Navegando por Palavras-chave "necrosis"

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    Effect of nicotine treatment and withdrawal on random-pattern skin flaps in rats
    (Elsevier B.V., 2008-09-01) Campos, Jose Humberto O.; Gomes, Heitor Carvalho [UNIFESP]; dos-Santos, Washington L. C.; Cardeal, Mauricio; Ferreira, Lydia Masako [UNIFESP]; Escola Bahiana Med & Saude Publ; Universidade Federal de São Paulo (UNIFESP); Fundacao Oswaldo Cruz
    Background: Tobacco use is associated with a high incidence of skin necrosis after surgery. the ideal timing for the cessation of tobacco use before plastic surgery has not, however, been precisely determined. the aim of this work was to define the ideal duration of nicotine withdrawal prior to random-pattern skin flap surgery in rats.Methods: Groups of 11 animals were subcutaneously injected with saline or nicotine (2 mg/kg) twice a day and subjected to random-pattern skin flap surgery according to the following protocol: Group I: continuously injected with saline 4 weeks before and I week after the surgery; Group II: injected with nicotine for 4 weeks until the day of the surgery; Group III: injected with nicotine for 4 weeks until one day before the surgery; Group IV: injected with nicotine for 4 weeks until 5 days before the surgery; Group V: injected with nicotine for 4 weeks until 10 days before the Surgery; Group VI: continuously injected with nicotine for 4 weeks before and I week after the surgery. McFARLANE skin flaps were performed on the dorsal skin, and the rats were sacrificed I week after the surgery.Results: the necrotic area was smaller in group I (8.85 cm(2)) than in group II (12.15 cm(2)), III (12.88 cm(2)) and VI (14.84 cm(2)) (ANOVA p < 0.0001). There was no difference between groups I, IV (10.13 cm(2)) and V (9.27 cm(2)).Conclusions: in conclusion, 5 days before surgery was considered the ideal time for nicotine withdrawal in this experimental model. (C) 2008 Published by Elsevier GmbH.
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    Electroporation of Vascular Endothelial Growth Factor Gene in a Unipedicle Transverse Rectus Abdominis Myocutaneous Flap Reduces Necrosis
    (Lippincott Williams & Wilkins, 2010-02-01) Rezende, Fernando C. [UNIFESP]; Gomes, Heitor C.; Lisboa, Bianca; Lucca, Aldrein F. [UNIFESP]; Han, Sang W.; Ferreira, Lydia M.; Div Plast Surg; Interdisciplinary Ctr Gene Therapy CINTERGEN; Universidade Federal de São Paulo (UNIFESP)
    Necrosis in TRAM (transverse rectus abdominis myocutaneous) still occurs in flap breast reconstruction. Blood flow may be improved by vascular endothelial growth factor (VEGF), an endogenous protein that stimulates neovascularization. Experimental studies of gene therapy with plasmid vector expressing human VEGF (hVEGF) presented inadequate results. Low level of gene expression could be the cause. To prove that high level of VEGF gene expression can minimize necrosis of TRAM flap, electroporation of VEGF plasmid was tested.Forty-two adult, male, Wistar-EPM rats were randomly distributed in 6 groups of 7 animals and 50 jig of vectors were injected in the intradermal layer of TRAM flap donor region, by electroporation: LacZ (beta-galactosidase gene): CG (no substance injected and flap elevated); P2G (empty gT plasmid in area 2); PV2G (gT-VEGF(165) in area 2); P4G (empty gT plasmid in area 4); PV4G (gT-VEGF(165) in area 4). Five days after flap elevation, the animals were euthanized and the degree of necrosis was analyzed by histology and paper template method.Dermal X-gal staining after electroporation with pSV(2)lacZ proved high rate of gene transfer. Mean values of necrosis by the paper template method were: CG (74.5%), P2G (62.2%), PV2G (41.1%), P4G (76.6%), and PV4G (59%). Degree of necrosis, preservation of muscle layer, and degree of infiltrates seen by histology were in accordance with mean values of necrosis.Intradermal injection of gT-VEGF(165) in area 2, by electroporation, was effective in reducing unipedicle I-RAM flap necrosis, in rats.
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    Ultrastructural identification of dentate granule cell death from pilocarpine-induced seizures
    (Elsevier B.V., 2000-08-01) Covolan, Luciene [UNIFESP]; Smith, R. L.; Mello, LEAM; Universidade Federal de São Paulo (UNIFESP)
    Cell loss in the hippocampal formation is a common event in patients with temporal lobe epilepsy. the belief that dentate granule neurons are relatively resistant to excitotoxic injury has recently been challenged both, in epileptic patients and in animal models of temporal lobe epilepsy. the nature of dentate granule cell damage in epilepsy has been reported as either apoptotic, necrotic or both. the lack of a consensus on this topic stems from use of different animal models and different experimental techniques for characterizing the apoptotic/necrotic process. Using electron microscopy for defining the, nature of cell loss and one of the main animal models of status epilepticus (SE) we have focussed on the nature of the degenerative process in dentate granule cells. Ultrastructural morphological changes of these cells were evaluated 2.5-48 h after pilocarpine-induced status epilepticus. A variety of morphologies ranging from apoptosis to necrosis, could be seen at 2.5 h after SE onset and continued at least over the following 48 h. Some cells displayed coalescence of chromatin against nuclear membranes. in such cases however, chromatin did not have well-defined edges las it should, if it were apoptosis). Condensation of cytoplasm. present in both processes was also frequently found. Neither obvious apoptotic budding-off of cytoplasm nor typical membrane-bound apoptotic bodies were found. Our results indicate that in the dentate granule cell layer pilocarpine-induced SE promotes a degenerative process in which apoptotic and necrotic features overlap. (C) 2000 Elsevier Science B.V. All rights reserved.
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    Vitamin E prevents cell death induced by mild oxidative stress in chicken skeletal muscle cells
    (Elsevier B.V., 2005-07-01) Nunes, Viviane A. [UNIFESP]; Gozzo, Andrezza Justino [UNIFESP]; Cruz-Silva, Ilana [UNIFESP]; Juliano, Maria Aparecida [UNIFESP]; Viel, Tania A. [UNIFESP]; Godinho, Rosely O. [UNIFESP]; Meirelles, Flavio V.; Sampaio, Misako U. [UNIFESP]; Sampaio, Claudio A M [UNIFESP]; Araujo, Mariana S. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    Apoptosis and necrosis are two forms of cell death that can occur in response to various agents and oxidative damage. in addition to necrosis, apoptosis contributes to muscle fiber loss in various muscular dystrophies as well participates in the exudative diathesis in chicken, pathology caused by dietary deficiency of vitamin E and selenium, which affects muscle tissue. We have used chicken skeletal muscle cells and bovine fibroblasts to study molecular events involved in the cell death induced by oxidative stress and apoptotic agents. the effect of vitamin E on cell death induced by oxidants was also investigated. Treatment of cells with anti-Fas antibody (50 to 400 ng/mL), staurosporine (0.1 to 100 mu M) and TNF-alpha (10 and 50 ng/mL) resulted in a little loss of Trypan blue exclusion ability. Those stimuli conducted cells to apoptosis detected by an enhancement in caspase activity upon fluorogenic substrates but this activity was not fully blocked by the caspase inhibitor Z-VAD-fmk. Oxidative stress induced by menadione (10, 100 and 250 mu M) promoted a significant reduction in cell viability (10%, 20% and 35% for fibroblasts; 20%, 30% and 75% for muscle cells, respectively) and caused an increase in caspase activity and DNA fragmentation. H2O2 also promoted apoptosis verified by caspase activation and DNA fragmentation, but in higher doses induced necrosis. Vitamin E protected cells from death induced by low doses of oxidants. Although it was ineffective in reducing caspase activity in fibroblasts, this vitamin diminished the enzyme activity in muscle cells. These data suggested that oxidative stress could activate apoptotic mechanisms; however the mode of cell death will depend on the intensity and duration of the stimulus, and on the antioxidant status of the cells. (C) 2005 Elsevier Inc. All rights reserved.