1,721,205 research outputs found
Mitochondria as sensors of sphingolipids
Much of the action in the mammalian apoptotic program takes place at the mitochondrial level. Physicochemical characteristics and integrity of mitochondrial membranes may play a crucial role in the recruitment and multimerization of pro-apoptotic Bcl-2 family members, opening of the permeability transition pore complex (PTPC) and the release of mitochondrial components which trigger the 'intrinsic' pathways of cellular apoptosis and activate executioner caspases. Recent evidence has accumulated pointing toward the mitochondrial membranes as the key targets for lipid and glycolipid mediators of stress-induced apoptosis. Mitochondrial membranes may thus act as 'sensors' of cellular stress by quantitating the local accumulation of specific lipids and glycolipids. Acute accumulation of ceramides, directly or indirectly, profoundly affects mitochondrial functions. GD3 ganglioside, a glycolipid which is actively synthesized and transiently accumulates in the early stages of apoptosis, relocates to the mitochondrial membranes causing the opening of the PTPC and the release of apoptogenic factors. Mitochondrial membranes appear to represent a common destination where protein and glycolipid mediators of stress converge and where crucial decisions about cellular adaptation or apoptotic cell death are taken
Corticosteroidi per nebulizzazione nella tosse da rinofaringite nel bambino
Il BDP è comunemente impiegato nel trattamento delle flogosi delle vie aeree superiori al fine di controllare i fenomeni infiammatori acuti che si evidenziano in corso di rinofaringiti e faringolaringiti, e delle loro complicanze quali tracheiti, tracheolaringiti, rinosinusiti e otolaringiti. Il FP presenta una maggiore attività antinfiammatoria una maggior rapidità d’azione e una minore biodisponibiltà orale rispetto al BDP.
Lo scopo di questo studio è stato quello di confrontare l’efficacia e la tollerabilità di FP con BDP per via aerosolica nel trattamento di infiammazioni delle vie aeree superiori in età pediatrica.
Sono stati arruolati 278 bambini di età compresa tra 4 e 14 anni, con infiammazione delle vie aeree superiori. I bambini ricevevano in regime di doppio cieco FP al dosaggio di 0.25 mg due volte al giorno oppure BDP al dosaggio di 0.4 mg due volte al giorno per 5-7 giorni.
Al termine del trattamento 76 (54.7%) pazienti nel gruppo FP e 74 (54.8%) nel gruppo BDP sono risultati guariti (n.s.).
Questo studio suggerisce pertanto un possibile impiego del FP in alternativa al BDP nel trattamento delle flogosi delle vie aeree superiori
La responsabilità professionale in campo medico con particolare riferimento all'odontostomatologia
GD3 in cellular ageing and apoptosis
Lipid and glycolipid mediators are important components of the adaptive responses to stress, including apoptosis. In mammalian cells, the intracellular accumulation of ganglioside GD3, an acidic glycosphingolipid, contributes to mitochondrial damage, a crucial event during the apoptotic program. GD3 is a minor ganglioside in most normal tissues. Its expression increases during development and in pathological conditions such as cancer and neurodegenerative disorders. Interestingly, GD3 expression also increases with the normal ageing process. Moreover, GD3 can also mediate biological events like proliferation and differentiation. Since organism integrity requires a tight balance between cell proliferation, apoptosis and senescence, controlling the intracellular level of GD3 appears of particular importance for cell fate determination
The ganglioside GD3 as the greek goddess Hecate: Several faces turned towards as many directions
The disialoganglioside GD3 can mediate biological functions as diverse as proliferation, differentiation, and apoptosis. Since intracellular level of GD3 is crucial for the cell, understanding the mechanisms by which GD3 metabolism is tightly regulated seems of particular importance. GD3 can be enlisted among the most potent natural inducers of mitochondrial damage and apoptosis. However, some cell types resist GD3-mediated mitochondrial damage through complex mechanisms which are beginning to be unveiled. © 2005 IUBMB
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