Disease relevance of Necrosis

• C6 gliomas exhibit morphological characteristics of human glioblastoma multiforme such as necroses with palisading cells [1].
• In mice at 500 microg/mL, occasional focal retinal necroses were observed, suggesting isolated retinal toxicity at this concentration of moxifloxacin [2].
• The myocardial necroses could be a consequence of the induced hypertension, or a direct effect of angiotensin II, or a combination of effects, although their predominance in the left ventricle suggests high systemic arterial pressure is an important factor [3].
• Alpha-2-macroglobulin a serum protein with a large hydrodynamic radius was also demonstrated in grade III and IV gliomas, whereas IgM and beta-lipoprotein being the largest serum proteins tested were almost restricted to blood vessels and tumour necroses [4].
• The penetration of ciprofloxacin into human pancreatic and peripancreatic necroses in acute necrotizing pancreatitis [5].

High impact information on Necrosis

• When measured histometrically, it appeared that the loss of the horn and the formation of necroses, 3-10 times larger than in the placebo groups, were mainly responsible for the tumor regressions caused by the retinoid [6].
• Forty-eight hours thereafter focal, but evidently cadmium-induced necroses occurred in the grafts [7].
• In GBM, PHF3 expression is concentrated in cells surrounding necroses [8].
• Glibenclamide does not enlarge myocardial necroses [9].
• The first one induces necroses and the expression of pathogen-related proteins, includes tyrosine protein kinases and mitogen-activated protein kinases, and depends on the overall structure and charge distribution [10].

Chemical compound and disease context of Necrosis

• The myocardial necroses were found principally in the left ventricle; only at the highest doses of angiotensin II were right ventricular lesions present [3].
• Cells in spheroids with central necroses were more sensitive to ACNU than cells in monolayer, although a large fraction of the cells in these spheroids was resistant to 5-Fu [11].
• The dependence of cardiac necrosis production on the presence or normal aggregability of platelets points out at platelet-dependent microvascular alterations as a main cause of isoproterenol-induced cardiac necroses [12].
• Pathological evaluation showed severe inflammatory responses and necroses only in liver sections from rats in the pyrazole plus LPS group; blood transaminase levels were significantly elevated only in the combination group [13].
• Aminoethoxyvinylglycine (AVG)-treated, ethylene-nonproducing N. benthamiana plants developed much larger necroses than ethylene-producing plants, whereas addition of ethylene to AVG-treated leaves restricted disease spreading [14].

Biological context of Necrosis

• The viable motheaten (mev) mice are characterized by a moth-eaten appearance of the coat, immunodeficiency, autoimmunity, generalized inflammatory disease, paws necroses, and early death [15].

Anatomical context of Necrosis

• Furthermore, cases with elevated numbers of leukocytes and macrophages, microfocal C5b-9((m))(+) necroses, and enteroviral VP1 capsid protein within the myocardium were detected [16].
• In about 30% of the animals treated with MNNG, degenerative liver changes were found, especially single cell and focal necroses, cystic alterations, and bile-duct proliferations [17].
• The development of necroses and the course of the mitotic index in the embryonic spinal cord of 10-day-old mouse embryos (NMRI) were investigated between 1.5 h and 4 h after either an intraperitoneal application of 500 mg/kg hydroxyurea (HU) or 1 mg/kg colchicine or a simultaneous application of both substances [18].
• The autopsy and toxicological analyses revealed that death was caused by an overdose of methadone and that the necroses in the groins were fistulas facilitating administration of the drugs directly into larger veins [19].
• Moreover, moxonidine treatment very effectively decreased the number of necroses (1 necrosis in 71 fetuses in the l-NNA + moxonidine group versus 15 necroses in 79 fetuses in the l-NNA group, P < 0.01) [20].

Gene context of Necrosis

• VEGF is particulary upregulated in palisading cells adjacent to necroses and has subsequently been shown to be hypoxia-inducible in glioma cells in vitro [21].
• SF/HGF expression was not up regulated around necroses or at tumor margins [22].
• Intestinal changes seen in the EGF-R (-/-) mice vary in severity, the end-point being severe mucosal lesions and necroses [23].
• We show that the protective response is composed of CD8(+) and interferon-gamma (IFNgamma)-producing CD4(+) cells, and that the most overt effects of these components on tumor growth in situ are to provoke overt focal necroses and to decrease the stromal bed [24].
• Preoperative embolisation did not influence Ki67 PI, but four of the 15 embolised tumours showed substantially increased MIB1 PIs around embolisation necroses [25].

Analytical, diagnostic and therapeutic context of Necrosis

• The pathogenesis of local skin necroses after intramuscular injection of various drugs such as phenylbutazone (Embolia cutis medicamentosa, Nicolau's syndrome) is not clear [26].
• Brain necroses after intraarterial chemotherapy and irradiation of malignant gliomas--a complication of both ACNU and BCNU [27]?
• Scintigraphy was used to study the distribution of the substance in the body of the experimental animal after intravenous (i.v.) application; long-term studies of embolized auricular arteries in rabbits revealed parchment-like necroses after 5 to 10 days and the presence of radiopaque substances in the ear stumps after 6 weeks [28].

References