Relevant bibliographies by topics / Apoptosis/Necrosis

Academic literature on the topic 'Apoptosis/Necrosis'

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Published: 11 March 2023

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Journal articles on the topic "Apoptosis/Necrosis"

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Peter, Marcus E. "Apoptosis meets necrosis." Nature 471, no. 7338 (March 2011): 310–12. http://dx.doi.org/10.1038/471310a.

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Zhivotovsky, Boris. "Apoptosis, Necrosis and Between." Cell Cycle 3, no. 1 (January 2004): 63–65. http://dx.doi.org/10.4161/cc.3.1.606.

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Hurtley, S. M. "Apoptosis, necrosis, and pyroptosis." Science 352, no. 6281 (March 31, 2016): 48–50. http://dx.doi.org/10.1126/science.352.6281.48-j.

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Proskuryakov, S. Ya, V. L. Gabai, A. G. Konoplyannikov, I. A. Zamulaeva, and A. I. Kolesnikova. "Immunology of Apoptosis and Necrosis." Biochemistry (Moscow) 70, no. 12 (December 2005): 1310–20. http://dx.doi.org/10.1007/s10541-005-0263-4.

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Zhivotovsky, Boris, Afshin Samali, and Sten Orrenius. "Determination of Apoptosis and Necrosis." Current Protocols in Toxicology 00, no. 1 (May 1999): 2.2.1–2.2.34. http://dx.doi.org/10.1002/0471140856.tx0202s00.

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Liu, Huiping, Bradley C. McPherson, and Zhenhai Yao. "Preconditioning attenuates apoptosis and necrosis: role of protein kinase Cε and -δ isoforms." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (July 1, 2001): H404—H410. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h404.

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Preconditioning reduces cardiomyocyte necrosis in vivo and in vitro, but it is unknown whether preconditioning blocks apoptosis. We wanted to compare the effects of preconditioning on necrosis and apoptosis in cardiomyocytes. Necrosis was detected with propidium iodide, and apoptosis was quantified by three complementary techniques: flow cytometry, TdT-mediated dUTP nick-end labeling assay, and DNA-laddering electrophoresis. Apoptosis increased with simulated ischemia time (6 h, 19 ± 1%; 12 h, 27 ± 2%; 18 h, 40 ± 4%; 24 h, 54 ± 4%; and 36 h, 83 ± 4%; n = 6 for each group). Simulated ischemia and reoxygenation contributed equally to apoptosis (12-h ischemia, 27 ± 2%, n = 6; 12-h ischemia and 12-h reoxygenation, 51 ± 4%, n = 6; and 24-h ischemia, 54 ± 5%, n = 8). Necrosis occurred primarily during reoxygenation; none was detected during simulated ischemia. Preconditioning with 10 min of simulated ischemia reduced necrosis (18 ± 6%, n = 8) but had no effect on apoptosis. However, three 1-min cycles of simulated ischemia separated by 5 min of reoxygenation reduced necrosis and apoptosis similarly. The protein kinase C (PKC) inhibitors Go6976 (0.1 μM) or chelerythrene (4 μM) abolished the effect of preconditioning. Preconditioning selectively activated PKCε but had no effect on PKCδ and on total PKC enzyme activity. Preconditioning protected against necrosis and apoptosis, but the preconditioning ischemia required for blocking apoptosis was less than that for reducing necrosis. Activation of PKCε isoform is important in mediating the protection.
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SNIDER, B. JOY, FRANK J. GOTTRON, and DENNIS W. CHOI. "Apoptosis and Necrosis in Cerebrovascular Disease." Annals of the New York Academy of Sciences 893, no. 1 OXIDATIVE/ENE (November 1999): 243–53. http://dx.doi.org/10.1111/j.1749-6632.1999.tb07829.x.

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Jaeschke, Hartmut, Jaspreet S. Gujral, and Mary Lynn Bajt. "Apoptosis and necrosis in liver disease." Liver International 24, no. 2 (April 2004): 85–89. http://dx.doi.org/10.1111/j.1478-3231.2004.0906.x.

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Nicotera, Pierluigi, and Stuart A. Lipton. "Excitotoxins in Neuronal Apoptosis and Necrosis." Journal of Cerebral Blood Flow & Metabolism 19, no. 6 (June 1999): 583–91. http://dx.doi.org/10.1097/00004647-199906000-00001.

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Neuronal loss is common to many neurodegenerative diseases. Although necrosis is a common histopathologic feature observed in neuropathologic conditions, evidence is increasing that apoptosis can significantly contribute to neuronal demise. The prevalence of either type of cell death, apoptosis or necrosis, and the relevance for the progression of disease is still unclear. The debate on the occurrence and prevalence of one or the other type of death in pathologic conditions such as stroke or neurotoxic injury may in part be resolved by the proposal that different types of cell death within a tissue reflect either partial or complete execution of a common death program. Apoptosis is an active process of cell destruction, characterized morphologically by cell shrinkage, chromatin aggregation with extensive genomic fragmentation, and nuclear pyknosis. In contrast, necrosis is characterized by cell swelling, linked to rapid energy loss, and generalized disruption of ionic and internal homeostasis. This swiftly leads to membrane lysis, release of intracellular constituents that evoke a local inflammatory reaction, edema, and injury to the surrounding tissue. During the past few years, our laboratories have studied the signals and mechanisms responsible for induction or prevention of apoptosis/necrosis in neuronal injury and this is the subject of this review.
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McConkey, David J. "Biochemical determinants of apoptosis and necrosis." Toxicology Letters 99, no. 3 (November 1998): 157–68. http://dx.doi.org/10.1016/s0378-4274(98)00155-6.

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Dissertations / Theses on the topic "Apoptosis/Necrosis"

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Schobesberger, Martina. "Oligodendroglial degeneration in distemper : apoptosis or necrosis? /." [S.l.] : [s.n.], 1998. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Dunlop, J. "Modulation of human neutrophil apoptosis by tumour necrosis factor-alpha." Thesis, University of Edinburgh, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649799.

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Many pro-inflammatory mediators have been demonstrated to inhibit neutrophil apoptosis in vitro, suggesting that such agents act not only in a priming or secretagogue capacity but also increase neutrophil functional longevity by delaying apoptosis. We have examined whether this hypothesis holds true for all neutrophil priming agents, in particular TNFα, a potent neutrophil priming agent which has been variably reported to either induce, delay, or have no effect on the rate of constitutive neutrophil apoptosis. We have shown that following a 20 hr incubation the rate of neutrophil apoptosis is inhibited by TNFα, however more detailed analysis demonstrated the ability of this cytokine to promote apoptosis in a subpopulation of cells at earlier (2-8 hr) times. FMLP, PAF, inositol hexakisphosphate, LPS, LTB and GM-CSF which represent a broad spectrum of alternative neutrophil priming and activating agents all inhibited apoptosis at 6 and 20 hr. The early pro-apoptotic effect of TNFα was confirmed by DNA fragmentation and propidium iodide binding and shown to be concentration-dependent with a near-identical EC50 value (2.8 ng/ml) to that observed for TNFα-priming of fMLP-stimulated superoxide anion generation. Moreover, the early cytocidal effect of this cytokine was detectable within 2 hr, abolished by TNFα neutralizing antibody, and was not associated with any change in cell viability or recovery. Of note, TNFα-stimulated apoptosis was abolished by pre-incubation of neutrophils with selective blocking antibodies to both the TNFR55 (which contains the classical death-domain sequence and is entirely responsible for the TNFα priming effect in suspension neutrophils) and TNFR75 receptor subtypes. Moreover, the TNFR55-selective mutants (E146K, R23W-S86T) induced neutrophil apoptosis but with a potency 14-fold lower than wild type TNFα while the TNFR75-selective mutant (D143F) did not induce apoptosis. These data indicate that TNFα has the ability apparently unique to this priming agent to induce apoptosis in human neutrophils at early time points via a mechanism whereby the TNFR75 facilitates and permits TNFR55-mediated induction of cell death.
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Medan, Djordje. "Apoptosis-necrosis paradox implications to the pathogenesis of inflammatory disorders /." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2763.

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Thesis (M.S.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains ix, 75 p. : ill. (some col.) Vita. Includes abstract. Includes bibliographical reference.
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Murray, Joanna. "Modulation of human neutrophil apoptosis by tumour necrosis factor-α." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/22514.

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Abdo, Michael A. "Tumour necrosis factor : alpha signal transduction in rat corpus luteum apoptosis." University of Western Australia. School of Anatomy and Human Biology, 2002. http://theses.library.uwa.edu.au/adt-WU2003.0024.

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[Formulae and special characters can only be approximated here. Please see the pdf version of the abstract for an accurate reproduction.] Apoptosis is a morphologically distinct form of cell death that is involved in the regulation of normal and aberrant cell systems. The complexities of the apoptotic cell death pathway arise from variation in both the cellular specialisation and initial stimulus. The corpus luteum (CL) is an endocrine gland that whilst critical to the maintenance of pregnancy in the rat, regresses at the completion of each oestrous cycle and pregnancy. This regression is facilitated through apoptosis; though, the stimulus and factors involved in the apoptotic pathway are poorly understood. Previous studies suggest that CL regression is not initiated through failure of luteotrophic support, but rather the active production of a luteolytic factor, of which tumour necrosis factor -alpha (TNFα) is one possible candidate. Several publications have reported the participation of the immune system in ovarian events. There is evidence that TNFα expression within the ovary is coordinated between cells of the immune system and the hormonal regulation of the CL. This study has focussed on the role of TNFα in CL apoptosis and the factors involved in this apoptotic pathway. TNFα-induced cell death is governed by the presence of the two TNFα receptors (TNFR) and several second messenger systems that include; the sphingolipids, mitogen-activated protein (MAP) kinases, nitric oxide (NO), nuclear factor-kappaB (NF-κB) and the caspases. These factors and their interactions were assessed in the rat CL during pregnancy and post-partum, and in vitro. Apoptosis was measured through the analysis of DNA fragmentation using DNA 3’ end labelling and single cell electrophoresis (COMET assay). Assessment of mRNA and protein expression was through Real-time RT-PCR and Western blot analysis; proteins were localised within the CL by immunocytochemistry. In addition, specific measurement of sphingolipid expression and nitric oxide (NO) production was by high performance liquid chromatography (HPLC) and NO assay respectively. Following parturition, TNFα mRNA and protein expression increased corresponding to the onset of CL apoptosis and increased expression of the chemotactic factor monocyte chemoattractant protein -1 (MCP-1). Furthermore, CL apoptosis was induced by treatment with recombinant TNFα in a time- and dose-dependent manner. A similar effect was observed in isolated luteal cells. Simultaneously, the functional regression of the CL was assessed by measurement of both progesterone synthesis and steroidogenic acute regulatory (StAR) protein expression. StAR mRNA and protein expression declined toward parturition in vivo. Immunocytochemical studies revealed the presence of TNFα receptors 1 (TNFR1) and 2 (TNFR2) in luteal cells. Furthermore, TNFR mRNA was isolated from CL throughout pregnancy and post-partum. Subsequently, the role of the sphingolipids ceramide and sphingosine was examined during CL apoptosis in vitro. Ceramide and sphingosine were found to be potent apoptotic agents when administered in vitro (50µM). The downstream signal transduction of TNFα and ceramide was assessed through MAP kinase expression. Both TNFα and ceramide increased expression of the pro-apoptotic p38 MAP kinase with no change to the non-apoptotic extracellular signal-related kinase (ERK1&2). Despite previous reports of c-Jun NH2 terminal kinase (JNK) involvement in the cell death pathway, JNK expression was not evident in the rat CL. The caspases are a family of cysteine proteases central to the regulation and execution of apoptosis. General inhibition of the caspase cascade in vitro was effective in preventing apoptosis regardless of the apoptotic stimulus (TNFα, ceramide and sphingosine), suggesting that this pathway is central to CL apoptosis. Specific inhibition of several caspases produced a varying effect; inhibition of caspases 3, 6 and 8 significantly reduced the level of TNFα-induced apoptosis, thus supporting their classification as either regulatory or effector caspases. NO is endowed with the unique ability to initiate and to block apoptosis and this dichotomy extends to the cytotoxic actions of TNFα. Inhibition of NO production by treating CL with L-NAME prevented the onset of apoptosis, whilst NO production increased in response to increasing levels of apoptosis following trophic withdrawal. However, this effect was not seen during TNFα-induced apoptosis, suggesting that the actions of NO are independent of TNFα. The data presented within this study examine multiple elements of the TNFα cell death pathway in a single system. The results suggest that these elements are involved in TNFα signal transduction and furthermore, in rat CL apoptosis. It can be said that TNFα plays an active role in CL regression through the activation of the caspases, the sphingolipids and the MAP kinases.
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Antoine, Daniel James. "Chemical and molecular markers of hepatic drug bioactivation, apoptosis and necrosis." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501593.

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Hepatotoxicity represents one of the most prevalent drug-induced adverse effects seen in the clinic and is a major cause of attrition of new chemical entities in development. Some adverse drug reactions are associated with metabolic activation to a chemically reactive intermediate. The hepatotoxicity associated with acetaminophen (APAP; paracetamol) and furosemide (FS) in mice is initiated by the formation of a reactive metabolite which has been well characterised. APAP hepatotoxicity is a major clinical problem, and with FS represents an important tool to investigate mechanisms of drug induced liver injury (DILI) in animal models.
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Sattiraju, Sandhya Ramani. "Apoptosis and necrosis drive muscle fiber loss in lipin1 deficient skeletal muscle." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1598626794423032.

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Latif, Lubna Salah Eldin Abdel. "Assessment of Cell Death Parameters in Bovine Parvovirus-Infected EBTr Cells." BYU ScholarsArchive, 2005. https://scholarsarchive.byu.edu/etd/445.

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Bovine parvovirus (BPV) is a helper-independent parvovirus. It has a small icosahedral capsid with a single stranded DNA genome. It is a highly stable virus with a narrow host range. It causes acute gastroenteritis in calves. It is considered to be a cytolytic virus because it kills the host cells. However, the mechanism by which the virus causes cell death is not known. The work described in this thesis assessed different parameters of cell death in BPV infected embryonic bovine tracheal (EBTr) cells. There are several ways for viruses to induce cell death. Viruses can induce apoptosis in the infected cell. They can also kill the host cell by necrosis. Several approaches were used in this work to look for evidence of apoptosis and necrosis. Cells undergoing apoptosis exhibit cardinal signs that distinguish them from other dying cells. Among these signs are the exposure of phosphatidylserine to the outer surface of the plasma membrane, DNA fragmentation into non-random DNA sections that are multimers of 180bp, nuclear morphology changes and caspase activation. These signs were studied in this research and data collected from these experiments did not show any positive sign of apoptosis in infected cells due to virus infection. Cells undergoing a necrotic cell death have a different pattern. The cells swell then burst releasing their cytoplasmic contents. The DNA is fragmented in a random fashion. Cellular morphology was studied in this research and the data suggested that BPV infected cells swell, then shrink and detach from the surface of the culture vessel. Moreover, formation of apoptotic bodies was not detected in dying infected cells. Release of cytoplasmic contents was also assessed by looking at concentrations of LDH enzyme, viral haemagglutinin, and the number of infectious viral particles in the media of infected cells. Data from the different approaches employed in this study do not support the hypothesis that BPV kills the infected EBTr cell by apoptosis, rather, infected cells in culture become necrotic, swell, release their cytoplasmic contents, and detach.
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Crott, Jimmy. "Effect of vitamin C supplements on chromosome damage, apoptosis and necrosis ex vivo /." Title page and introduction only, 1997. http://web4.library.adelaide.edu.au/theses/09S.B/09s.bc9516.pdf.

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Thesis (B. Sc.(Hons.))--University of Adelaide, Dept. of Physiology, 1997.
Spine title: Effect of vitamin C on chromosome damage, apoptosis and necrosis. Includes bibliographical references (leaves 30-34).
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Pistilli, Emidio E. "The extrinsic apoptotic pathway in aged skeletal muscle roles of tumor necrosis factor-[alpha] and interleukin-15 /." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4912.

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Thesis (Ph. D.)--West Virginia University, 2006.
Title from document title page. Document formatted into pages; contains x, 189 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Books on the topic "Apoptosis/Necrosis"

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Ennis, Maurice. Tumour necrosis factor alpha and ultraviolet light activation of programmed cell death by apoptosis in D. melanogaster. Ottawa: National Library of Canada, 2001.

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C, Hemmings Hugh, ed. Regulatory protein modification: Techniques and protocols. Totowa, N.J: Humana Press, 1997.

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service), SpringerLink (Online, ed. Death receptors and cognate ligands in cancer. Heidelberg: Springer, 2009.

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Ntuli, Tobias M., ed. Cell Death - Autophagy, Apoptosis and Necrosis. InTech, 2015. http://dx.doi.org/10.5772/59648.

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Aerts, Joeri. Progesterone Induces Apoptosis in Eosinophilic Granulocytes & Induces Tumour Necrosis Factor-Alpha / Tumour Necrosis Factor Receptor. Leuven Univ Pr, 2002.

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Dynamic changes in cell death after lung transplantation: Apoptosis and necrosis in ischemia-reperfusion injury. Ottawa: National Library of Canada, 2000.

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(Editor), N. G. Bazan, U. Ito (Editor), V. L. Marcheselli (Editor), T. Kuroiwa (Editor), and I. Klatzo (Editor), eds. Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis and/or Necrosis, Neuronal Recovery vs. Death, and Protection Against Infarction. Springer, 2001.

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Klatzo, I., T. Kuroiwa, U. Ito, N. G. Bazan, and V. L. Marcheselli. Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis and/or Necrosis, Neuronal Recovery vs. Death, and Protection Against Infarction. Springer London, Limited, 2012.

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Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis and/or Necrosis, Neuronal Recovery vs. Death, and Protection Against Infarction. Springer, 2011.

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Bahjat, Frances Rena. Characterization and genetic analysis of the resistance of nonobese diabetic mice to tumor necrosis factor-alpha-mediated hepatocyte apoptosis and lethality. 2002.

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Book chapters on the topic "Apoptosis/Necrosis"

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Clarke, Peter G. H. "Apoptosis Versus Necrosis." In Cell Death and Diseases of the Nervous System, 3–28. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-4612-1602-5_1.

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Korhonen, Laura, and Dan Lindholm. "Apoptosis and Necrosis." In Neuroprotection, 151–72. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603867.ch8.

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Coleman, Jack, Rui Liu, Kathy Wang, and Arun Kumar. "Detecting Apoptosis, Autophagy, and Necrosis." In Methods in Pharmacology and Toxicology, 77–92. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3588-8_5.

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Narula, Jagat, and Leo Hofstra. "Imaging Myocardial Necrosis and Apoptosis." In Atlas of Nuclear Cardiology, 197–216. London: Current Medicine Group, 2003. http://dx.doi.org/10.1007/978-1-4615-6496-6_12.

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Mierke, Claudia Tanja. "Cell Proliferation, Survival, Necrosis and Apoptosis." In Cellular Mechanics and Biophysics, 743–824. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58532-7_16.

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Gibson, Peter R. "Apoptosis or Necrosis-Colonic Epithelial Cell Survival." In Novartis Foundation Symposia, 133–50. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470090480.ch10.

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Radu-Ionita, Florentina, Ecaterina Bontas, and Ion C. Tintoiu. "Hepatocellular Death: Apoptosis, Autophagy, Necrosis and Necroptosis." In Liver Diseases, 37–52. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-24432-3_4.

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Russell, Lonnie D. "Cell Loss During Spermatogenesis: Apoptosis or Necrosis?" In Male Sterility and Motility Disorders, 203–14. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1522-6_18.

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Fulda, Simone. "Tumor-Necrosis-Factor-Related Apoptosis-Inducing Ligand (TRAIL)." In Advances in Experimental Medicine and Biology, 167–80. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6458-6_8.

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Woolbright, Benjamin L., and Hartmut Jaeschke. "Measuring Apoptosis and Necrosis in Cholestatic Liver Injury." In Methods in Molecular Biology, 133–47. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9420-5_9.

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Conference papers on the topic "Apoptosis/Necrosis"

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Mugnano, Martina, Alejandro Calabuig, Simonetta Grilli, Lisa Miccio, and Pietro Ferraro. "Monitoring cell morphology during necrosis and apoptosis by quantitative phase imaging." In SPIE Optical Metrology, edited by Pietro Ferraro, Simonetta Grilli, Monika Ritsch-Marte, and David Stifter. SPIE, 2015. http://dx.doi.org/10.1117/12.2186771.

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Niles, Andrew L., Kevin R. Kupcho, Terry L. Riss, Dan F. Lazar, and James J. Cali. "Abstract 710: Real-time apoptosis and necrosis detection in 3D spheroid cellmodels." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-710.

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Niles, Andrew L., Kevin R. Kupcho, Terry L. Riss, Dan F. Lazar, and James J. Cali. "Abstract 710: Real-time apoptosis and necrosis detection in 3D spheroid cellmodels." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-710.

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Smith, Katisha D., and Liang Zhu. "In Vivo Experimental Study of Rat Brain and Spinal Temperatures During Non-Invasive Spinal Cord Hypothermia Using a Cooling Pad." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53129.

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Traumatic injury causes mechanical tissue disruption that immediately follows a traumatic event. After the initial event, secondary injury often occurs. It is a cellular and molecular response to external trauma, including ischemia, inflammation, apoptosis, necrosis, and edema in the central nervous system (CNS). Since secondary injuries can lead to paralysis and permanent neurological damage, most current treatment are devoted to delaying or preventing secondary neurological injury.
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Leszczynski, Dariusz, Costas M. Pitsillides, R. Rox Anderson, and Charles P. Lin. "Induction of apoptosis and necrosis following pulsed laser irradiation of intracellular pigment microparticles." In Biomedical Topical Meeting. Washington, D.C.: OSA, 1999. http://dx.doi.org/10.1364/bio.1999.cwc5.

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Edelmann, Martin, Thomas Meier, Markus Rupp, and Kathia Vilpoux. "Laser induced temperature distribution in cell layers." In European Conference on Biomedical Optics. Washington, D.C.: Optica Publishing Group, 2001. http://dx.doi.org/10.1364/ecbo.2001.4433_10.

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Thermal stimulation of single cells and cell layers is used for investigations of temperature associated processes like necrosis or apoptosis. Simulations of temperature distributions in layered structures on various substrates are presented. In order to verify the simulations a diode pumped IR-cw laser system was developed. The TEM00 output beam at a wavelength of 2.8 µm was focused on biological material to compare visible effects with the calculations.
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Inada, Shunko A., Hiroshi Amano, Isamu Akasaki, Akimichi Morita, and Keiko Kobayashi. "Effect of UV irradiation on the apoptosis and necrosis of Jurkat cells using UV LEDs." In SPIE OPTO: Integrated Optoelectronic Devices, edited by Klaus P. Streubel, Heonsu Jeon, and Li-Wei Tu. SPIE, 2009. http://dx.doi.org/10.1117/12.809929.

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Shen, Dee, Eric Chan, Praveen Pande, and Wayne F. Patton. "Abstract 2876: A novel multi-parametric assay of cell death pathways: Autophagy, apoptosis, and necrosis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2876.

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Baselt, Tobias, Christopher Taudt, Alexander Kabardiadi-Virkovski, Ina Pade, Andrés Fabián Lasagni, and Peter Hartmann. "Non-disruptive Supercontinuum based scattering analyses of cartilage and collagen before and after apoptosis and necrosis." In Tissue Optics and Photonics, edited by Zeev Zalevsky, Valery V. Tuchin, and Walter C. Blondel. SPIE, 2020. http://dx.doi.org/10.1117/12.2555422.

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Loeuillard, Emilien, Jingchun Yang, Haidong Dong, Gregory J. Gores, and Sumera Ilyas. "Abstract 2738: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mediates tumor immune evasion in cholangiocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2738.

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Reports on the topic "Apoptosis/Necrosis"

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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Related Apoptosis-Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada486929.

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2

Behbakht, Kian. Modulators of Response to Tumor Necrosis-Related Apoptosis-Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada508266.

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3

Behbakht, Kian. Modulators of Response to Tumor Necrosis-Factor-Related Apoptosis Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada532993.

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4

Belenska-Todorova, Lyudmila Filipova, Valeriya Gyurkovska, and Nina Dimitrova Ivanovska. Neutralization of Tumour Necrosis Factor-related Apoptosis-inducing Ligand Ameliorates the Symptoms of Zymosan-induced Septic Shock. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, November 2021. http://dx.doi.org/10.7546/crabs.2021.11.15.

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5

Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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6

Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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