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Massive Necrosis (massive + necrosis)
Selected AbstractsMassive necrosis of cervical ectopic decidua presenting in labourBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 4 2000A. S. Gornall Subspecialty Trainee (Fetomaternal Medicine) No abstract is available for this article. [source] Nuclear factor ,B decoy oligodeoxynucleotides prevent endotoxin-induced fatal liver failure in a murine modelHEPATOLOGY, Issue 2 2003Ichiro Ogushi Endotoxin syndrome is a systemic inflammatory response mediated by inflammatory cytokines. Nuclear factor ,B (NF-,B) is the dominant regulator of the production of these cytokines by inflammatory cells. The aim of this study was to assess the efficacy of in vivo transfer of synthetic double-stranded oligodeoxynucleotides (ODN) with high affinity against NF-,B (NF-,B/decoy/ODN) as a therapeutic strategy for treating endotoxin-induced fatal liver injury. Liver injury was induced by administration of lipopolysaccharide (LPS) to Propionibacterium acnes -primed BALB/C mice. NF-,B/decoy/ODN was transferred into the portal vein using a fusigenic liposome with hemagglutinating virus of Japan. NF-,B/decoy/ODN was preferentially transferred to Kupffer cells, and activation of NF-,B after the LPS challenge was suppressed, leading to decreased inflammatory cytokine production. As a result, the massive necrosis and hepatocyte apoptosis observed in the control mice was dramatically attenuated and the survival rate improved. In conclusion, NF-,B/decoy/ODN transfer in vivo effectively suppressed endotoxin-induced fatal liver injury in mice. [source] Telomerase inhibition by stable RNA interference impairs tumor growth and angiogenesis in glioblastoma xenograftsINTERNATIONAL JOURNAL OF CANCER, Issue 9 2006Roberto Pallini Abstract Telomerase is highly expressed in advanced stages of most cancers where it allows the clonal expansion of transformed cells by counteracting telomere erosion. Telomerase may also contribute to tumor progression through still undefined cell growth-promoting functions. Here, we inhibited telomerase activity in 2 human glioblastoma (GBM) cell lines, TB10 and U87MG, by targeting the catalytic subunit, hTERT, via stable RNA interference (RNAi). Although the reduction in telomerase activity had no effect on GBM cell growth in vitro, the development of tumors in subcutaneously and intracranially grafted nude mice was significantly inhibited by antitelomerase RNAi. The in vivo effect was observed within a relatively small number of population doublings, suggesting that telomerase inhibition may hinder cancer cell growth in vivo prior to a substantial shortening of telomere length. Tumor xenografts that arose from telomerase-inhibited GBM cells also showed a less-malignant phenotype due both to the absence of massive necrosis and to reduced angiogenesis. © 2005 Wiley-Liss, Inc. [source] Continuous infusion of prostaglandin E1 via the superior mesenteric artery can prevent hepatic injury in hepatic artery interruption through passive portal oxygenationLIVER INTERNATIONAL, Issue 2 2000Tsutomu Sato Abstract:Aims/Background: Hepatic artery interruption (HAI) causes severe ischemic liver damage, especially following hepatopancreatobiliary surgery. In order to inhibit a decrease in oxygen delivery after HAI, continuous infusion of PGE1 via the superior mesenteric artery (SMA) was administered in pigs and changes in hepatic blood flow and oxygen delivery were investigated. Furthermore, its effectiveness in the prevention of liver injury was evaluated by histology and serum enzyme levels. Methods: Animals were subjected to HAI without PGE1 infusion (control group n=6) and to continuous infusion of PGE1 (0.02 ,g/kg/min) into the SMA (PGE1 group n=6). Results and Conclusion: PGE1 infusion via the SMA not only increased the portal blood flow but also elevated the oxygen content of the portal blood. The reduction in oxygen delivery to the liver was 50% in the control group, and only 13% in the PGE1 group. Serum aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels 24 h after HAI in the control group were 3415±1283 IU/L and 9839±2959 respectively while in the PGE1 group they were 939±426 IU/L and 5510±1545 IU/L respectively. Histological examination showed massive necrosis in the control group at 72 h but only focal liver cell necrosis in the PGE1 group. Based on this finding and the fact that this treatment can be performed easily and safely, continuous infusion of PGE1 via the SMA may be a useful intervention to prevent severe liver damage after hepatic artery interruption. [source] Necrotizing sialometaplasia of the parotid gland associated with angiocentric T-cell lymphoma: A case report and review of the LiteraturePATHOLOGY INTERNATIONAL, Issue 4 2010Takako Yoshioka A very rare case of necrotizing sialometaplasia of the parotid gland associated with angiocentric T-cell lymphoma was described. A 66-year-old male had left neck and pharyngeal masses and biopsy specimen showed a monotonous proliferation of atypical lymphoid cells with massive necrosis in the parotid gland. Angiocentric pattern or vascular invasion by the lymphoid cells was observed and the involved parotid gland exhibited squamous metaplasia of the ducts and acini; necrotizing sialometaplasia. Immunohistochemical analysis revealed a cytotoxic T-cell phenotype of the lymphoid cells (CD3+, CD4-, CD5+, CD8+, CD56-, Granzyme B+, TIA-1+, Perforin-) but in situ hybridization showed no relation to Epstein-Barr virus. Although necrotizing sialometaplasia is relatively rare in the parotid gland, angiocentric T-cell lymphoma should be considered for a causative condition of necrotizing sialometaplasia. [source] |