Relevant bibliographies by topics / Delayed Death Inhibitors

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Reports

Academic literature on the topic 'Delayed Death Inhibitors'

Author: Grafiati
Published: 6 September 2023
Last updated: 31 July 2025

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Journal articles on the topic "Delayed Death Inhibitors"

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Amberg-Johnson, Katherine, and Ellen Yeh. "Host Cell Metabolism Contributes to Delayed-Death Kinetics of Apicoplast Inhibitors inToxoplasma gondii." Antimicrobial Agents and Chemotherapy 63, no. 2 (2018): e01646-18. http://dx.doi.org/10.1128/aac.01646-18.

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ABSTRACTToxoplasma gondiiand related human parasites contain an essential plastid organelle called the apicoplast. Clinically used antibiotics and other inhibitors that disrupt apicoplast biogenesis cause a mysterious “delayed-death” phenotype in which parasite growth is unaffected during the first lytic cycle of inhibitor treatment but is severely inhibited in the second lytic cycle even after drug removal. Critical to understanding the complex downstream cellular effects of these drug classes are the timing of apicoplast loss during inhibitor treatment and how it relates to this peculiar gro
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Ramya, T. N. C., Satyendra Mishra, Krishanpal Karmodiya, Namita Surolia, and Avadhesha Surolia. "Inhibitors of Nonhousekeeping Functions of the Apicoplast Defy Delayed Death in Plasmodium falciparum." Antimicrobial Agents and Chemotherapy 51, no. 1 (2006): 307–16. http://dx.doi.org/10.1128/aac.00808-06.

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ABSTRACT Targeting of apicoplast replication and protein synthesis in the apicomplexan Toxoplasma gondii has conventionally been associated with the typical “delayed death” phenotype, characterized by the death of parasites only in the generation following drug intervention. We demonstrate that antibiotics like clindamycin, chloramphenicol, and tetracycline, inhibitors of prokaryotic protein synthesis, invoke the delayed death phenotype in Plasmodium falciparum, too, as evident from a specific reduction of apicoplast genome copy number. Interestingly, however, molecules like triclosan, cerulen
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Kindy, Mark S. "Inhibition of Tyrosine Phosphorylation Prevents Delayed Neuronal Death following Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 13, no. 3 (1993): 372–77. http://dx.doi.org/10.1038/jcbfm.1993.50.

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Protein tyrosine phosphorylation plays an important role in the regulation of neuronal function. We examined the effects of inhibition of tyrosine phosphorylation on ischemic neuronal damage in the CA1 region of the hippocampus. In the gerbil hippocampus, genistein and lavendustin A, tyrosine kinase inhibitors, were administered 30 min before initiation of 5-min ischemia and reperfusion. Both genistein and lavendustin A blocked tyrosine phosphorylation and prevented delayed neuronal death (DND). However, genistin, an inactive analogue of genistein, did not block DND. Genistein was dose-depende
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Weil, M., M. D. Jacobson, and M. C. Raff. "Are caspases involved in the death of cells with a transcriptionally inactive nucleus? Sperm and chicken erythrocytes." Journal of Cell Science 111, no. 18 (1998): 2707–15. http://dx.doi.org/10.1242/jcs.111.18.2707.

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We show that mouse sperm die spontaneously within 1–2 days in culture and that treatment with either staurosporine (STS) and cycloheximide (CHX) or a peptide caspase inhibitor does not accelerate or delay the cell death. Chicken erythrocytes, by contrast, are induced to die by either serum deprivation or treatment with STS and CHX, and embryonic erythrocytes are more sensitive than adult erythrocytes to both treatments. Although these erythrocyte deaths display a number of features that are characteristic of apoptosis, they are not blocked, or even delayed, by peptide caspase inhibitors, and m
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Jäckle, Tina, Cornelia Hasel, Ingo Melzner, S. Brüderlein, Peter M. Jehle, and Peter Möller. "Sustained hyposmotic stress induces cell death: apoptosis by defeat." American Journal of Physiology-Cell Physiology 281, no. 5 (2001): C1716—C1726. http://dx.doi.org/10.1152/ajpcell.2001.281.5.c1716.

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We describe sustained hyposmotic stress as a novel type of environmental condition enforcing apoptosis. In a dose- and time-dependent fashion, hyposmotic stress leads to a delayed type of apoptosis with considerable variations in constitutive sensitivity among different cell types. For example, after 48 h at 84 mosmol/l, the death rate ranged from 10.8 ± 0.7% in AsPc1 human pancreatic carcinoma cells to 72.0 ± 1.6% in HK-2 human kidney tubule cells. Caspase inhibitors rendered cells more resistant to hyposmolar stress; the caspase 3 inhibitor Ac-Asp-Glu-Val-aspartic acid aldehyde was the most
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Shishido, Yoshiyuki, Masayoshi Furushiro, Shuichi Tanabe, Shigenobu Shibata, Shusuke Hashimoto, and Teruo Yokokura. "Effects of prolyl endopeptidase inhibitors and neuropeptides on delayed neuronal death in rats." European Journal of Pharmacology 372, no. 2 (1999): 135–42. http://dx.doi.org/10.1016/s0014-2999(99)00185-5.

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Lewin, Matthew, José Gutiérrez, Stephen Samuel, et al. "Delayed Oral LY333013 Rescues Mice from Highly Neurotoxic, Lethal Doses of Papuan Taipan (Oxyuranus scutellatus) Venom." Toxins 10, no. 10 (2018): 380. http://dx.doi.org/10.3390/toxins10100380.

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There is an unmet need for economical snakebite therapies with long shelf lives that are effective even with delays in treatment. The orally bioavailable, heat-stable, secretory phospholipase A2 (sPLA2) inhibitor, LY333013, demonstrates antidotal characteristics for severe snakebite envenoming in both field and hospital use. A murine model of lethal envenoming by a Papuan taipan (Oxyuranus scutellatus) demonstrates that LY333013, even with delayed oral administration, improves the chances of survival. Furthermore, LY333013 improves the performance of antivenom even after it no longer reverses
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Duval, R., V. Bellet, S. Delebassée, and C. Bosgiraud. "Implication of caspases during maedi–visna virus-induced apoptosis." Journal of General Virology 83, no. 12 (2002): 3153–61. http://dx.doi.org/10.1099/0022-1317-83-12-3153.

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Maedi–visna virus (MVV) causes encephalitis, pneumonia and arthritis in sheep. In vitro, MVV infection and replication lead to strong cytopathic effects characterized by syncytia formation and subsequent cellular lysis. It was demonstrated previously that MVV infection in vitro induces cell death of sheep choroid plexus cells (SCPC) by a mechanism that can be associated with apoptotic cell death. Here, the relative implication of several caspases during acute infection with MVV is investigated by employing diverse in vitro and in situ strategies. It was demonstrated using specific pairs of cas
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Nakagomi, T., T. Sasaki, T. Kirino, et al. "Effect of cyclooxygenase and lipoxygenase inhibitors on delayed neuronal death in the gerbil hippocampus." Stroke 20, no. 7 (1989): 925–29. http://dx.doi.org/10.1161/01.str.20.7.925.

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STEFANELLI, Claudio, Francesca BONAVITA, Ivana STANIC', et al. "ATP depletion inhibits glucocorticoid-induced thymocyte apoptosis." Biochemical Journal 322, no. 3 (1997): 909–17. http://dx.doi.org/10.1042/bj3220909.

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In quiescent thymocytes, mitochondrial de-energization was not correlated to apoptotic death. In fact, thymocytes treated with oligomycin, a highly specific inhibitor of ATP synthase, alone or with atractyloside to block ATP translocation from the cytoplasm, were alive, even if their mitochondria were depolarized, as revealed by flow cytometry after Rhodamine 123 staining. Furthermore, oligomycin was a powerful inhibitor of apoptosis induced in rat thymocytes by dexamethasone and, to a lesser extent, by the calcium ionophore A23187 and etoposide, but was without effect when apoptosis was induc
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Dissertations / Theses on the topic "Delayed Death Inhibitors"

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Belekar, M. A. "Pharmacological and genetic studies on delayed death inhibitors of apicomplexan parasites." Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 2019. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/5197.

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Discovering new drugs against apicomplexan parasites, preferably acting via novel mechanisms or extending our chemical toolkit for well determined targets are much needed. We have done detailed screening effort to identify novel inhibitors of Toxoplasma gondii using three different chemical libraries- “Sigma LOPAC”, MMV “Malaria Box” and MMV “Pathogen Box”. Sigma LOPAC is a collection of 1280 bioactive small molecules from Sigma Aldrich and have known mechanism of action in mammalian system and these molecules could be used to identify some unusual and new druggable targets in apicomplexan pa
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Belekar, M. "Pharmacological and genetic studies on delayed death inhibitors of apicomplexan parasites." Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 2019. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/5850.

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Burns, Amy Lee. "Investigation of azithromycin analogues and proteasome-like inhibitors as quick-killing antimalarials." Thesis, 2019. http://hdl.handle.net/2440/123090.

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Malaria is caused by mosquito-borne parasites of the genus Plasmodium which were responsible for ~435,000 of deaths annually, with >90% caused by the deadliest species, P. falciparum. Over the last two decades, global implementation of vector control and artemisinin combination therapies have resulted in significant reductions in the global burden of malaria. Of current concern is the spread of multi-drug resistant parasites that have severely limited the efficacy of antimalarials, including front-line artemisinins, highlighting the urgent need to identify new antimalarials for use as treatmen
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Book chapters on the topic "Delayed Death Inhibitors"

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Birkoben, Tom, Mirko Hansen, Marina Ignatov, Martin Ziegler, and Hermann Kohlstedt. "A Bio-inspired Perceptual Decision-Making Circuit Based on the Hassenstein-Reichardt Direction Detector." In Springer Series on Bio- and Neurosystems. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-36705-2_13.

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AbstractDecision-making belongs to one of the most prominent principles in the nerve system of living species. The crucial trade-off between time to decide (speed) and accuracy is essential for a creature to react to environmental stimuli and most importantly, relevant for survival. In-depth studies of coherent motion tasks in primates, based on two-choice decision experiments, led to a profound understanding of neuronal information processing and even bridged the gap to behavioural psychology. Three fundamental processing stages are needed to successfully perform a two-choice decision experim
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Cappato, Riccardo. "Primary prevention of sudden death in idiopathic dilated cardiomyopathy." In ESC CardioMed, edited by Gerhard Hindricks. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0554.

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Idiopathic dilated cardiomyopathy is characterized by early ventricular enlargement and systolic contractile dysfunction with congestive heart failure not secondary to recognizable causes. Symptoms of congestive heart failure develop at a later stage, usually between 18 and 50 years of age, although they may occasionally occur earlier as a first manifestation of the underlying disease. Mechanisms of life-threatening arrhythmias are facilitated by subendocardial scarring, electrolyte unbalance, stretch-induced electrophysiological changes, autonomic impairment, conduction delay, or proarrhythmi
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Becker, Richard C., and Frederick A. Spencer. "Aspirin." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0012.

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Aspirin, considered the prototypic platelet antagonist, has been available for over a century and currently represents a mainstay both in the prevention and treatment of vascular events that include stroke, myocardial infarction, peripheral vascular occlusion, and sudden death. Aspirin irreversibly acetylates cyclooxygenase (COX), impairing prostaglandin metabolism and thromboxane A2 (TXA2) synthesis. As a result, platelet aggregation in response to collagen, adenosine diphosphate (ADP), and thrombin (in low concentrations) is attenuated (Roth and Majerus, 1975). Because aspirin more selective
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Reports on the topic "Delayed Death Inhibitors"

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Granot, David, and Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, 2003. http://dx.doi.org/10.32747/2003.7585189.bard.

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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed c
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