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Luigi Pentimalli, Andrea Modesti, Andrea Vignati, Enrico Marchese, Alessio Albanese, Federico Di Rocco, Anna Coletti, Paolo Di Nardo, Cristina Fantini, Barbara Tirpakova and Giulio Maira

progress in research, however, basic genetic mechanisms related to intracranial aneurysms remain unclear. Other authors have suggested that apoptosis (genetically programmed cell death) may be involved in aneurysm growth and rupture. In a number of congenital and/or acquired pathological conditions, apoptotic phenomena may become pronounced, damaging arterial walls. 14, 20 An attempt to delineate the mechanisms of apoptotic smooth-muscle cell death in intracranial aneurysms has been proposed by Stehbens, 37 who studied the involvement of phosphorylated c-Jun NH 2

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Evelyne Emery, Philipp Aldana, Mary Bartlett Bunge, William Puckett, Anu Srinivasan, Robert W. Keane, John Bethea and Allan D. O. Levi

A poptosis is an important biological process in eukaryotes in which individual cells die by activating an intrinsic suicide mechanism. Apoptosis is distinguished from necrotic cell death by morphological and biochemical criteria. Apoptosis is an active process of cell destruction characterized by cell shrinkage, chromatin aggregation with genomic fragmentation, and nuclear pyknosis. 27, 31 In contrast, necrosis is characterized by passive cell swelling, intense mitochondrial damage with rapid energy loss, and disruption of internal homeostasis. Necrosis

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Kotaro Ogihara, Alexander Y. Zubkov, David H. Bernanke, Adam I. Lewis, Andrew D. Parent and John H. Zhang

-treated control group at 24 hours. Transmission Electron Microscopy Findings: the Apoptotic Body Transmission electron microscopy is another specific method used to identify apoptotic changes in cells. As shown in Fig. 3 , ultrastructural analysis of endothelial cells incubated with saline or OxyHb (100 µM) for 24 hours revealed morphological changes in endothelial cells that were typical of the stages of apoptotic changes. Figure 3A shows a normal endothelial cell treated with saline for 24 hours. Figure 3B–D shows dynamic changes in cells undergoing apoptosis

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Mubarak Al-Ghatany, Mubarak Al-Shraim, Allan D. O. Levi and Rajiv Midha

were treated nonsurgically. Delayed, subacute deterioration secondary to involvement of several segments above the original injury level, which is unrelated to mechanical instability or syrinx formation, is rare and its mechanism has not been fully elucidated. Apoptosis has been increasingly cited as a key factor in the pathobiological action of disease afflicting the CNS. In this article we will try to shed the light on the role of apoptosis in the mechanism of progressive SPAM, based on the pathological finding in our case. Recent evidence of apoptosis

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Narendra Nathoo, Pradeep K. Narotam, Devendra K. Agrawal, Catherine A. Connolly, James R. van Dellen, Gene H. Barnett and Runjan Chetty

, presents an attractive target for pharmacological and genetic manipulation. Recently it has become increasingly clear that apoptosis of both neurons and oligodendrocytes may contribute to the overall diseased state associated with clinical 7, 22 and experimental TBI. 3, 8, 21, 28 In 1999 Clark and associates 7 were the first to document the presence of apoptosis in humans with TBI. In their study, brain tissue samples were collected in patients who had undergone resection for impending cerebral herniation and were compared with postmortem samples. In another

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David H. Harter, Patrick F. Doherty and Lawrence S. Chin

Apoptosis is a carefully regulated process involved in developmental and immunological events. The alteration of apoptotic pathways is important in the establishment and progression of neoplasia. Apoptosis allows for the orderly removal of excess cells but, in contrast to necrosis, it is not an inflammatory process. Many of the molecular components and effectors of apoptosis have been described. In this review the authors briefly discuss the current understanding of apoptosis in the context of the two prevailing hypotheses, the “conflicting signal” and “dual signal” theories.

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Vladimir V. Didenko, Hop N. Ngo, Candace Minchew and David S. Baskin

—mediated destruction. Recently it was reported that in some tumors, including hepatocellular carcinoma, melanoma, and colon cancer, an immune evasion strategy has been developed that is based on FasL-mediated destruction of invading lymphocytes. 9, 12, 15 Various immune privileged sites, such as the eye or testis, rely on FasL expression for maintenance of their immune privileged positions because FasL expression induces apoptosis in entering activated immune cells. Similarly, in the tumors mentioned earlier, invading T lymphocytes that express Fas are stimulated to apoptosis by

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Toshinari Meguro, Christoph P. R. Klett, Betty Chen, Andrew D. Parent and John H. Zhang

cells of cerebral arteries are damaged. They may incur cellular distortion, formation of intracellular vacuoles, disruption of tight junctions, or widening of interendothelial spaces. The damage may lead to the detachment of endothelial cells. 3, 5, 13 We recently found that OxyHb induces apoptotic changes in cultured vascular endothelial cells. 17 This result may provide us with some suggestions about the pathogenesis and therapeutic strategies of cerebral vasospasm. Apoptosis induced by OxyHb has many mechanisms that remain unclear. It has been documented that the

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Dali Yin, Norihiko Tamaki and Takashi Kokunai

H uman malignant gliomas are among the most difficult tumors to treat successfully. Improving the efficacy of chemotherapy depends on knowledge of the underlying mechanism by which anticancer agents kill glioma cells, as well as the tumor's mechanisms of resistance. In recent studies 2, 20, 22 it has been demonstrated that chemotherapy results in dramatic changes in cellular gene expression and the induction of apoptosis in many tumor cell types. In a variety of lesions, the susceptibility of tumor cells to apoptotic cell death following chemotherapy is a major

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Hamed Reihani Kermani, Hamid Hoboubati, Saeed Esmaeili-Mahani and Majid Asadi-Shekaari

apoptosis in the discs was significantly increased by CUS, but this process was not intensified in degenerated discs after CUS. F ig . 2. Bar graph showing results of Western blot analysis of Bax/Bcl2 protein across experimental groups. Each value in the graph represents the mean ± SEM band density ratio for each group (*p < 0.05, **p < 0.01 compared with control group). Histopathological Findings Staining With the TUNEL Method Apoptotic cells were examined using the TUNEL method ( Fig. 3 ). The degenerated, CUS, and degenerated/CUS groups exhibited