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Inflammation apoptosis

Holmin, S. and Mathiesen T. Intracerebral administration of interleukin-1 beta and induction of inflammation, apoptosis, and vasogenic edema. J. Neurosurg. 92, 108, 2000. [Pg.304]

Figure 20.34 A simple representation of the processes of necrosis and apoptosis leading to the death of cells. Necrosis is initiated by a decrease In the ATP/ADP concentration ratio, which slows ion pumps, which leads to cation imbalance (e.g. ca ion entry into the cytosol) and hence intracellular damage, entry of water and lysis which can lead to local inflammation. Apoptosis is initiated by specific extracellular or intracellular factors, which lead to cell shrinkage and disruption into apoptotic bodies which are removed by phagocytes. Figure 20.34 A simple representation of the processes of necrosis and apoptosis leading to the death of cells. Necrosis is initiated by a decrease In the ATP/ADP concentration ratio, which slows ion pumps, which leads to cation imbalance (e.g. ca ion entry into the cytosol) and hence intracellular damage, entry of water and lysis which can lead to local inflammation. Apoptosis is initiated by specific extracellular or intracellular factors, which lead to cell shrinkage and disruption into apoptotic bodies which are removed by phagocytes.
The importance of NF-kB to inflammation, apoptosis resistance and tumour progression has resulted in the development of unique NF-kB inhibitors as part of cancer therapeutic regimens for GI and other cancers. Efforts are also being made to understand the efficacy of using natural substances obtained from plants, such as feverfew (e.g. parthenolide), bee glue (e.g. caffeic acid phenylethyl ester), tea (e.g. EGCG), spices (e.g. curcumin from turmeric) and mulberry figs (e.g. morin, a flavone) for the prevention both of persistent NF-kB activation and of the development of inflammatory pre-neoplastic lesions. [Pg.55]

There is incomplete understanding of the disease mechanism beyond substrate storage, although several processes (such as inflammation, apoptosis, defects of autophagy and activation of the ER-stress response) may have a contributory role (Ballabio and Gieselmann, 2009). [Pg.792]

Sjogren s is also hypothesized to be triggered by a virus, which initiates the inflammatory response in lacrimal and salivary glands. The genetic factors play a role in modulating the immune response to the inflammation. In a normally mounted immune response to inflammation, apoptosis of the activated immune cells reverses the process once the virally infected cells are neutralized. In Sjogren s syndrome the normal apoptotic process does not occur due to a combination of genetic and neuroendocrine factors. [Pg.288]

Caspase-4 lch-2, ICErelll Caspase-1 Inflammation/apoptosis (note this could be the human form of mouse caspase-11). Related to human caspase-5 and caspase-1... [Pg.162]

Caspase-5 ICErellll, TY Inflammation/apoptosis (related to human caspase-4 and caspase-1)... [Pg.162]

Of the available MRI and CT measurements, abnormalities detected on diffusion-weighted MR imaging (DWI) are considered the most reliable estimate of the infarct core. Within this region, cell death occurs via a variety of mechanisms including excitotoxicity, oxida-tive/nitrosative stress, inflammation, apoptosis, and peri-infarct depolarization [55]. The loss of cellular energy metabolism causes a failure of membrane ionic... [Pg.251]

Yang, H., et al.. The many faces of HMGBl molecular structure-functional activity in inflammation, apoptosis, and chemotaxis. JLeukoc Biol, 2013. 93 p. 865-73. [Pg.427]

Cellular processes modulated by CO -inflammation -apoptosis/cell death... [Pg.548]


See other pages where Inflammation apoptosis is mentioned: [Pg.283]    [Pg.448]    [Pg.469]    [Pg.64]    [Pg.502]    [Pg.166]    [Pg.785]    [Pg.805]    [Pg.901]    [Pg.1126]    [Pg.419]    [Pg.419]    [Pg.1]    [Pg.14]    [Pg.172]   
See also in sourсe #XX -- [ Pg.50 ]




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Apoptosis and inflammation

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