11 research outputs found

    Nurses' perceptions of aids and obstacles to the provision of optimal end of life care in ICU

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    Contains fulltext : 172380.pdf (publisher's version ) (Open Access

    Down-regulation of Bcl-2 in rat substantia nigra after focal cerebral ischemia

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    After occlusion of the middle cerebral artery in rats, a robust neuronal loss occurs in the ipsilateral substantia nigra reticulata. In this study we have assessed whether degeneration of the substantia nigra is accompanied by changes in the expression of the anti-apoptotic protein Bcl-2. Neuronal loss was assessed by neuronal nuclei (NeuN) immunoreactivity. A significant decrease of Bcl-2 expression was observed in the substantia nigra 12, 24 and 72 h after middle cerebral artery occlusion. These results suggest that the secondary neuronal loss in the substantia nigra could be related with the modification of proteins regulating programmed cell death. Exo-focal cell death may explain the appearance of neuropsychiatric symptoms that are not correlated with the primary site of lesion. © 2004 Lippincott Williams & Wilkins.Peer Reviewe

    Estrogen dissociates Tau and alpha-amino-3-hydroxy-5-methylisoxazole-4- propionic acid receptor subunit in postischemic hippocampus

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    During cerebral ischemia, part of the damage associated with the hyperactivation of glutamate receptors results from the hyperphosphorylation of the microtubule-associated protein Tau. Previous studies have shown that estradiol treatment reduces neural damage after cerebral ischemia. Here, we show that transient occlusion of the middle cerebral artery results in the hyperphosphorylation of Tau and in a significant increase in the association of Tau with glycogen synthase kinase-3β and alpha-amino-3-hydroxy-5- methylisoxazole-4-propionic acid type glutamate receptor subunits 2/3 in the hippocampus. Estradiol treatment decreased hippocampal injury, inhibited glycogen synthase kinase-3β and decreased the hyperphosphorylation of Tau and the interaction of Tau with glycogen synthase kinase-3β and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor. These findings suggest that ischemia produces a strong association between Tau and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor, and estradiol can exert at least part of its neuroprotective activity through inhibition of glycogen synthase kinase-3β. © 2006 Lippincott Williams & Wilkins.Peer Reviewe

    Soluble or soluble/membrane TNF-± inhibitors protect the brain from focal ischemic injury in rats

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    Tumor Necrosis Factor-alpha (TNF-α) is an immunomodulatory and proinflammatory cytokine implicated in neuro-inflammation and neuronal damage in response to cerebral ischemia. The present study tested the hypothesis that anti-TNF-α agents may be protective against cerebral infarction. Transient focal ischemia was artificially induced in anesthetized adult male Wistar rats (300–350 g) by middle cerebral artery occlusion (MCAO) with an intraluminal suture. TNF-α function was interfered with either a chimeric monoclonal antibody against TNF-α (infliximab-7 mg/kg) aiming to TNF-α soluble and membrane-attached form; or a chimeric fusion protein of TNF-α receptor-2 with a fragment crystallizable (Fc) region of IgG1 (etanercept-5 mg/kg) aiming for the TNF-α soluble form. Both agents were administered intraperitoneally 0 or 6 h after inducing ischemia. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining. Cerebral infarct volume was significantly reduced in either etanercept or infliximab-treated group compared with non-treated MCAO rats 24 h after reperfusion. These results suggest that anti-TNF-α agents may reduce focal ischemic injury in rats

    "Organización, fragmentación y posibilidades de cambio: la brecha como vacío fértil"

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    En este trabajo buscamos comprender los complejos procesos de aprendizaje colectivo, y explorar y diseñar herramientas que posibiliten desarrollarlo. De este modo, observamos brechas y fragmentaciones en la red organizativa, que se enquistan en un vacío estéril que impide el flujo y tensión creativa que requieren los procesos de transformación y cambio. Primeramente se explicitan conceptos, seguido de ejemplos de brechas en torno a las cuales venimos trabajando. Finalmente concluimos con una síntesis integradora para abrir nuevos horizontes que nos conduzcan a una articulación compleja de dichas brechas

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