998 resultados para Library Administration.
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View to entrance stair as seen from exterior court.
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View to south-east elevation with corrugated steel cladding, plywood, concrete block and colonnade, as seen from exterior.
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View to south-east elevation; entrance stair, plywood and sheet steel cladding and colonnade, as seen from exterior.
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View of timber batten screen to verandah behind and entrance stair, as seen from exterior.
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View of timber batten screen to north-east elevation with verandah behind.
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View of steel-framed timber screen to verandah.
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View of second floor reading area with rigid frames and air-conditioning ducting.
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View to south-east elevation as seen from exterior.
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North-west elevation as seen from Building K.
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View to entrance verandah on north-east elevation and sunshades to north-west elevation.
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Using light and electron microscopic histological and immunocytochemical techniques, we investigated the effects of the glucocorticoid dexamethasone on T cell and macrophage apoptosis in the central nervous system (CNS) and peripheral nervous system (PNS) of Lewis rats with acute experimental autoimmune encephalomyelitis (EAE) induced with myelin basic protein (MBP). A single subcutaneous injection of dexamethasone markedly augmented T cell and macrophage apoptosis in the CNS and PNS and microglial apoptosis in the CNS within 6 hours (h). Pre-embedding immunolabeling revealed that dexamethasone increased the number of apoptotic CD5+ cells (T cells or activated B cells), αβ T cells, and CD11b+ cells (macrophages/microglia) in the meninges, perivascular spaces, and CNS parenchyma. The induction of increased apoptosis was dose-dependent. Daily dexamethasone treatment suppressed the neurological signs of EAE. However, the daily injection of a dose of dexamethasone (0.25 mg/kg). which, after a single dose, did not induce increased apoptosis in the CNS or PNS, was as effective in inhibiting the neurological signs of EAE as the high dose (4 mg/kg), which induced a marked increase in apoptosis. This indicates that the beneficial clinical effect of glucocorticoid therapy in EAE does not depend on the induction of increased apoptosis. The daily administration of dexamethasone for 5 days induced a relapse that commenced 5 days after cessation of treatment, with the severity of the relapse tending to increase with dexamethasone dosage.