Relevant bibliographies by topics / Delayed death

Academic literature on the topic 'Delayed death'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Delayed death"

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Kirino, Takaaki. "Delayed neuronal death." Neuropathology 20, s1 (September 2000): 95–97. http://dx.doi.org/10.1046/j.1440-1789.2000.00306.x.

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Maled, Venkatesh. "Delayed Death in Hanging." Indian Journal of Forensic Medicine and Pathology 9, no. 1 (2016): 29–37. http://dx.doi.org/10.21088/ijfmp.0974.3383.9116.5.

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Strojan, Marjan, and Alasdair Mackinnon. "A Sudden Death Delayed." Iowa Review 36, no. 2 (October 2006): 58–59. http://dx.doi.org/10.17077/0021-065x.6125.

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Torre, Carlo. "Delayed Death from “Fisting”." American Journal of Forensic Medicine and Pathology 8, no. 1 (March 1987): 91. http://dx.doi.org/10.1097/00000433-198703000-00026.

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Abe, K., M. Aoki, J. Kawagoe, T. Yoshida, A. Hattori, K. Kogure, and Y. Itoyama. "Ischemic Delayed Neuronal Death." Stroke 26, no. 8 (August 1995): 1478–89. http://dx.doi.org/10.1161/01.str.26.8.1478.

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Gordon, Jeffrey M., Ruthy Shaco-Levy, Daniel Feuermann, Mahmoud Huleihil, and Solly Mizrahi. "Photothermally induced delayed tissue death." Journal of Biomedical Optics 11, no. 3 (2006): 030504. http://dx.doi.org/10.1117/1.2210948.

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MOREHEAD, RICHARD S. "Delayed Death From Pulmonary Tuberculosis." Southern Medical Journal 93, no. 5 (May 2000): 507–10. http://dx.doi.org/10.1097/00007611-200005000-00015.

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MOREHEAD, RICHARD S. "Delayed Death From Pulmonary Tuberculosis." Southern Medical Journal 93, no. 5 (May 2000): 507–10. http://dx.doi.org/10.1097/00007611-200093050-00015.

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Goswami, Rajesh Ban, and A. Dutta. "A Retrospective Observational Study of Delayed Death in Rescued Hanging Cases." Indian Journal of Forensic Medicine and Pathology 11, no. 2 (2018): 111–14. http://dx.doi.org/10.21088/ijfmp.0974.3383.11218.12.

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Aggarwal, N. K., Upender Kishore, and B. B. L. Agarwal. "Hanging-Delayed Death (A Rare Phenomenon)." Medicine, Science and the Law 40, no. 3 (July 2000): 270–72. http://dx.doi.org/10.1177/002580240004000314.

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Hanging is one of the most common methods of suicide in India in which death of the individual occurs instantaneously. However, a few cases have been reported in literature in which death has occurred after a certain period of time or the patient has survived after prolonged resuscitative measures. A case of a 20-year-old female is described who survived for nine days after hanging, remaining unconscious throughout in the hospital. She died due to cerebral damage caused by cerebral anoxia.
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Dissertations / Theses on the topic "Delayed death"

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Shi, Ruoyang. "BNIP3 regulates excessive mitophagy in the delayed neuronal death in stroke." Springer, 2012. http://hdl.handle.net/1993/23688.

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Autophagy is a physiological process by which the cell eliminates damaged organelles, toxic agents, and long-lived proteins by degradation through lysosomal system. Mitophagy, the specific autophagic elimination of mitochondria, regulates mitochondrial number to match metabolic demand and is a core machinery of quality control to remove damaged mitochondria. A neuroprotective role of physiological autophagy/mitophagy has been discovered. However, recent studies suggested that highly accelerated autophagy/mitophagy might contribute to neuronal death in various pathological situations including cerebral ischemia. In this study, we aimed to investigate the activation of excessive autophagy, particularly, the more specific mitophagy, in neuronal tissues and its contribution to ischemia/hypoxia (I/H)-induced delayed neuronal death. I/H injury was induced by oxygen and glucose deprivation (OGD) followed by reperfusion (RP) on primary cortical neurons in vitro. Cerebral ischemia was induced by unilateral common carotid artery occlusion and hypoxia in neonatal mice in vivo. In order to determine the extent to which autophagy contributes to neuronal death in cerebral ischemia, we performed multiple methods and found that in both primary cortical neurons and SH-SY5Y cells exposed to OGD for 6 h and RP for 24, 48, and 72 h, respectively, an increase of autophagy was observed as determined by the increased ratio of LC3-II to LC3-I and Beclin 1 expression. Using Fluoro-Jade C and monodansylcadaverine double-staining, and electron microscopy we found the increment in autophagy after OGD/RP was accompanied by increased autophagic cell death, and this increased cell death was inhibited by the specific autophagy inhibitor, 3-methyladenine. The presence of large autolysosomes and numerous autophagosomes in cortical neurons were confirmed by electron microscopy. Autophagy activities were increased dramatically in the ischemic brains 3-7 days postinjury from a rat model of neonatal cerebral I/H as shown by increased punctate LC3 staining and Beclin-1 expression. We thus obtained the conclusion that excessive activation of autophagy contributes to neuronal death in cerebral ischemia. BNIP3 (Bcl-2/adenovirus E19 kD interacting protein 3), a member of a unique subfamily of death-inducing mitochondrial proteins, is highly associated with mitochondrial dysfunction and delayed neuronal death in stroke. It is known that BNIP3-induced neuronal death is caspase-independent and characterized by early mitochondrial damage. Recent evidence suggested that the BNIP3 family of proteins might be important regulators of mitophagy. Here, using both stroke models, we found that homodimer (60 kD) of BNIP3/NIX (BNIP3L) were highly expressed in a ‘delayed’ manner. Particularly, significant mitophagic activation was confirmed by electron microscopy. In contrast, both neonatal mitophagy and apoptosis were significantly inhibited in the BNIP3 knockout (KO) mice after I/H, which was also accompanied by a significantly increased autophagic response. In addition, the infarct volume in the BNIP3 KO mice was significantly reduced as compared to wild-type (WT) mice after 7 or 28 days recovery, showing a prominent neuroprotection of BNIP3 gene silencing. A protein-to-protein interaction of mitochondria-localized BNIP3 (60 kD) with the autophagosome marker, LC3, was confirmed by co-ip, immunocytochemistry and further quantified by ELISA, indicating BNIP3 was an effective LC3-binding target on damaged mitochondria. These data demonstrated a novel role of BNIP3 in regulating neuronal mitophagy and cell death during ischemic stroke.
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Clausen, Fredrik. "Delayed Cell Death after Traumatic Brain Injury : Role of Reactive Oxygen Species." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4296.

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Chapman, Courtney Myfanwy. "Novel pharmaceutical combination confers protection from delayed cell death following transient cerebral ischemia." Thesis, Montana State University, 2009. http://etd.lib.montana.edu/etd/2009/chapman/ChapmanC0509.pdf.

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Stroke is a leading cause of death and disability throughout the world; ischemia is the most common form of stroke. Medical procedures such as cardio-pulmonary bypass surgery can cause ischemic stroke can be caused. There are no treatments to limit neural impairment following stroke. The current research investigates neuroprotection offered by treatment with a novel drug combination consisting of Simvastatinâ„¢, Gemfibrozilâ„¢, Troglitazoneâ„¢, and Spironolactoneâ„¢. Animals were treated with the drug cocktail three weeks proceeding and one week subsequent to surgery. Ischemic insult was induced by clamping the carotid arteries for 5 min. Sham subjects underwent similar surgical procedures, but the carotids were not clamped. Twenty-four hrs following the surgical procedure locomotor activity was monitored in an open field for 5 min. Seven to fourteen days following ischemia or the sham procedure animals were sacrificed and sections containing the hippocampal CA1 region were mounted on slides and stained with cresyl violet. The CA1 region was rated on a 4-point scale for level of damage. Rodents generally show increased locomotor activity following transient global ischemia in an open field. In our study, ischemic animals that received vehicle demonstrated increased activity relative to the animals that received the drug treatment on all behavioral measures. Ischemic animals that received vehicle treatment had significantly more neural damage in the hippocampal CA1 region than ischemic animals receiving the drug. The appearance of neurons in the CA1 hippocampal regions of animals in the sham condition was not significantly different from ischemic animals in the drug treatment condition. It is concluded that the drug treatment is effective in offering neuroprotection during transient global ischemia. The next step is to characterize the biochemical mechanisms behind the neuroprotection conferred by the drug treatment. Contrasting the protein expression levels of animals receiving the vehicle treatment with animals receiving the drug treatment following an ischemic insult will assist in elucidating these pathways. Predictions are made regarding the biochemical mechanisms affected by the drug treatment based on previous research on the biochemical pathways affected by each pharmaceutical.
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Kamme, Fredrik. "Changes in gene expression during delayed neuronal death after cerebral ischemia in the rat." Lund : Laboratory for Experimental Brain Research, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/40337178.html.

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Daré, Elisabetta. "Neurotoxicity of methylmercury : analysis of molecular mechanisms and behavioral alterations /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-145-4.

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Youssef, Ihsen. "Étude des mécanismes moléculaires impliqués dans la mort neuronale induite par le peptide de ß-amyloïde soluble : recherche et validation fonctionnelle de cibles cellulaires." Thesis, Vandoeuvre-les-Nancy, INPL, 2006. http://www.theses.fr/2006INPL068N/document.

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Le vieillissement des populations est corrélé à l’augmentation des pathologies neurodégénératives liées à l’âge, plus particulièrement la maladie d’Alzheimer. La recherche de marqueurs précoces de la maladie ainsi que l’élaboration de nouvelles stratégies thérapeutiques constituent un enjeu de taille. Parmi les mécanismes moléculaires de la formation des plaques amyloïdes actuellement explorés, les formes oligomériques tronquées de peptide amyloïde (Aß), notamment le peptide Aß3(?pE)??42? retrouvé à des stades précoces de la maladie, joueraient un rôle déterminant. Ces travaux de thèse ont permis de montrer, dans un premier temps, que l’injection intracérébrale de ce peptide chez la souris entraîne des altérations de la mémoire de travail et des capacités d’apprentissage, associées à une accumulation d’espèces réactives dérivées de l’oxygène dans des régions cérébrales spécifiques (hippocampe et bulbes olfactifs) de ces animaux. Des essais menés in vitro sur des cultures primaires de neurones de souris montrent leur implication dans les voies apoptotiques impliquant l’activation des caspases et la cascade métabolique de l’acide arachidonique. La seconde étape de ces travaux a constitué en l’étude des effets protecteurs d’un peptide antiapoptotique d’origine endogène, l’humanine (HN) et son variant S14G (HNG). In vitro, un effet protecteur de ces peptides a été mesuré après traitement de neurones en culture par le peptide A[bêta]3?(pE)42.??? Les résultats les plus marquants résident dans les observations faites in vivo : en effet, ces peptides inhibent l’effet délétère de l’injection intracérébroventriculaire du peptide Aß3?(pE??)42?? en restaurant les performances mnésiques des animaux dans les tests comportementaux. A la lumière de ces résultats, les peptides HN pourraient constituer de nouveaux outils thérapeutiques dans le traitement ou la prévention des dommages cellulaires précoces liés à la présence des oligomères solubles du peptide Aß
Aging of population is correlated to the increase of neurodegenerative disease, more particularly Alzheimer disease. Defining early diagnostic markers and new therapeutic strategies are highly relevant. Among the molecular pathways which are currently developed, N-terminal-truncated forms of amyloid-ß (Aß) peptide have been recently suggested to play a pivotal role in the disease. Among them, Aß3(?pE)42 ?peptide is the dominant Aß species in amyloid plaques. We first investigated the effects of soluble oligomeric Aß3(pE) 42 after intracerebroventricular injection on mice learning capacities and the molecular mechanisms of in vitro neurotoxicity. Mice injected with soluble Aß3(pE) 42 displayed impaired spatial working memory and delayed memory acquisition. These cognitive alterations were associated with free radical overproduction in hippocampus and olfactory bulbs. In vitro, Aß3(pE) 42 oligomers induced a redox-sensitive neuronal apoptosis involving caspase activation and an arachidonic acid-dependent pathway. The second goal of this work was to investigate the protective effects of the apoptosis rescue endogenous peptide humanin (HN) and its S14G mutant (HNG). In vitro, we measured their inhibitory effect on neuronal death and apoptotic events resulting from soluble Ab oligomer treatment. What’s of particular interest is the in vivo restoration of soluble Aß3(pE) 42 oligomer-induced mnesic impairment. Thus, HN peptides might serve as new drug candidates for treatment or prevention of early cellular damages linked to soluble A[bêta] oligomers
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Steinman, Christopher T. "Delay and Death-thought Accessibility: A Meta-analysis." Kent State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=kent1461077859.

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Willis, Angela. "TIME ON FLORIDA'S DEATH ROW: A THEORY OF "BENIGN NEGLECT"." Master's thesis, University of Central Florida, 2008. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/3896.

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This thesis attempts to identify and explain what influences the length of time an inmate spends on Florida's death row. A systematic random sample of 33 Florida death row inmates was drawn from the Florida Department of Corrections death row roster and the Florida Commission on Capital Cases inmate roster. Documented for each death row inmate was how long he spent on Florida's death row navigating the various stages and steps in Florida's post-conviction capital punishment process. The data show that petitions to the state trial courts and appeals to the Florida Supreme Court take the longest time in Florida's post-conviction capital punishment process. It also shows a considerable amount of "dead time," which refers to any additional time that an inmate spends on death row with no legal actions pending. A theory of "benign neglect" is proposed as the most likely explanation for the excessive delays.
M.S.
Department of Criminal Justice and Legal Studies
Health and Public Affairs
Criminal Justice MS
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Sullivan, Robert A. "Reign delay, preaching sermons to strengthen faith for people who fear death and dying." Chicago, Ill. : McCormick Theological Seminary, 2002. http://www.tren.com.

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Stefanus, Frieda N. "Understanding the perceptions of women who experienced any delay in accessing appropriate health care services during childbirth in Otjiwarongo district hospital, Namibia." University of Western Cape, 2019. http://hdl.handle.net/11394/7646.

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Master of Public Health - MPH
Access to appropriate health care service during childbirth is a great challenge to many women in Africa and Namibia is no exception. More than 70% of women in Otjozondjupa region experienced some form of delay during childbirth, and while maternal mortality continued to rise over the years in Namibia it is currently at about 265/100 000, which is too high for a middle-income country. Hence, this study aimed to get a deeper understanding of the perceptions of women who experienced any of the three delays in accessing appropriate health care during childbirth in Otjiwarongo hospital.
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Books on the topic "Delayed death"

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Justice delayed: The Catherine Janet Walsh story. Pittsburgh, PA: The Artists' Orchard, LLC, 2015.

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Delayed legacy: A son's amazing search for the full story of his father's death after D-Day. San Antonio, Tex: Maverick Pub., 2005.

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The Delaney women. Waterville, Me: Wheeler Pub., 2003.

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Østerbø, Olav. Mathematical modelling and analysis of communication networks: Transient characteristics of traffic processes and models for end-to-end delay and delay-jitter. Trondheim, Norway]: NTNU, 2003.

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Crosscut. Oxford: ISIS Large Print, 2006.

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Sneyd, Elizabeth J. An in-depth analysis of real and perceived barriers to speech and language program participation for children with speech and language delays: A question of barriers to service? St. Catharines, Ont: Brock University, Dept. of Child and Youth Studies, 2005.

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Delayed Death: Temptation in Florence #1. Beate Boeker, 2013.

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Death of a Bookseller Pub Delayed 2022. British Library Publishing, 2022.

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Gaylord Fact Finders Genealogical Society., ed. Delayed death records index, 1934-1947, Otsego County, Michigan. Gaylord, Mich. (P.O. Box 1524, Gaylord 49735): Gaylord Fact Finders, 1995.

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IV, Conrad John Netting. Delayed Legacy: A Son's Search for the Story of His Father's Death after D-Day. Trinity University Press, 2016.

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Book chapters on the topic "Delayed death"

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Kirino, T., T. Nakagomi, H. Kanemitsu, and A. Tamura. "Delayed Neuronal Death and Ischemic Tolerance." In Thrombolytic Therapy in Acute Ischemic Stroke III, 19–28. Tokyo: Springer Japan, 1995. http://dx.doi.org/10.1007/978-4-431-68459-6_3.

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Katoh, Akira, Toshitaka Nabeshima, Hirohisa Ishimaru, Hiroshi Ohtsuka, Taneo Fukuta, and Tsutomu Kameyama. "Carbon Monoxide (CO)-Induced Delayed Amnesia and Delayed Neuronal Death." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 757–60. Boston, MA: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_154.

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Garcia, J. H., Z. R. Ye, K. F. Liu, and J. A. Gutierrez. "Delayed Neuronal Death in Experimental Ischemic Stroke." In Maturation Phenomenon in Cerebral Ischemia III, 267–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58602-6_32.

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Gusev, Eugene, and Veronica I. Skvortsova. "Delayed Neuronal Death Following Acute Focal Brain Ischemia." In Brain Ischemia, 101–2. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9248-2_7.

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Wieloch, T., K. Bergstedt, M. Cardell, I. Gustafson, T. Honoré, B. R. Hu, F. Boris-Möller, B. Nellgård, and E. Westerberg. "Importance of Postischemic Neurotransmission in Delayed Neuronal Death." In Maturation Phenomenon in Cerebral Ischemia, 107–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77134-7_12.

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Biswas, Debabrata, and Tanmoy Banerjee. "Collective Behavior-II: Amplitude Death and the Corresponding Transitions in Coupled Chaotic Time-Delayed Systems." In Time-Delayed Chaotic Dynamical Systems, 79–97. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70993-2_5.

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Diemer, N. H., T. Bruhn, T. Christensen, M. Nielsen, and F. F. Johansen. "Glutamate-Mediated Mechanisms in Delayed Neuronal Death After Cerebral Ischemia." In Maturation Phenomenon in Cerebral Ischemia II, 53–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60546-8_7.

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Shigeno, T., T. Mima, K. Takakura, G. Katoh, Y. Hashimoto, S. Furukawa, and D. I. Graham. "Amelioration of Delayed Neuronal Death of the Hippocampus by Nerve Growth Factor." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 467–70. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5847-3_95.

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Hu, B. R., M. E. Martone, and C. L. Liu. "Protein Aggregation, Unfolded Protein Response and Delayed Neuronal Death after Brain Ischemia." In Maturation Phenomenon in Cerebral Ischemia V, 225–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18713-1_22.

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Wiessner, Christoph, P. Vogel, T. Neumann-Haefelin, and K. A. Hossmann. "Molecular Correlates of Delayed Neuronal Death Following Transient Forebrain Ischemia in the Rat." In Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma, 1–7. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-9465-2_1.

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Conference papers on the topic "Delayed death"

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Gordon, Jeffrey M., Ruthy Shaco-Levy, Daniel Feuermann, Mahmoud Huleihil, and Solly Mizrahi. "Delayed tissue death probed with sunlight surgery." In Biomedical Optics 2005, edited by Steven L. Jacques and William P. Roach. SPIE, 2005. http://dx.doi.org/10.1117/12.583432.

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Wang, Zaihua, and Haiyan Hu. "An Energy Analysis of Amplitude Death of a Pair of Oscillators With Delayed Coupling." In ASME 2005 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2005. http://dx.doi.org/10.1115/detc2005-84437.

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This paper presents an energy analysis of the amplitude death, a phenomenon that the individual oscillators cease to oscillate when coupled and go to an equilibrium motion instead, of a pair of coupled oscillators with time delay that are slightly perturbed from two undamped oscillators and with delayed coupling. The energy analysis reveals that amplitude death, as well as the stability of the phase-locked periodic solutions, can be justified by the sign of the averaged total powers along a special function with harmonic entries, rather than along arbitrary solution of the coupled oscillators as in the application of the method of Lyapunov’s function for stability analysis. An illustrative example is given to show the effectiveness of the present method.
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Emelianova, Yulia P., Valeriy V. Emelyanov, and Nikita M. Ryskin. "Amplitude death and broadband synchronization in the coupled delayed-feedback electronic oscillators." In 2014 International Conference on Computer Technologies in Physical and Engineering Applications (ICCTPEA). IEEE, 2014. http://dx.doi.org/10.1109/icctpea.2014.6893266.

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Yao, Yu, Nan Zhang, Fu-Xiang Gao, and Ge Yu. "Bifurcation in a delayed worm propagation model with birth and death rates." In 2012 International Conference on Systems and Informatics (ICSAI 2012). IEEE, 2012. http://dx.doi.org/10.1109/icsai.2012.6223326.

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Lima, Thayane Araújo, and Cláudio Brandão dos Santos Filho. "Lethality rate in children with meningitis in 2019 and associated risk factors." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.677.

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Background: Early diagnosis, identification of the pathogen and time until the start of adequate antibiotic therapy are important variables that improve the clinical outcomes of meningitis in children. However, even with an early approach and adequate treatment with effective antibiotics, death and neurological sequelae may occur as a result of the infection. Objectives: Determine the lethality rate of meningitis among children aged 0 to 9 years and define the factors associated with mortality. Design and setting: Case-control study based on secondary data from the Notifiable Diseases Information System (SINAN). Methods: It covers the notifications registered in 2019 and includes the variables: deaths, age group, sex, residence in the Legal Amazon or in the Semi-Arid. Statistical analysis - Odds-Ratio (OR) - was performed using Microsoft Excel for Windows®. Results: The deaths of children due to meningitis, in the studied period, totaled 316, which corresponds to a lethality rate of 4.2%. The associated risk factors were: residence in the Legal Amazon (OR = 3.7) and in the Semi-Arid (OR = 2.2). The age group (OR = 1.6) and sex (OR = 1.0) were not associated with death from meningitis. Conclusions: Reside in the Legal Amazon and the Semi-Arid are risk factors justified by the scarcity of resources and the isolation of these regions, resulting in precarious and more delayed health care. This factor culminates in deaths due to the need for early intervention and treatment of meningitis. The low educational rates found in these areas, culminates in poor access to information regarding the importance of vaccination.
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Rosa, Isabella Inês Rodrigues, Alexandre Santana Valadares, Douglas Marques de Paula, Tiago Paiva Prudente, Maria Elvira Freitas Martins, Guilherme Ferreira Barros, and Ana Laura de Sene Amâncio Zara. "ASPECTS OF BREAST CANCER DIAGNOSIS AND DELAYED TREATMENT IN BRAZIL." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2077.

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Objective: Breast cancer is one of the leading causes of death in women worldwide. Several studies highlight the correlation between delayed treatment and high mortality. However, few researchers have addressed the main reasons for long delays in the healthcare system. This study aims to analyze different aspects influencing the postponement of treatment in Brazil. Methodology: An ecological approach using the secondary data from the Oncology Panel of the Brazilian Unified Health System (SUS). The data were collected on February 13, 2020, and included the diagnoses of breast cancer (ICD-10: C50 and D05) from 2015 to 2020. The aspects analyzed included the waiting time for the first treatment, procedure, staging, and region. Anatomopathological diagnoses made after a surgical procedure were not included. Results: According to the Brazilian laws, oncological patients need to start treatment within 60 days (5). However, the data reveal that only 45.22% of breast cancer patients (stages 2–4) started the treatment within 60 days. This is more alarming when looking at the procedures. Over half of the patients submitted to chemotherapy and 76.8% submitted to radiotherapy received their treatment after 60 days from the diagnosis. Interestingly, our geographic analysis did not reveal significant disparities among regions. The lower-income regions had 49.01–57.07% of patients treated after the recommended time frame. The higher-income regions had values from 43.44% to 54.44%. Conclusion: Despite the knowledge that later treatments result in worse outcomes and the legal right of earlier treatment, our results show a current controversial frame in Brazil. Most patients take longer than recommended, and the worst scenario is for radiotherapy patients. No substantial differences were found among lower- and higher-income regions, although it is likely that further analysis with different approaches could be more sensitive to deny or confirm this assumption.
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Adam, H., A.-C. Docherty Skogh, Å. Edsander Nord, I. Schultz, J. Gahm, P. Hall, J. Frisell, M. Halle, and J. de Boniface. "Abstract P4-13-14: Risk of recurrence and death in breast cancer patients after delayed deep inferior epigastric perforator flap reconstruction." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p4-13-14.

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Para, Andrea N., and David Ku. "Creating a Low Volume Model of Occlusive Thrombosis." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53624.

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Heart disease is the leading cause of death in industrialized countries. Heart attacks and strokes can cause mortality within an hour following plaque rupture. Unfortunately, as it is impossible to study heart attacks in real time, little is known about the mechanism which contributes to mortality. The mechanism of thrombosis under high shear is currently in dispute. Some investigators have shown that GPIIb/IIIa is important in stabilizing a thrombus under high shear conditions.[1] We have independently shown occlusive thrombosis in a gravity-fed tubular stenosis is predicated on a delayed phase of Rapid Platelet Accumulation (RPA) that occurs only at pathologically high shear rates with fast occlusion times consistent with Acute Coronary Syndrome.[2] However, Ruggeri has recently shown that platelet deposition and aggregation can occur at high shear model independent of GPIIb/IIIa which must be activated for binding.[3] Thus, the role of GPIIb/IIIa on high shear thrombosis to occlusion is not known.
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Karimi, Mahmood, and Ramesh R. Rao. "Human Body Composition Estimation and Model-Free Control Design for Weight Management." In ASME 2014 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/dscc2014-6354.

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It is well known that obesity, a chronic disease, can lead to increased risk of other serious chronic diseases and even death. Knowledge of daily changes in lean muscle mass and body fat can be helpful in developing personalized diet and exercise routines to correct this problem. In this paper, it is assumed that measurements of individual body composition components are available only periodically although the total body weight is tracked on a daily basis. The control input is physical activity whose profile can be constrained to accommodate individual preferences while the energy intake can be arbitrary. We present switching and time delayed feedback based model-free control methods for the dynamic management of body mass and its major components. Additionally, based on human body weight dynamics, estimation of body composition using soft switching-based observer is proposed. Simulation results validate the performance of the proposed controllers and the observer under disturbances in recording energy intake and energy expenditure figures.
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Golubev, A. P. "LATE BRONZE AGE COLLAPSE - UNKNOWN GLOBAL АNTROPOGENIC ECOLOGICAL CRISIS XIII - XII CENTURIES BC." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute, 2021. http://dx.doi.org/10.46646/sakh-2021-1-7-11.

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The Late Bronze Age Collapse, or the Crisis of Producers, is the definition for the process of the gradual decline of agricultural production in the states of the Fertile Crescent and Indus Valley regions, which culminated at the end of XIII-XII centuries BC. It was caused not by individual private mistakes, but by fundamental and irreparable defects in the then dominant system of agriculture in region mentioned. First of all, they were the widespread deforestation, overgrazing and salinization of arable lands as a result of excessive irrigation. This led to a catastrophic decline in their fertility and food shortages. The crisis of producers became the main reason for the death of largest states of those epoch (the First Babylonian Kingdom, Ancient Egypt, Harappa, etc.), which were at the forefront of the world civilizational progress, which delayed the technological and cultural development of the peoples of the Eastern Mediterranean, the Middle East and South Asia, by at least for a millennium.
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Reports on the topic "Delayed death"

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Granot, David, and Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, January 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 cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .
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Freire, Mariana, Diana Martins, Maria Filomena Botelho, and Fernando Mendes. Biomarkers of resistance mechanisms in innovative lung cancer treatments - A systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0011.

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Review question / Objective: This systematic review aims to provide an overview of the immunotherapy resistance mechanisms and identify potential biomarkers associated with immunotherapy response in NSCLC, as well as examine new treatment options to overcome this hurdle. Condition being studied: Lung Cancer (LC) remains one of the leading cancers worldwide. In 2020, were globally estimated 2 206 771 new cases and 1 796 144 deaths, representing the uttermost frequent cause of cancer death. LC is classified histologically into small cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC), being the last one the most common, representing 80 to 85% of all LC. The three predominantly subtypes of NSCLC are lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large cell carcinoma (LCLC). NSCLC is usually diagnosed in advanced-staged disease due to ambiguous and delayed severe symptoms.
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Candrilli, Sean D., and Samantha Kurosky. The Response to and Cost of Meningococcal Disease Outbreaks in University Campus Settings: A Case Study in Oregon, United States. RTI Press, October 2019. http://dx.doi.org/10.3768/rtipress.2019.rr.0034.1910.

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Invasive meningococcal disease (IMD) is a contagious bacterial infection that can occur sporadically in healthy individuals. Symptoms are typically similar to other common diseases, which can result in delayed diagnosis and treatment until patients are critically ill. In the United States, IMD outbreaks are rare and unpredictable. During an outbreak, rapidly marshalling the personnel and monetary resources to respond is paramount to controlling disease spread. If a community lacks necessary resources for a quick and efficient outbreak response, the resulting economic cost can be overwhelming. We developed a conceptual framework of activities implemented by universities, health departments, and community partners when responding to university-based IMD outbreaks. Next, cost data collected from public sources and interviews were applied to the conceptual framework to estimate the economic cost, both direct and indirect, of a university-based IMD outbreak. We used data from two recent university outbreaks in Oregon as case studies. Findings indicate a university-based IMD outbreak response relies on coordination between health care providers/insurers, university staff, media, government, and volunteers, along with many other community members. The estimated economic cost was $12.3 million, inclusive of the cost of vaccines ($7.35 million). Much of the total cost was attributable to wrongful death and indirect costs (e.g., productivity loss resulting from death). Understanding the breadth of activities and the economic cost of such a response may inform budgeting for future outbreak preparedness and development of alternative strategies to prevent and/or control IMD.
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Wolfenson, David, William W. Thatcher, Rina Meidan, Charles R. Staples, and Israel Flamenbaum. Hormonal and Nutritional Stretegies to Optimize Reproductive Function and Improve Fertility of Dairy Cattle during Heat Stress in Summer. United States Department of Agriculture, August 1994. http://dx.doi.org/10.32747/1994.7568773.bard.

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The BARD program includes two main parts. In the first, experiments were conducted to complete our understanding of the mechanisms responsible for the impairment of reproductive functions under heat stress. Experiments focused on follicular development and function, since results obtained in our previous BARD project indicate that the preovulatory follicle is susceptible to heat stress. The theca cells, sensitive to thermal stress, produced less androgen during the summer, as well as during the autumn. Similarly, luteinized theca cells obtained from cows in summer produced much less progesterone than in winter. Granulosa cells and luteinized granulosa cells were less susceptible to heat stress. A delayed effect of heat stress on follicular development, on suppression of dominance and on steroid production by theca and granulosa cells was noted. This may be related to the low fertility of cows during the cool months of autumn. In the second part, experiments were conducted aiming to improve fertility in summer. The timed AI program was developed using two injections of GnRH coupled with PGF2a. It was found effective in improving reproductive performance in lactating cows. Limitations induced by heat stress on estrus detection were eliminated with the timed AI management program. Replacing the second injection of GnRH with hCG instead of GnRH agonist increased plasma progesterone levels post ovulation but did not improve fertility. Use of the timed AI program in summer, shortened days open and increased the net revenue per cow, however, it did not protect the embryo fiom temperature-induced embryonic mortality. Incorporation of a GnRH-agonist implant into the timed AJ program was examined. The implant increased plasma progesterone and LH concentrations and altered follicular dynamics. The use of a GnRH-implant enhanced pregnancy rate in cows with low body conditions. In a timed embryo transfer experiment, the use of fresh or frozen in vitro produced embryos was compared in the summer to improve fertility. The use of flesh embryos (but not frozen ones) improved pregnancy rate, however, substantial embryonic death occurred between 21 and 45 days. The timed AI program, which is now being used commercially, shortened days open, and increased pregnancy rate during summer. Other approaches which were found to improve fertility in small-scale studies, need to be tested again in large-scale field trials.
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Tuite, Ashleigh R., David N. Fisman, Ayodele Odutayo, Pavlos Bobos, Vanessa Allen, Isaac I. Bogoch, Adalsteinn D. Brown, et al. COVID-19 Hospitalizations, ICU Admissions and Deaths Associated with the New Variants of Concern. Ontario COVID-19 Science Advisory Table, March 2021. http://dx.doi.org/10.47326/ocsat.2021.02.18.1.0.

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New variants of concern (VOCs) now account for 67% of all Ontario SARS-CoV-2 infections. Compared with early variants of SARS-CoV-2, VOCs are associated with a 63% increased risk of hospitalization, a 103% increased risk of intensive care unit (ICU) admission and a 56% increased risk of death due to COVID-19. VOCs are having a substantial impact on Ontario’s healthcare system. On March 28, 2021, the daily number of new SARS-CoV-2 infections in Ontario reached the daily number of cases observed near the height of the second wave, at the start of the province-wide lockdown, on December 26, 2020. The number of people hospitalized with COVID-19 is now 21% higher than at the start of the province-wide lockdown, while ICU occupancy is 28% higher (Figure 1). The percentage of COVID-19 patients in ICUs who are younger than 60 years is about 50% higher now than it was prior to the start of the province-wide lockdown. Because the increased risk of COVID-19 hospitalization, ICU admission and death with VOCs is most pronounced 14 to 28 days after diagnosis, there will be significant delays until the full burden to the health care system becomes apparent.
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Ruterbusch, V. L., M. J. Swiergosz, and W. A. Gerth. Effects of Delays at Depth on Diver Inspired Oxygen Partial Pressures in Simulated Lockouts Using the MK 25 MOD 2 UBA. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada442954.

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Baral, Aniruddha, Jeffery Roesler, and Junryu Fu. Early-age Properties of High-volume Fly Ash Concrete Mixes for Pavement: Volume 2. Illinois Center for Transportation, September 2021. http://dx.doi.org/10.36501/0197-9191/21-031.

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High-volume fly ash concrete (HVFAC) is more cost-efficient, sustainable, and durable than conventional concrete. This report presents a state-of-the-art review of HVFAC properties and different fly ash characterization methods. The main challenges identified for HVFAC for pavements are its early-age properties such as air entrainment, setting time, and strength gain, which are the focus of this research. Five fly ash sources in Illinois have been repeatedly characterized through x-ray diffraction, x-ray fluorescence, and laser diffraction over time. The fly ash oxide compositions from the same source but different quarterly samples were overall consistent with most variations observed in SO3 and MgO content. The minerals present in various fly ash sources were similar over multiple quarters, with the mineral content varying. The types of carbon present in the fly ash were also characterized through x-ray photoelectron spectroscopy, loss on ignition, and foam index tests. A new computer vision–based digital foam index test was developed to automatically capture and quantify a video of the foam layer for better operator and laboratory reliability. The heat of hydration and setting times of HVFAC mixes for different cement and fly ash sources as well as chemical admixtures were investigated using an isothermal calorimeter. Class C HVFAC mixes had a higher sulfate imbalance than Class F mixes. The addition of chemical admixtures (both PCE- and lignosulfonate-based) delayed the hydration, with the delay higher for the PCE-based admixture. Both micro- and nano-limestone replacement were successful in accelerating the setting times, with nano-limestone being more effective than micro-limestone. A field test section constructed of HVFAC showed the feasibility and importance of using the noncontact ultrasound device to measure the final setting time as well as determine the saw-cutting time. Moreover, field implementation of the maturity method based on wireless thermal sensors demonstrated its viability for early opening strength, and only a few sensors with pavement depth are needed to estimate the field maturity.
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Elnour Abdelkarim, Zeinab. Assessing Sudan's Electoral Legal Framework. International Institute for Democracy and Electoral Assistance, May 2022. http://dx.doi.org/10.31752/idea.2022.18.

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Assessing Sudanʼs Electoral Legal Framework provides an in-depth insight and analysis of Sudanʼs current legal framework for elections. It measures Sudanʼs legal electoral framework against a common international understanding of the principles, norms and obligations that define credible and democratic elections. The objective of this analysis is not to criticize or pass judgement on the countryʼs existing electoral processes; instead, it offers an unbiased assessment of how Sudanʼs existing electoral laws and country context create an enabling or disabling environment for free and fair elections. It provides comprehensive and constructive recommendations to strengthen existing legislation and improve fairness, uniformity, reliability, consistency and professionalism in Sudanʼs future elections. This Report also assesses the status of core democratic principles and freedoms that provide the foundation for credible elections and highlights any restrictions on these fundamental rights and liberties that could interfere with the countryʼs upcoming elections or delay its political transition. It calls upon the transitional government to protect citizensʼ rights and liberties and prevent abuses that may influence public trust, fairness, and openness of electoral and other transitional processes. Lastly, this Report discusses political, socio-economic, and legal issues impacting Sudanʼs roadmap to democratic transition before the October 2021 military coup.
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