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Necrotic process

The source of free radicals is multiplied under these circumstances, arachidonic acid metabolism, activation of xanthine oxidase, perturbation of electron flow within the respiratory chain, and NOS activation. Structurally, excitotoxicity is generally described as a necrotic process involving initial swelling of the cell and of the endoplasmic reticulum, clumping of chromatin, followed by swelling of the... [Pg.350]

Biochemically, following the opening of the mitochondrial mega-pore and the MPT, if sufficient mitochondria are damaged to this level, then the cell will die by necrotic processes. Once the pore has opened, ATP can flow out and solutes such as Ca2+ can flow in. [Pg.229]

Propylthiouracil The therapeutic aim is the inhibition of a hyprer-metabolic status and the prevention of pericentral necrotizing processes. Dosage 300 mg/day. So far, no efficacy could be proved. [Pg.537]

Fig. 37.27 Numerous cystoid liver metastases due to a central necrotizing process (differential diagnosis liver abscesses)... Fig. 37.27 Numerous cystoid liver metastases due to a central necrotizing process (differential diagnosis liver abscesses)...
Coronary flow fractions (CFF) were collected and analyzed using previously published procedures (see Methods and refs. [10,11]). The first CFFs of reperfusion contained relatively high levels of iron and copper (Table 2). The values were dependent on the duration of ischemia, while the concentrations of group I CFFs were systematically and markedly lower (by a factor of 2-5) than the corresponding values of group III. The mobilization patterns of these metals from the tissue to the CFF were similar to each other, but distinctly different for iron, copper, and protein, indicating that this mobilization does not reflect a simple necrotic process, but rather a selective one [11]. [Pg.51]

Apoptotic/necrotic transformation of excitable cells. Effects of dipeptides directed to support stability of cellular structures increase the reliability of cellular functions under normal conditions and especially during oxidative stress, which accompanies effect of several extreme factors. It was found in experiments on individual neurons that carnosine prevents cell death induced by excitotoxic compounds, N-methyl-D-aspartic acid (NMDA) or kainate [93-95] or experimental hypoxia/reoxigenation [96]. Apoptosis induced by exposure of cerebellum neurons to kainic acid (see Table 6), was arrested if the cells were pre-incubated with carnosine or anserine and simultaneously heavy necrotic processes were substitute by light (reversible) necrosis. At the same time, N-acetylcamosine or homocaraosine did not reveal protecting action [94,95]. [Pg.211]

Only few detailed analyses of the intracellular events following epithelial injury have been performed using cells from the airways, and most mechanistic work has concentrated on pre-necrotic and necrotic processes in epitheUal cells of renal origin (Trump etal., 1980, 1981 Trump and Berezesky, 1984). Collectively these studies, which have employed a wide range of stimuli to evoke cellular injury (ischaemia, metabolic poisons, chaotropic agents and ionophores), suggest that similar patterns of intracellular events accompany injury evoked by the different stimuli. [Pg.193]

Acute Phase Response. In inflammatory or necrotic processes, serum AAT levels begin to rise after approximately 24 hours and peak at 3 to 4 days if the insult is acute and short lived. Synthesis is stimulated by cytokines, particularly the IL-6 family, and by AAT-elastase complexes taken up via SEC-R. Cytokines induce a broader APR, whereas uptake by the SEC-R induces only AAT synthesis. The acute phase response of AAT probably occurs in an attempt to control... [Pg.550]

The proximate cause of PUD is relative or absolute gastric acid hypersecretion. The etiology of the disease is still unknown. Many pathophysiologic abnormalities have been proposed as explanations for the mechanism(s) by which this excess acidity causes gastric and duodenal ulceration. Our understanding of what the cytoprotective controls are that prevent this necrotic process in healthy individuals is simultaneously increasing. [Pg.630]

Fetykov, A.L, et al. The effectiveness of cold plasma treatment of diabetic feet syndrome, complicated hy purulo-necrotic process. In 2nd International Conference on Plasma Medicine, San Antonio, TX, USA (2009)... [Pg.381]

Liver Fibrosis Liver fibrosis is a common end result of inflammation and/or necrosis. While the liver does have considerable regenerative capabilities, cytokine release associated with the inflammatory/necrotic process can lead to fibrosis that can have a deleterious effect on hepatic function, not only from the aspect of decreased hepatic functional mass but also from the standpoint of compromising blood supply. Animal models of hepatic fibrosis would be valuable from the standpoint of facilitating the development of noninvasive biomarkers as well as development of interventional agents. [Pg.266]

As discussed earlier, MPTP has been shown to be causal in the development of PD. The structural similarity between MPTP and organophosphate pesticides sng-gests that such pesticides might also cause PD, and epidemiological studies have demonstrated such relationships [33]. In an in vitro study, it was demonstrated that coadministration to the organophosphate endosnlfan = 3.83) and the dithio-carbamate zineb (A w = 0.39) resnlts in synergistic apoptotic/necrotic process... [Pg.261]


See other pages where Necrotic process is mentioned: [Pg.350]    [Pg.15]    [Pg.59]    [Pg.243]    [Pg.258]    [Pg.535]    [Pg.431]    [Pg.280]    [Pg.57]    [Pg.299]    [Pg.401]    [Pg.718]    [Pg.59]    [Pg.307]    [Pg.550]    [Pg.165]    [Pg.59]    [Pg.285]    [Pg.159]    [Pg.505]    [Pg.263]    [Pg.4]    [Pg.555]    [Pg.155]   
See also in sourсe #XX -- [ Pg.419 ]




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