479 research outputs found

    Tra Venezia e Mantova. Confronti per l’attribuzione dell’Angelo Annunciante di Palazzo Ducale

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    Gigliola Gorio aims to attribute the Archangel Gabriel of Palazzo Ducale in Mantua to the Venetian artist Andrea da San Felice, the author of the Doge Giovanni Dolfin monument, whose catalogue has been studied and deepened in recent years. The attribution is supported by stylistic analogies with the indisputable works of the artist, who belonged to Andriolo de Santis’ workshop. There are a lot of references to Gothic Venetian artists in 14th century sculptures in Mantova, for example in what remains of the monument to Guido, Francesco and Ludovico Gonzaga once in the church of San Francesco. A new fragment that belonged to this monument has been discovered in a private collection

    Acetylcholine compartments in mouse diaphragm. Comparison of the effects of black widow spider venom, electrical stimulation, and high concentrations of potassium

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    The authors have studied the effects of 25 mM potassium, electrical stimulation of the phrenic nerve, and crude black widow spider venom on the ultrastructure, electrophysiology, and acetylcholine (ACh) contents of mouse diaphragms. About 65% of the ACh in diaphragms is contained in a depletable store in the nerve terminals. The rest of the ACh is contained in a nondepletable store that may correspond to the store that remains in denervated muscles and includes, in addition, ACh in the intramuscular branches of the phrenic nerve. About 4% of the ACh released from the depletable store at rest is secreted as quanta and may come from the vesicles, while 96% is secreted in a nonquantized form and comes from an extravesicular pool is uncertain: it could be < 10%, or as great as 50%, of the depletable store. K causes a highly (but perhaps not perfectly) selective increase in the rate of quantal secretion so that quanta account for about 50% of the total ACh released from K-treated diaphragms. K, or electrical stimulation of the phrenic nerve, depletes both the vesicular and extravesicular pools of ACh when hemicholinium no. 3 (HC-3) is present. However, most of the vesicles are retained under these conditions so that the diaphragms are able to increase slightly their rates of release of ACh when K is added. Venom depletes the terminals of their vesicles and abolishes the release of quanta of ACh. It depletes the vesicular pool of ACh (since it depletes the vesicles), but may only partially deplete the extravesicular pool (since it reduces resting release only 10-40%). The rate of release of ACh from the residual extravesicular pool does not increase when 25 mM K is added. Although we cannot exclude the possibility that stimulation may double the rate of release of ACh from the extravesicular pool, our results are compatible with the idea that the ACh released by stimulation comes mainly from the vesicles and that, when synthesis is inhibited by HC-3, ACh may be exchanged between the extravesicular pool and recycled vesicles

    GANGLIOSIDE ENHANCEMENT OF NEURONAL DIFFERENTIATION, PLASTICITY, AND REPAIR

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    Gangliosides are carbohydrate-rich complex lipids of large size and great complexity which are found in cell membranes, especially neuronal cell membranes. They are present in the external leaflet of the membrane. The hydrophobic moiety, consisting of sphingosine and fatty acid (stearic acid, 95%), is inserted into the membrane, while the hydrophilic moiety, consisting of sialic acid (NANA) and other carbohydrates, protrudes towards the extracellular fluid. Although gangliosides were discovered some 50 years ago, their potential role in neuronal functions has been appreciated only recently. During development, their composition and concentration change in a variety of animal species. Their role is indicated from studies which have shown that abnormalities in ganglioside metabolism can have a severe impairing effect on normal development. The mouse mutant weaver is characterized by cerebellar granule cell death, which is correlated by the lack of GM1 expression on the neuronal surface. On the other hand, inborn metabolic errors causing ganglioside accumulation in neurons (GM1 gangliosides) are correlated to an aberrant neurite outgrowth. A further appreciation of ganglioside action has been obtained either by adding gangliosides to neurons in culture or by treating animals during neuronal regeneration. It was found that these agents increased the rate and extent of sprouting of regenerating axons and enhanced neuronal differentiation and sprouting in vitro. Such effects were dependent upon the presence of the growth factor in the bathing medium; ganglioside incorporation, however, did not alter nerve growth factor (NGF) binding and internalization, indicating that some membrane events triggered by ganglioside incorporation may be relevant in neuronal differentiation and sprouting. More recently, we have obtained evidence showing that neurons from animals treated with gangliosides are more resistant to anoxia and ionic unbalances. It seems that ganglioside treatment prevents the decay of some key enzyme activity, such as Na+-K+-ATPase occurring after trauma. Indeed, the recent literature suggests that gangliosides may play an important role during development and, when injected into animals, enhance reparatory events in the central and peripheral nervous system

    Reversibility and mode of action of Black Widow spider venom on the vertebrate neuromuscular junction

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    Black widow spider venom (BWSV) stimulates transmitter release and depletes synaptic vesicles from muscles bathed in a sodium free medium containing 1 mM EGTA. However, frog neuromuscular junctions treated with BWSV in glucosamine Ringer's and post-treated with antivenin recover normal function. This suggests that probably the permanent block of neuromuscular transmission is due to changes in permeability of the nerve ending plasma membrane to cations such as Na+. When BWSV is applied in a medium lacking divalent cations and containing 1 mM EGTA, in most of the cases no effect is observed. The authors found that this inhibition can be overcome in 3 ways: by adding divalent cations to the medium; by increasing the tonicity of the medium with sucrose; by raising the temperature of the medium. These results suggest that the lack of divalent cations influences the membrane fluidity. Moreover, in view of the report by Yahara and Kaimoto-Sameshima (1977) that hypertonic media induce capping of surface receptors in lymphocytes and thymocytes, the authors think that these data further support the hypothesis that BWSV stimulates release by a dual mode of action; namely, it increases the nerve ending permeability to cations and also stimulates release directly via a process of redistribution of membrane components, a process which may also inhibit vesicle recycling

    Caroline Deby, pittrice tra Italia e Francia. Appunti e spunti per l’attività di una ritrovata artista romantica

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    The paper stems from the research carried out on the heritage of the Museum of Risorgimento in Brescia, on the occasion of its rearrangement. Archival investigations have returned the name of the Camillo Ugoni’s portrait author, Caroline Deby (mar- ried Vallée), whose path is retraced and analyzed. She was a romantic painter active between Italy and France from the 1820s and met Camillo Ugoni in Brescia before his exile

    Perinatal morphine .2. Changes in cortical plasticity

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    We have previously shown that perinatal exposure to morphine impairs reactive plasticity of serotonin (5-HT) neurons following selective neonatal lesion (Gorio et al., J Neurosci Res 34:462-471, 1993), This study shows that morphine inhibits also that the compensatory sprouting of intact axons after partial denervation, Neonatal 6-OHDA injection causes norepinephrine (NE) depletion in the frontal cortex, which triggers a compensatory increase of dopamine, serotonin (5-HT), and met-enkephalin content correlated by the increased density of tyrosine hydroxylase- and 5-HT-positive axons, In perinatal morphine-treated rats, no compensatory changes are observed after neonatal 6-OHDA depletion of NE in the frontal cortex. (C) 1995 Wiley-Liss, Inc

    PERINATAL MORPHINE .1. EFFECTS ON SYNAPSIN AND NEUROTRANSMITTER SYSTEMS IN THE BRAIN

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    We have previously shown that rat perinatal exposure to morphine causes dopaminergic and met-enkephalin (ME) and substance P (SP) changes in the striatum during the early postnatal period (Tenconi et al.: Int J Dev Neurosci 10:517-526, 1992); in addition it increases the susceptibility to neurotoxic lesions and impairs regenerative capacity of the serotoninergic system (Gorio et al.: J Neurosci Res 34: 462-471, 1993). Our study shows that ME and SP levels increase postnatally in several areas of the rat brain, reaching the highest values between 30 and 60 days, after which the peptide content subsides to lower levels. Perinatal exposure to morphine increases such ME and SP levels during the early stages of postnatal life. No effect of morphine on 5-HT and NE is observed, while the dopaminergic system is mainly affected in the mesencephalon. The pre- and postnatal brain expression of synapsin I mRNA is gradually and progressively localized in discrete areas of the brain. In the brain of rats perinatally exposed to morphine, the abundance of synapsin I mRNA expression is markedly reduced. Therefore, perinatal exposure to morphine affects early postnatal synaptic development in the brain as shown by the altered peptidergic and monoaminergic content and by the reduced synapsin I mRNA expression. (C) 1995 Wiley-Liss, Inc

    Selezione dall'archivio Gorio

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    La selezione è il risultato di un lavoro di analisi critica, condotta sull'opera architettonica di Gorio, sulla base dei materiali originali del progettista depositati presso gli Archivi di Architettura Cesarch-Inarch a Roma. La documentazione selezionata e pubblicata è organizzata per sezioni e ogni scheda, con foto, tavole di progetto e disegni, è accompagnata da note e riflessioni critiche
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