipoles performed a random walk in space, yielding nonphysical artefacts in the reconstructions; such artefacts are not observed when using the proposed model. The algorithm is validated with simulated data, in which it provided an average localisation error which is approximately half that of the bootstrap filter. An application to complex real data derived from a somatosensory experiment is presented. Assessment of model fit via marginal likelihood showed a clear preference for the proposed model and the associated reconstructions show better localisation

    La retorica e la poetica di Vico, ossia la prima concezione estetica del linguaggio

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    La retorica e la poetica di Vico, ossia la prima concezione estetica del linguaggio / Andrea Sorrentino. - Torino : Bocca, 1927 Dedica manoscritta dell\u27autore: A Sua Eccellenza / On.le Professore Emilio Bodrero / con la piu\u27 alta stima e la piu\u27 viva devozione / l\u27autore / Andrea Sorrentino / Prof.re di lettere italiane e latine / nel R. Liceo "T. Tasso" di Salerno https://galileodiscovery.unipd.it/discovery/fulldisplay?context=L&vid=39UPD_INST:VU1&search_scope=MyInst_and_CI&tab=Everything&docid=alma99000985961020604

    Effect of bradykinin antagonists, NG- monomethyl-L- Arginine and L- NG- Nitro - Arginine on phospholipase A2 induced oedema in rat paw.

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    1. 1. The rat paw oedema produced by a local injection of phospholipase A2 from Naja mocambique mocambique has been shown to be mainly driven by the liberation of serotonin and kinins. 2. 2. Using specific bradykinin receptor antagonists we have shown that kinins are acting through B2 receptors. 3. 3. Using endothelium-derived relaxing factor (EDRF) synthesis inhibitors NG-monomethyl-l-arginine and l-NG-nitro arginine we have tested the possible envolvement of EDRF as mediator. 4. 4. Our work supports the view that extracellular phospholipases A2 are involved in inflammation, and suggests a role for EDRF as mediator of extravasation in this model of inflammatio

    A variational approach to the study of the existence of invariant lagrangian graphs

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    This paper surveys some recent results by the author and some collaborators, on the existence of invariant Lagrangian graphs for Tonelli Hamiltcmian systems
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