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Li, Leilei, Deyong Guo, Yi Wang, Ke Wang, and Runan Lian. "Anatomy of Mine Rescue Teams’ Casualty Incidents: A Basis for Medical Emergency Preparedness and Injury Prevention." Disaster Medicine and Public Health Preparedness 13, no. 4 (March 5, 2019): 695–99. http://dx.doi.org/10.1017/dmp.2018.140.
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ABSTRACTObjectiveMine rescue teams bear a high risk of injury. To improve medical emergency preparedness and injury prevention, this work analyzed the causes and severity of mine rescue teams’ casualty incidents, the primary injuries, and the link between the causes and the occurrences of the casualty incidents.MethodsA total of 81 cases from 1953 to 2013 were used to analyze the casualty incidents of mine rescue teams based on the frequency of accidents. A panel with 4 rescue experts was set up to ensure the accuracy of the analysis.ResultsThe 81 casualty incidents occurred in 7 types of rescue work and were due to 6 causes. Organizational and personal factors were the leading cause, followed by rescue skill and equipment factors. Problems with decision-making and command have gradually become the primary inducement of casualty incidents in recent years, with an average death toll reaching up to 6 to 7 people. The main injuries causing death to team members were blast injury, burns, poisoning, suffocation, blunt trauma, and overwork injury. Some of the injured died because of medical emergency response failure.ConclusionThe construction of emergency medical teams and the preparedness of disaster medicine need to be improved to reduce the mortality of the injured team members. Actions according to the causes of casualty incidents should be adopted for injury prevention. (Disaster Med Public Health Preparedness. 2019;13:695–699)
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Bittle, Steven, and Laureen Snider. "Law, Regulation, and Safety Crime: Exploring the Boundaries of Criminalizing Powerful Corporate Actors." Canadian Journal of Law and Society / Revue Canadienne Droit et Société 30, no. 03 (June 11, 2015): 445–64. http://dx.doi.org/10.1017/cls.2015.16.
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AbstractThis article interrogates the laws that govern safety crimes, harmful but typically unintentional acts of negligence that occur in the production of goods and services. Acts that injure employees at work are commonly depicted in legal discourses as accidents and penalized through administrative laws, although other negligent acts such as driving offences causing injury or death are treated as potentially criminal events. Through a discourse analysis of legal and regulatory texts and documents, the authors argue that the constitution of workplace safety crime is rooted in complex historical factors that shape state responses to corporate wrongdoing. This article documents the roots of this “common sense” view of workplace crime, empirically focusing on Canadian corporate negligence law, and concludes with tentative strategies of resistance and change.
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Henshall, David C., and Roger P. Simon. "Epilepsy and Apoptosis Pathways." Journal of Cerebral Blood Flow & Metabolism 25, no. 12 (May 11, 2005): 1557–72. http://dx.doi.org/10.1038/sj.jcbfm.9600149.
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Epilepsy is a common, chronic neurologic disorder characterized by recurrent unprovoked seizures. Experimental modeling and clinical neuroimaging of patients has shown that certain seizures are capable of causing neuronal death. Such brain injury may contribute to epileptogenesis, impairments in cognitive function or the epilepsy phenotype. Research into cell death after seizures has identified the induction of the molecular machinery of apoptosis. Here, the authors review the clinical and experimental evidence for apoptotic cell death pathway function in the wake of seizure activity. We summarize work showing intrinsic (mitochondrial) and extrinsic (death receptor) apoptotic pathway function after seizures, activation of the caspase and Bcl-2 families of cell death modulators and the acute and chronic neuropathologic impact of intervening in these molecular cascades. Finally, we describe evolving data on nonlethal roles for these proteins in neuronal restructuring and cell excitability that have implications for shaping the epilepsy phenotype. This review highlights the work to date on apoptosis pathway signaling during seizure-induced neuronal death and epileptogenesis, and speculates on how emerging roles in brain remodeling and excitability have enriched the number of therapeutic strategies for protection against seizure-damage and epileptogenesis.
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Bezborodov, D. A., and R. M. Kravchenko. "Criminal Liability of Athletes for Damage Caused as a Result of Violation of the Rules of Sports Events." Rossijskoe pravosudie 12 (November 13, 2020): 100–105. http://dx.doi.org/10.37399/issn2072-909x.2020.12.100-105.
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The article deals with issues related to the characteristics of the qualification of causing injury or death to an athlete during sports events. The article analyzes the possibility of applying the provisions of certain circumstances that exclude the criminality of the act. Take into account that the relationship between the participants of sports competitions and sports training, while relationships at the same time are not regulated by the law and sports regulations sports, and the internal rules of sports organizations, defining the organization of the training process. Therefore, the issues related to the influence of special rules regulating the procedure for conducting sports competitions and other sporting events on the features of criminal liability (in particular, guilt), both athletes and other persons who ensure the conduct of sports events, are studied specifically. It is taken into account that modern legislation and law enforcement often ignores this requirement, which, in particular, is expressed in the failure to include the facts of sports injuries in the list of crimes in the field of sports. First of all, the article analyzes the issues of criminal-legal assessment of an athlete's act in the event of injury to health or death to another athlete, given that in sports, harm is usually caused unintentionally, by negligence. Therefore, the work analyzes the risks, harm to health, as well as measures that should have been taken by the organizers of the competition to avoid causing harm, taking into account that all these issues are evaluative. The characteristic of harming an athlete while observing the rules of events by his opponent is given. The question of how the rules relating to a particular sport can exempt a person from liability for causing harm is being investigated.
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Shrot, Shai, Andrea Poretti, Elizabeth W. Tucker, Bruno P. Soares, and Thierry AGM Huisman. "Acute brain injury following illicit drug abuse in adolescent and young adult patients: spectrum of neuroimaging findings." Neuroradiology Journal 30, no. 2 (February 27, 2017): 144–50. http://dx.doi.org/10.1177/1971400917691994.
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The use of illicit drugs is currently a major medical problem among adolescents. Several illicit drugs have a high abuse potential and can be neurotoxic causing high morbidity and mortality. The clinical manifestation of adolescents with acute drug-induced neurotoxicity is often characterized by non-specific symptoms and findings. Early diagnosis is important to prevent death and permanent long-term neurological impairments. We report on clinical and neuroimaging findings in five adolescents with acute brain imaging following illicit drug intoxication to highlight the role of neuroimaging findings in the diagnostic work-up of pediatric acute drug-induced neurotoxicity. Our patients reveal two main neuroimaging patterns of brain injury: diffuse symmetric subcortical white matter injury with preferential cerebellar involvement (leukoencephalopathy pattern) or multiple foci of ischemic infarctions in a non-arterial territory distribution (ischemic pattern). Familiarity with these two neuroimaging patterns of findings in the evaluation of magnetic resonance imaging studies in adolescents with acutely altered mental status may suggest the correct diagnosis, narrow the differential diagnosis, and consequently allow early initiation of targeted laboratory investigations and treatment, potentially improving outcome.
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Jaswal, Priya, Priyanka ., and Jhilli Basu. "Climatological Nephropathy: An Overview." International Journal of Health Sciences and Research 11, no. 9 (September 7, 2021): 83–96. http://dx.doi.org/10.52403/ijhsr.20210913.
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Globally hike in temperature provokes the heat waves, results in heat stress and becomes a silent health peril to the existing population. Today, heat stress or climatological stress is one of the dominant pathological conditions which comes in focus when the body means of handling its thermoregulatory function starts to fail, show its associated symptoms followed by eventual loss of consciousness and finally death. The condition of heat stress along with intermittent dehydration worsens the renal damage and enhances the risk of Acute Kidney Injury (AKI), results in chronic kidney disease (CKD). Therefore, CKD comes up as a leading cause of death, specifically in those patients having long-lasting medical conditions like heart problem, hypertension, diabetes and obesity etc. High temperature, work rate, humidity and working time wearing accessories, all become mitigating factors for causing heat stress. Distinguish molecular ups and downs specifically decrease production of uric acid (polyol-fructokinase pathway), increase ROS (oxidative stress), intracellular Ca2+ overload (mitochondrial dysfunctioning) and decrease NO (vascular endothelial dysfunctioning) has been responsible for the severe outcomes of Climatological Nephropathy (CN) or Heat Stress Nephropathy (HSN). However, prevention is the best approach to dealing with heat-related illness, therefore, the Government established some valuable policies as a preventive measures. This review epitomizes the alarming outcomes of the heat stress followed by recurrent dehydration and also enlightened the global talk of HSN, pathogenicity, molecular level peculiarities and recommended measures for HSN. Key words: Acute Kidney Injury, Chronic Kidney Disease, Nephropathy, Mitochondrial Dysfunctioning.
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Rasineni, Karuna, Serene M. L. Lee, Benita L. McVicker, Natalia A. Osna, Carol A. Casey, and Kusum K. Kharbanda. "Susceptibility of Asialoglycoprotein Receptor-Deficient Mice to Lps/Galactosamine Liver Injury and Protection by Betaine Administration." Biology 10, no. 1 (December 31, 2020): 19. http://dx.doi.org/10.3390/biology10010019.
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Background: Work from our laboratory has shown that the ethanol-induced increase in apoptotic hepatocellular death is closely related to the impairment in the ability of the asialoglycoprotein receptor (ASGP-R) to remove neighboring apoptotic cells. In this study, we assessed the role of ASGP-R in fulminant liver failure and investigated whether prior treatment with betaine (a naturally occurring tertiary amine) is protective. Methods: Lipopolysaccharide (LPS; 50 μg/kg BW) and galactosamine (GalN; 350 mg/kg BW) were injected together to wild-type and ASGP-R-deficient mice that were treated for two weeks prior with or without 2% betaine in drinking water. The mice were sacrificed 1.5, 3, or 4.5 h post-injection, and tissue samples were collected. Results: LPS/GalN injection generate distinct molecular processes, which includes increased production of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), thus causing apoptosis as evident by increased caspase-3 activity. ASGP-R deficient animals showed increased liver caspase activities, serum TNF-α and IL-6 levels, as well as more pronounced liver damage compared with the wild-type control animals after intraperitoneal injection of LPS/GalN. In addition, prior administration of betaine was found to significantly attenuate the LPS/GalN-induced increases in liver injury parameters. Conclusion: Our work underscores the importance of normal functioning of ASGP-R in preventing severe liver damage and signifies a therapeutic role of betaine in prevention of liver injuries from toxin-induced fulminant liver failure.
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Ribeiro, Juliana O., Marília G. P. A. Ferreira, Isabela C. S. Marques, Carolina Alvarenga, Andrigo B. Nardi, Sérgio B. Garcia, Gabriel Luiz Montanhim, and Paola C. Moraes. "A new experimental model of intrinsic denervation in ileum from wistar rats through intramural microinjections of benzalkonium chloride." Pesquisa Veterinária Brasileira 39, no. 4 (April 2019): 263–70. http://dx.doi.org/10.1590/1678-5150-pvb-5861.
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ABSTRACT: Extensive literature is available about the intrinsic denervation of segments of the digestive tube through the application of CB in the serosa of the viscera. However, this technique has some disadvantages like causing peritonitis, flanges and high mortality, limiting its use in humans. The aim of the present study was to evaluate the feasibility of benzalkonium chloride (CB) to induce intrinsic chemical denervation, through applications of CB in the intramural ileum of wistar rats, as well as deepen the knowledge about the evolution of neuronal injury caused in the process. We used 40 rats, divided into two groups (control-GC and benzalkonium-GB) of 20 animals each, divided into four sub-groups according to the time of postoperative assessment of 24, 48 hours, 30 and 90 days. The animals were submitted to intramural microinjections of sterile saline solution 0.9% (GC) or benzalkonium chloride (GB) in ileal portion, and subsequent histopathological analysis and immunohistochemistry for evaluation of neuronal injury. A significant decrease (p<0.05) was found of the neuronal myenteric count over time in groups, GB3, GB4 and GB2. The specific positive immunolabeling for H2AX and Caspase-3 confirmed the results obtained in the histopathological evaluation, denoting the ignition of irreversible cell injury in 24 hours, evolving into neuronal apoptosis in 48 hours after application of the CB 0.3%. Under the conditions in which this work was conducted, it can be concluded that the application of CB 0.3% by means of microinjections intramural in the ileal wall is able to induce intrinsic chemical denervation of the diverticulum of wistar rats and that the main mechanism of neuronal death is induction of apoptosis.
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Chattha, Hassan S., Kenneth W. Corscadden, and Qamar U. Zaman. "Hazard Identification and Risk Assessment for Improving Farm Safety on Canadian Farms." Journal of Agricultural Safety and Health 23, no. 3 (2017): 155–74. http://dx.doi.org/10.13031/jash.11959.
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Abstract. Agriculture is one of the most hazardous industries worldwide. The number of serious accidents on farms, despite sophisticated technology, development of effective prevention methods, and high-quality training and improved skill levels of farmers, is still very high. The purpose of this study was to develop and apply a generic farm safety protocol to hazards that have been identified in previously published literature and demonstrate the potential benefits of such a protocol with a view to raising awareness of farm safety. Hazards in agriculture were categorized, and literature highlighting the risks associated with hazards was collated. A protocol was developed and applied to establish the likelihood of a hazard causing injury and the consequence of that injury should adverse effects of hazards be realized. The results indicated farm ownership, farm being used as a primary residence, and missing rollover protective structures as the greatest farm risks with expected likelihood and extreme consequence such as death or permanent disablement. Other hazards that require immediate attention while developing mitigation strategies include accident history and existing medical conditions of the farmer, working environment (i.e., alone and isolated), water bodies in the proximity of the farm, lack of periodic machine maintenance, uncovered power take-off and other rotating parts of the tractor, missing safety decals, auger entanglements, and unprotected use of pesticides. Intervention strategies may be guided by considering the results presented in this study. Moreover, farm safety specialists should increase their efforts to promote effective injury prevention methods and enforce safe work environments. The developed protocol addresses almost all common aspects of farming hazards and can be used to mitigate risks associated with hazards in any farm setting. Keywords: Agriculture, Farm safety, Generic protocol, Hazards, Likelihood.
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Tarlinskaja, Marina. "Rhythm and meaning: "Rhythmical deviations" as italics." Sign Systems Studies 40, no. 1/2 (September 1, 2012): 65–81. http://dx.doi.org/10.12697/sss.2012.1-2.04.
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English iambic pentameter allows rhythmical deviations that occupy three (seldom four, more often two) adjacent metrical positions. These deviations, though metrical, are noticed by the listener or reader. Starting from the first quarter of the 16th century, poets (Surrey) have used rhythmical deviations to emphasize ("italicize") semantically important segments in the line. Such rhythmical deviations have become part of the English poetic traditions. It has turned out that rhythmical deviations used to italicize meaning are filled with recurring rhythmical and grammatical structures and repeated lexicon. M. L. Gasparov used a special term to denote the recurring rhythmicalgrammatical structures: "clichés"; while calling clichés incorporating recurrent lexicon "formulas". I have discovered that formulas are part of the English poetic tradition: the same formulas recur in poetic texts of the 16th–20th cc. They are not plagiarisms, allusions or reminiscences; they are a common basket of goods that belong to all English poets, used by all and owned by none. The recurrent deviations usually occur on metrical positions "weak-strong-weak-strong" and as a rule contain a monosyllabic (rarely – disyllabic) verbpredicate followed by a monosyllabic grammatical word (e.g. an article), an adjectiveattribute and a noun – a direct object to the verb. The recurring lexicon includes verbs of motion, particularly verbs of fast, aggressive motion, an action directed downwards or causing an injury or death, and recurring nouns referring to moving objects or agents (hands, arms, wings; spear, sword). I term such recurring formulas "rhythmical italics".
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Prisyajnyuk, V., S. Semychayevsky, M. Yakimenko, and M. Osadchuk. "ON JUSTIFICATION OF QUALITY INDICATORS AND METHODS OF THEIR EVALUATION OF SPECIAL FIRE PROTECTION EQUIPMENT." Municipal economy of cities 1, no. 161 (March 26, 2021): 290–95. http://dx.doi.org/10.33042/2522-1809-2021-1-161-290-295.
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During the elimination of emergencies, fires and their consequences, units of the State Emergency Service of Ukraine work in a specific environment, which is due to adverse factors affecting them. Fire hazards are manifestations that cause or may lead to burns, poisoning by volatile combustion products or injury or death, causing material and other damage. Dangerous factors of fire include: fever, smoke, deterioration of the gas environment. To date, a number of different (both in terms of technical characteristics and type) special protective equipment is used to perform the tasks assigned by the State Emergency Service of Ukraine, which may not always protect the firefighter from the effects of certain dangerous factors that occur in a fire. The current national standards in Ukraine set only the minimum technical requirements for such equipment, which are insufficient to identify substandard products that fall into the equipment of these units. Therefore, in order to prevent the use of such low-quality protective equipment, it is necessary to study all possible risks and dangers that arise during emergency response by the State Emergency Service of Ukraine and develop reasonable requirements for special protective equipment and appropriate test methods. The above determines the relevance of the study aimed at implementing in Ukraine modern requirements for quality indicators of special protective equipment for firefighters, methods and procedures for their evaluation. This is necessary to implement the requirements of the Technical Regulations for construction products, buildings and structures in order to ensure the safety of rescue teams during firefighting. In order to assist in solving this problem at the Institute of Public Administration and Research on Civil Protection by order of the State Emergency Service of Ukraine plans to conduct research on "Substantiation of quality indicators and methods of assessing special protective equipment firefighter" (topic code: Protective equipment - indicators quality "), which will develop a draft national standard of Ukraine, which sets requirements for quality indicators of special protective equipment for firefighters, methods and procedures for their evaluation.
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Gaoneng, Yu. "Causing Death by Inflicting Injury: Causation and Sentencing." Journal of Criminal Law 72, no. 2 (April 2008): 113–16. http://dx.doi.org/10.1350/jcla.2008.72.2.486.
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Mouncey, Paul R., Alvin Richards-Belle, Karen Thomas, David A. Harrison, M. Zia Sadique, Richard D. Grieve, Julie Camsooksai, et al. "Reduced exposure to vasopressors through permissive hypotension to reduce mortality in critically ill people aged 65 and over: the 65 RCT." Health Technology Assessment 25, no. 14 (February 2021): 1–90. http://dx.doi.org/10.3310/hta25140.
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Background Vasopressors are administered to critical care patients to avoid hypotension, which is associated with myocardial injury, kidney injury and death. However, they work by causing vasoconstriction, which may reduce blood flow and cause other adverse effects. A mean arterial pressure target typically guides administration. An individual patient data meta-analysis (Lamontagne F, Day AG, Meade MO, Cook DJ, Guyatt GH, Hylands M, et al. Pooled analysis of higher versus lower blood pressure targets for vasopressor therapy septic and vasodilatory shock. Intensive Care Med 2018;44:12–21) suggested that greater exposure, through higher mean arterial pressure targets, may increase risk of death in older patients. Objective To estimate the clinical effectiveness and cost-effectiveness of reduced vasopressor exposure through permissive hypotension (i.e. a lower mean arterial pressure target of 60–65 mmHg) in older critically ill patients. Design A pragmatic, randomised clinical trial with integrated economic evaluation. Setting Sixty-five NHS adult general critical care units. Participants Critically ill patients aged ≥ 65 years receiving vasopressors for vasodilatory hypotension. Interventions Intervention – permissive hypotension (i.e. a mean arterial pressure target of 60–65 mmHg). Control (usual care) – a mean arterial pressure target at the treating clinician’s discretion. Main outcome measures The primary clinical outcome was 90-day all-cause mortality. The primary cost-effectiveness outcome was 90-day incremental net monetary benefit. Secondary outcomes included receipt and duration of advanced respiratory and renal support, mortality at critical care and acute hospital discharge, and questionnaire assessment of cognitive decline and health-related quality of life at 90 days and 1 year. Results Of 2600 patients randomised, 2463 (permissive hypotension, n = 1221; usual care, n = 1242) were analysed for the primary clinical outcome. Permissive hypotension resulted in lower exposure to vasopressors than usual care [mean duration 46.0 vs. 55.9 hours, difference –9.9 hours (95% confidence interval –14.3 to –5.5 hours); total noradrenaline-equivalent dose 31.5 mg vs. 44.3 mg, difference –12.8 mg (95% CI –18.0 mg to –17.6 mg)]. By 90 days, 500 (41.0%) patients in the permissive hypotension group and 544 (43.8%) patients in the usual-care group had died (absolute risk difference –2.85%, 95% confidence interval –6.75% to 1.05%; p = 0.154). Adjustment for prespecified baseline variables resulted in an odds ratio for 90-day mortality of 0.82 (95% confidence interval 0.68 to 0.98) favouring permissive hypotension. There were no significant differences in prespecified secondary outcomes or subgroups; however, patients with chronic hypertension showed a mortality difference favourable to permissive hypotension. At 90 days, permissive hypotension showed similar costs to usual care. However, with higher incremental life-years and quality-adjusted life-years in the permissive hypotension group, the incremental net monetary benefit was positive, but with high statistical uncertainty (£378, 95% confidence interval −£1347 to £2103). Limitations The intervention was unblinded, with risk of bias minimised through central allocation concealment and a primary outcome not subject to observer bias. The control group event rate was higher than anticipated. Conclusions In critically ill patients aged ≥ 65 years receiving vasopressors for vasodilatory hypotension, permissive hypotension did not significantly reduce 90-day mortality compared with usual care. The absolute treatment effect on 90-day mortality, based on 95% confidence intervals, was between a 6.8-percentage reduction and a 1.1-percentage increase in mortality. Future work Future work should (1) update the individual patient data meta-analysis, (2) explore approaches for evaluating heterogeneity of treatment effect and (3) explore 65 trial conduct, including use of deferred consent, to inform future trials. Trial registration Current Controlled Trials ISRCTN10580502. Funding This project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 25, No. 14. See the NIHR Journals Library website for further project information.
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Peek-Asa, C., D. L. McArthur, and J. F. Kraus. "Determining injury at work on the California death certificate." American Journal of Public Health 87, no. 6 (June 1997): 998–1002. http://dx.doi.org/10.2105/ajph.87.6.998.
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WALDZINSKI, TOMASZ, CEZARY WALDZINSKI, ALEKSANDRA DURZYNSKA, EWA WALDZINSKA, MALGORZATA KNAS, and KAZIMIERZ KOCHANOWICZ. "Criminal liability for injuries of competitors arising in the course of sports competition in Polish criminal law." Baltic Journal of Health and Physical Activity Supplement 1, no. 1 (December 31, 2020): 11–18. http://dx.doi.org/10.29359/bjhpa.2020.suppl.1.02.
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Practicing both high performance and recreational sport involves not only many sacrifices, taking care of one's health and maintaining an appropriate shape, but also risks which result in damage to one's health and, in extreme cases – the death of a contestant. The athletes suffer various types of sports injuries during competitions or training sessions. Much of it is due to the behaviour of another contestant. Therefore, the question is when a sportsman, in the Polish legal system, will be liable for a penalty for the fact that during the competition he caused an injury (sporting injury) to his rival. The criminal liability of sportsmen may be subject to criminal law provisions concerning: causing serious bodily harm, causing other than serious bodily harm, unintentionally causing the death, violating personal inviolability. According to the criminal law, an injury caused as a result of sports activity should be defined as a bodily harm. It should also be pointed out that in the Polish legal system it has been developed by doctrine and reflected in court rulings, the sport risk justification excluding the unlawfulness of the act and thus excluding criminal liability of the competitor causing damage to the health or death of the competitor.
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Katanick, Dvora, Mark L. Taff, and Werner U. Spitz. "A Work-Related Death Due to a Penetrating Chest Injury." American Journal of Forensic Medicine and Pathology 7, no. 2 (June 1986): 163–64. http://dx.doi.org/10.1097/00000433-198607020-00016.
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Cherkasov, V. G., T. V. Lachtadyr, L. Ya Fedoniuk, and O. V. Shypitsyna. "Comparative analysis of the effects of various detoxification solutions on the structure of the kidneys in experimental burn disease in rats." Reports of Morphology 25, no. 2 (June 26, 2019): 16–27. http://dx.doi.org/10.31393/morphology-journal-2019-25(2)-02.
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The use of existing infusion solutions, as well as the development, scientific substantiation and implementation of the latest nephroprotective detoxification solutions, remain an urgent problem for combustiologists. The aim of this work is to compare the effects of various detoxification solutions (0.9 % NaCl solution and complex colloid-hyperosmolar solutions – lactoprotein with sorbitol and the newly developed HAES-LX-5 % solution) on the kidney structure in experimental burn disease in rats. The experimental rats were divided into seven groups (fifteen animals each): the first group was intact rats; the second, third and fourth groups were rats without reproduction of experimental burn disease, which had a separate intravenous infusion of 0.9 % NaCl solution, lactoprotein with sorbitol and HAES-LX-5 % at a dose of 10 ml/kg; the fifth, sixth and seventh groups were rats with experimental burn disease (by causing burn injury of the skin with an area of 21-23 % of the body surface), which under the same scheme had an intravenous infusion of the investigated solutions. All studies and the removal of rats from the experiment were performed under deep thiopental intraperitoneal anesthesia. Histological preparations of the renal cortex of the rat were stained with hematoxylin-eosin and examined on an Olympus BX51 microscope. Using ultramicrotome LKB-3 (Sweden) obtained semi-thin sections which were stained with toluidine blue and methylene blue – Azur II; and ultrathin sections were counterstained with uranyl acetate and lead citrate according to Reynolds and examined using a PEM-125K electron microscope. Morphometric measurements (estimation of the area of the vascular glomeruli, the area of the urinary lumen of the capsule of the renal corpuscles; the area of the renal tubules of the nephrons and the area of their lumens, the area of the renal corpuscles, the area of cytoplasm and nuclei of epithelial cells of tubules, and also their nuclear-cytoplasmic ratio) was carried out using the VideoTest-5.0, KAARA Image Base and Microsoft Excel on a personal computer. Statistical analysis of the obtained quantitative indicators was performed using the ІВМ SPSS v. 22.0. for Windows. Functionally different cells of nephrons have been found to die by necrosis, apoptosis and anoikis when infused with detoxification solutions during the development of burn disease; in epithelial cells of nephron tubules, mitophagy and mitoptosis occur. Mitoptosis in epithelial cells of rat tubules of nephrons with experimental burn skin injury is carried out in two ways related to: 1) destruction of the outer mitochondrial membrane; 2) preservation of the outer mitochondrial membrane and involvement of autophagic (mitophagic) mechanisms to release the cell from degraded mitochondrial material. In the first case, the mitochondria first condense, after which its matrix swells and the fragmentation of the cristae occurs due to the destruction of the junction of the cristae. Finally, the outer mitochondrial membrane breaks and the remnants of the cristae (in the form of vesicles) go into the cytoplasm. In the second case, the mitochondria condense, vesicular fragmentation of the cristae occurs, but the rupture of the outer mitochondrial membrane does not occur and the mitochondria are absorbed by the autophagosome (or transformed into the autophagosome). Next is the merger of autophagosomes with lysosomes and the formation of autophagolysosomes, which, under the conditions of effective digestion of the contents, are transformed into vacuoles. The latter are emptied by exocytosis and ensure the release of cells from degraded material. Only lactoprotein with sorbitol has a membrane-plastic effect on the strengthening (enhancement of structuring) of the mitochondrial membrane in part of the mitochondria of epithelial cells of nephron tubules, which is ultrastructurally manifested by an increase in the electron density and thickness of all components of the mitochondria. The maximum membrane effect of lactoprotein with sorbitol against mitochondria manifests itself fourteen days after the experimental burn skin injury and gradually (after twenty-one and thirty days) disappears, which is correlated with an improvement in the overall clinical condition and an improvement in the structural changes in the kidney of animals with burn disease. There is every reason to believe that increased structuration of mitochondria is a preventer of the spread of mitoptosis and mitophagy, the excess of which can lead to cell death.
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Rodrigues, Nhirneyla Marques, Ana Maria Quessada, Fabiane Leite da Silva, Esther Machado de Carvalho e. Silva, João Moreira da Costa Neto, and Wagner Costa Lima. "Epidemiology and Anesthetic Risk in Dogs with Aural Hematoma." Acta Scientiae Veterinariae 44, no. 1 (March 19, 2018): 6. http://dx.doi.org/10.22456/1679-9216.80930.
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Background: Otohematoma or aural hematoma in dogs is blood pooling within the ear cartilage plate, and stems from several causes (ear infections, ectoparasites and others). The formation of hematoma is by vascular injury, causing bleeding, generated by self-injury. This disease occurs especially in dogs of pendulous ears, and the concave surface of the ear is considered as the most frequent. The therapy to correct the lesion can be a clinical procedure; however, surgical drainage is the treatment of choice. This work aims to record the epidemiological aspects related to aural hematoma in dogs, as well as classify such patients as to the physical condition and anesthetic risk.Materials, Methods & Results: Twenty five dogs with aural hematoma submitted to surgical procedure were followed. During the data collection period (seven months), surgery to correct aural hematoma represented 19% of surgeries performed in dogs (total of surgeries: 474). The percentage of canine breeds affected was: mixed breed (64%; 16/25), german shepherd (24%; 6/25), labrador (4%; 1/25), waimaraner (4%; 1/25) and daschund (4%; 1/25). Most occurrences were observed in females aged 3-12 years. Most of the animals showed only one pina affected (96%; 24/25), and 52% (13/25) had hematoma in the right and 44% (11/25) in the left ear. Some of the patients had no hematologic abnormalities (48%; 12/25), but some animals showed normocytic normochromic anemia (36%, 9/25), leukocytosis (8%; 2/25) and thrombocytopenia (8%; 2/25). Among animals, there were only dogs classified as ASA II and ASA III with similar rates (56% and 44% respectively). No deaths were observed among cases analyzed.Discussion: The high prevalence of the disease in mongrel dogs can be explained by the great number of mongrel animals in the service analyzed. Aural hematoma was more frequent in older dogs probably because animals in this age group are more affected by otitis externa, which can predispose them to aural hematoma. Otohematoma was common in animals with pendulous ears, probably because these dogs are more prone to ear diseases than animals with erect ears. Females are more affected, and these data are different to those of other studies, and may be related to changes of the clientele among males and females. Only 4% (1/25) showed bilateral aural hematoma which, actually, is less common. Haematological abnormalities observed may be related to the appearance of aural hematoma, but were unspecific and common to several diseases. Animals classified as ASA II entered in this category for being carriers of mild haematological disorders, especially anemia (36%; 9/25). Dogs classified as ASA III showed signs of moderate systemic disease, and the main suspected disease was ehrlichiosis, which may be associated with aural hematoma. Animals underwent surgical procedure even though being classified as ASA II and III. Such procedure caused no detectable adverse effects and no deaths were recorded. It is expected that mortality is higher in patients classified in a higher grade. The absence of deaths can be related to ASA classification, which was only up to Grade III (moderate systemic disease). Moreover, surgery to drain aural hematoma is considered free of contamination, minimally invasive and without the involvement of important anatomical structures that could systemically compromise patients.
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Husky, Mathilde M., Victor Alvarez Fernandez, Geraldine Tapia, Florin Oprescu, Fernando Navarro-Mateu, and Viviane Kovess-Masfety. "Mental disorders and medical conditions associated with causing injury or death: A population-based study." Psychiatry Research 287 (May 2020): 112899. http://dx.doi.org/10.1016/j.psychres.2020.112899.
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Hong, Jung Yeon, Mi Na Kim, Eun Gyul Kim, Jae Woo Lee, Hye Rin Kim, Soo Yeon Kim, Soon Min Lee, Yoon Hee Kim, Kyung Won Kim, and Myung Hyun Sohn. "Clusterin Deficiency Exacerbates Hyperoxia-Induced Acute Lung Injury." Cells 10, no. 4 (April 19, 2021): 944. http://dx.doi.org/10.3390/cells10040944.
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Exposure to high oxygen concentrations leads to generation of excessive reactive oxygen species, causing cellular injury and multiple organ dysfunctions and is associated with a high mortality rate. Clusterin (CLU) is a heterodimeric glycoprotein that mediates several intracellular signaling pathways, including cell death and inflammation. However, the role of CLU in the pathogenesis of hyperoxic acute lung injury (HALI) is unknown. Wild-type (WT) and CLU-deficient mice and cultured human airway epithelial cells were used. Changes in cell death- and inflammation-related molecules with or without hyperoxia exposure in cells and animals were determined. Hyperoxia induced an increase in CLU expression in mouse lungs and human airway epithelial cells. Mice lacking CLU had increased HALI and mortality rate compared with WT mice. In vitro, CLU-disrupted cells showed enhanced release of cytochrome c, Bax translocation, cell death and inflammatory cytokine expression. However, treatment with recombinant CLU attenuated hyperoxia-induced apoptosis. Moreover, the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyses revealed metabolic pathways, hematopoietic cell lineage, response to stress and localization and regulation of immune system that were differentially regulated between WT and CLU−/− mice. These results demonstrate that prolonged hyperoxia-induced lung injury is associated with CLU expression and that CLU replenishment may alleviate hyperoxia-induced cell death.
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Rennekampff, Hans-Oliver, and Ziyad Alharbi. "Burn Injury: Mechanisms of Keratinocyte Cell Death." Medical Sciences 9, no. 3 (July 16, 2021): 51. http://dx.doi.org/10.3390/medsci9030051.
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Cutaneous burn injury is associated with epidermal loss in the zone of coagulation zone and delayed tissue loss in the zone of stasis. Thus, thermal stress can trigger both necrosis and regulated cell death (RCD) or apoptosis. Experimental in vitro and in vivo work has clearly demonstrated apoptotic events of thermally injured keratinocytes that are accompanied by morphological and biochemical markers of regulated cell death. However, in vivo data for the different pathways of regulated cell death are sparse. In vitro experiments with heat-stressed human keratinocytes have demonstrated death receptor involvement (extrinsic apoptosis), calcium influx, and disruption of mitochondrial membrane potential (intrinsic apoptosis) in regulated cell death. In addition, caspase-independent pathways have been suggested in regulated cell death. Keratinocyte heat stress leads to reduced proliferation, possibly as a result of reduced keratinocyte adhesion (anoikis) or oncogene involvement. Understanding the underlying mechanisms of RCD and the skin’s responses to thermal stress may lead to improved strategies for treating cutaneous burn trauma.
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Vasilchenko, Anna A. "Representation of Suffering in the Vocabulary of the Dialect Language Personality of a Siberian Peasant Woman." Vestnik Tomskogo gosudarstvennogo universiteta, no. 462 (2021): 14–21. http://dx.doi.org/10.17223/15617793/462/2.
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The article examines the semantic field “suffering” that represents a fragment of the emotional and sensual existence of a language personality. The linguopersonological research based on the material of the idiolectal vocabulary of Vera Vershinina, a Siberian old resident, continues the comprehensive description of a dialect language personality made by Tomsk dialectologists. The research sources are A Complete Dictionary of a Dialect Language Personality edited by E.V. Ivantsova, transcripts of the informant’s speech made through participation in the linguistic existence of the speaker. The article focuses on 52 lexical and phraseological units. The research aims to describe a fragment of an individual linguistic worldview representing suffering. The view on the research object develops in the following way: word – definition – examples represented in the dictionary – text – idiolectal discourse. At the first stage of the research, the lexical and phraseological units are divided into seven functional semantic classes (FSC) according to the categorial lexical seme uniting them. The researcher examines the numerical composition of each class, the linguistic features of its elements (presence of figurative units, features of the use of the examined words). The most developed is the FSC of emotional state, since suffering is perceived as a long and deep feeling caused by a certain reason, but infinite. Classes of emotional impact and receiving the emotional state characterize suffering as a feeling hurting physically, exhausting with its length and intensity. A large number of units with the semantics of weeping in the FSC of external expression of emotions can indicate that the informant replaces reflection with a detailed description of external manifestations of suffering. Classes of emotional characterization and attitude show the informant as a person deeply empathetic to the grief of others. The last FSC demonstrates that names of the feeling and the situation causing this feeling coexist in one unit, which is typical for representatives of the folk speech culture. At the second stage of the research, the author describes the most frequent situations associated with the actualization of the semantic field “suffering” in the informant’s speech. These situations include: disease or death; disability caused by an injury; difficult living conditions, etc. It corresponds to the core values of the traditional peasant culture: life and health of a person, wealth, stability of a family’s life. The material shows that, for the dialect speaker, suffering is one of the dominants of reality, a constant of everyday life fully accepted by the speaker. However, the informant does not ignore other people in her grief, she is empathetic towards their life because of such personal qualities as optimism and spiritual power.
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van der Weg, Kirian, Frits W. Prinzen, and Anton PM Gorgels. "Editor’s Choice- Reperfusion cardiac arrhythmias and their relation to reperfusion-induced cell death." European Heart Journal: Acute Cardiovascular Care 8, no. 2 (November 13, 2018): 142–52. http://dx.doi.org/10.1177/2048872618812148.
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Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.
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Glazebrook, P. R. "A BETTER WAY OF CONVICTING BUSINESSES OF AVOIDABLE DEATHS AND INJURIES?" Cambridge Law Journal 61, no. 2 (June 24, 2002): 405–22. http://dx.doi.org/10.1017/s0008197302001678.
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The Law Commission’s proposal for an offence of “corporate killing” (modelled on the common law crimeof gross negligence manslaughter) is criticised for vagueness and imprecison, for not comprehending serious non-fatal injuries, and for failing to recognise that in the absence of clear rules of attribution, any criminal liability imposed on an organisation can only be for failing to prevent something happening. It is suggested that offences (patterned on those of causing death by dangerous, or by careless and drunken driving) of causing death or serious injury by breaking (statutory) regulations would be a much better way of holding businesses and similar bodies as well as individuals liable for death and serious injuries that would not have occurred if those regulations had been obeyed.
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Samol, Monika A., Francisco A. Uzal, Patricia C. Blanchard, Rick M. Arthur, and Susan M. Stover. "Sudden death caused by spinal cord injury associated with vertebral fractures and fetlock failure in a Thoroughbred racehorse." Journal of Veterinary Diagnostic Investigation 33, no. 4 (May 27, 2021): 788–91. http://dx.doi.org/10.1177/10406387211018289.
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The most prevalent causes of death in racehorses are musculoskeletal injuries, causing ~83% of deaths within the racing industry in California and elsewhere. The vast majority of these injuries have preexisting lesions that predispose to fatal injury. A 4-y-old Thoroughbred colt suffered an acute suspensory apparatus failure, including biaxial proximal sesamoid bone fractures of the right front fetlock, causing loss of support of the fetlock joint and consequent fall with fractures of the cervical and sacral spine. Cervical fracture caused spinal cord damage that resulted in sudden death. A preexisting lesion in the medial proximal sesamoid bone likely predisposed to complete fracture of this bone and fetlock breakdown. Interestingly, a comparable osteopenic lesion was present in the intact medial proximal sesamoid bone of the left forelimb, which is consistent with bilateral repetitive overuse injury in racehorses. The morphologic features of the cervical and sacral spine fractures were compatible with acute injury; no evidence of preexisting lesions was seen. Most likely, these acute vertebral fractures occurred as a result of the horse falling. This case emphasizes the importance of performing a detailed autopsy in horses that suffer an appendicular musculoskeletal injury, particularly in fatal cases when the horse dies following a leg injury.
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’t Mannetje, Andrea, and Neil Pearce. "Quantitative estimates of work-related death, disease and injury in New Zealand." Scandinavian Journal of Work, Environment & Health 31, no. 4 (August 2005): 266–76. http://dx.doi.org/10.5271/sjweh.882.
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Mueller, P., L. C. Horn, P. Buehrdel, and H. J. Boehme. "Hydropericardium Causing Sudden Infant Death in Glycogenosis Type I: Osmotic Injury Due to Percutaneous Silastic Catheterization." Klinische Pädiatrie 216, no. 5 (September 2004): 294–96. http://dx.doi.org/10.1055/s-2004-816245.
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Zorov, D. B., E. Y. Plotnikov, S. S. Jankauskas, N. K. Isaev, D. N. Silachev, L. D. Zorova, I. B. Pevzner, N. V. Pulkova, S. D. Zorov, and M. A. Morosanova. "The phenoptosis problem: What is causing the death of an organism? Lessons from acute kidney injury." Biochemistry (Moscow) 77, no. 7 (July 2012): 742–53. http://dx.doi.org/10.1134/s0006297912070073.
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Halestrap, A. P., E. Doran, J. P. Gillespie, and A. O'Toole. "Mitochondria and cell death." Biochemical Society Transactions 28, no. 2 (February 1, 2000): 170–77. http://dx.doi.org/10.1042/bst0280170.
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Mitochondria play a central role in both apoptosis and necrosis through the opening of the mitochondrial permeability transition pore (MPTP). This is thought to be formed through a Ca2+-triggered conformational change of the adenine nucleotide translocase (ANT) bound to matrix cyclophilin-D and we have now demonstrated this directly by reconstitution of the pure components. Opening of the MPTP causes swelling and uncoupling of mitochondria which, unrestrained, leads to necrosis. In ischaemia/reperfusion injury of the heart we have shown MPTP opening directly. Recovery of hearts correlates with subsequent closure, and agents that prevent opening or enhance closure protect from injury. Transient MPTP opening may also be involved in apoptosis by initially causing swelling and rupture of the outer membrane to release cytochrome c (cyt c), which then activates the caspase cascade and sets apoptosis in motion. Subsequent MPTP closure allows ATP levels to be maintained, ensuring that cell death remains apoptotic rather than necrotic. Apoptosis in the hippocampus that occurs after a hypoglycaemic or ischaemic insult is triggered by this means. Other apoptotic stimuli such as cytokines or removal of growth factors also involve mitochondrial cyt c release, but here there is controversy over whether the MPTP is involved. In many cases cyt c release is seen without any mitochondrial depolarization, suggesting that the MPTP does not open. Recent data of our own and others have revealed a specific outer-membrane cyt c-release pathway involving porin that does not release other intermembrane proteins such as adenylate kinase. This is opened by pro-apototic members of the Bcl-2 family such as BAX and prevented by anti-apoptotic members such as Bcl-xL. Our own data suggest that this pathway may interact directly with the ANT in the inner membrane at contact sites.
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Deshpande, Rushikesh, and Chunbin Zou. "Pseudomonas Aeruginosa Induced Cell Death in Acute Lung Injury and Acute Respiratory Distress Syndrome." International Journal of Molecular Sciences 21, no. 15 (July 28, 2020): 5356. http://dx.doi.org/10.3390/ijms21155356.
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Pseudomonas aeruginosa is an important opportunistic pathogen responsible for the cause of acute lung injury and acute respiratory distress syndrome. P. aeruginosa isthe leading species isolated from patients with nosocomial infection and is detected in almost all the patients with long term ventilation in critical care units. P. aeruginosa infection is also the leading cause of deleterious chronic lung infections in patients suffering from cystic fibrosis as well as the major reason for morbidity in people with chronic obstructive pulmonary disease. P. aeruginosa infections are linked to diseases with high mortality rates and are challenging for treatment, for which no effective remedies have been developed. Massive lung epithelial cell death is a hallmark of severe acute lung injury and acute respiratory distress syndrome caused by P. aeruginosa infection. Lung epithelial cell death poses serious challenges to air barrier and structural integrity that may lead to edema, cytokine secretion, inflammatory infiltration, and hypoxia. Here we review different types of cell death caused by P. aeruginosa serving as a starting point for the diseases it is responsible for causing. We also review the different mechanisms of cell death and potential therapeutics in countering the serious challenges presented by this deadly bacterium.
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Saghir, Rabia. "Retrospective Autopsy based analysis of nature and prevalence of Fatal Injuries in Lahore." Pakistan Journal of Surgery and Medicine 1, no. 1 (February 1, 2020): 81–85. http://dx.doi.org/10.37978/pjsm.v1i1.96.
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Bacckground: Autopsy is a medical examination conducted after death to ascertain the cause of death. For Clinical autopsies, the permission of the next of kin is required. In suspicious deaths, an autopsy is a legal requirement and is performed by the coroner ormedico-legal surgeon.
Methodology: Retrospective analysis of records of forensic medicine from January 1st, 2016 to December 31st, 2016, was done to observe fatal injuries causing death, their nature, and prevalence. The deaths, in which cause of death was Fatal Injury were included in our study. These cases were analyzed with respect to age, gender, cause and manner of death, number and location of injuries and the approximate time lag between injury and death. All data were entered into SPSS.
Results: A total of 785 autopsies were conducted at the Department of Forensic Medicine and Toxicology, King Edward Medical University, Lahore in 2016, 42.8% fulfilled our inclusion criteria and were included in the study. Cases of firearm injuries were maximum constituting 46.4%, followed by RTA (13.7%) and blunt trauma (11.9%). Most victims were in the age bracket of 21-40 (55.1%) with a male to female ratio of 4.09:1. Head was the predominant site involved.
Conclusion: Fatal injury deaths are mostly due to firearm injuries. Victims are more commonly males and majority cases die immediately after sustaining the injury. Manner of death is predominantly homicidal. Efforts should be made to prevent and properly manage fatal injuries.
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Wood, Bruce W., and Charles C. Reilly. "240 Sudden Tree Decline and Death of Pecan." HortScience 35, no. 3 (June 2000): 432D—432. http://dx.doi.org/10.21273/hortsci.35.3.432d.
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This study reports on sudden death (or decline) of mature and apparently healthy pecan trees [Carya illinoinensis (Wangenh.) K. Koch]. Observations suggest that death and damage is due to winter cold injury (although the season's low was only -5 °C). The severity of this cold injury-like form of sudden death is closely associated with nut crop load (i.e., grams of kernels per square centimeter of trunk cross-sectional area) and premature defoliation. Both dead and declining trees not only produced relatively heavy crops, but also exhibited substantial premature pest-induced defoliation the previous autumn. The near absence of sugars and starch in roots and shoots of dead or declining trees at budbreak and the relatively high levels in healthy trees indicates that diminished assimilate reserves during the dormant season were the key factor causing death or decline. The diminished assimilate reserves prevented the accumulation of assimilate reserves necessary for maintaining live roots throughout the dormancy and prevented proper cold acclimation of shoot tissues. Distinct symptoms of sudden tree death or decline compared to typical cold damage are: a) a distinct top-to-bottom gradation of tree damage, with an increased proportion of dead shoots and shoots supporting abnormally small foliage being near the base of the canopy; b) dessicated and tan appearance of inner bark and phloem of the main trunk rather than brown coloration so typical of classical cold injury; c) death of roots by time of budbreak; and d) absence of resprouting from the trunk or root collar. These observations indicate that pecan trees can suddenly die due to being overly stressed for assimilates and that economic losses previously attributed to injury by severe winter cold sometimes may be due to depleted assimilate reserves during the dormant season as a result of overcropping and premature defoliation.
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Nieminen, A. L., A. K. Saylor, B. Herman, and J. J. Lemasters. "ATP depletion rather than mitochondrial depolarization mediates hepatocyte killing after metabolic inhibition." American Journal of Physiology-Cell Physiology 267, no. 1 (July 1, 1994): C67—C74. http://dx.doi.org/10.1152/ajpcell.1994.267.1.c67.
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The importance of ATP depletion and mitochondrial depolarization in the toxicity of cyanide, oligomycin, and carbonyl cyanide m-cholorophenylhydrazone (CCCP), an uncoupler, was evaluated in rat hepatocytes. Oligomycin, an inhibitor of the reversible mitochondrial ATP synthase (F1F0-adenosinetriphosphatase), caused dose-dependent cell killing with 0.1 microgram/ml being the minimum concentration causing the maximum cell killing. Oligomycin also caused rapid ATP depletion without causing mitochondrial depolarization. Fructose (20 mM), a potent glycolytic substrate in liver, protected completely against oligomycin toxicity. CCCP (5 microM) also caused rapid killing of hepatocytes. Fructose retarded cell death caused by CCCP but failed to prevent lethal cell injury. Although oligomycin (1.0 microgram/ml) was lethally toxic by itself, in the presence of fructose it protected completely against CCCP-induced cell killing. Cyanide (2.5 mM), an inhibitor of mitochondrial respiration, caused rapid cell killing that was reversed by fructose. CCCP completely blocked fructose protection against cyanide, causing mitochondrial depolarization and rapid ATP depletion. In the presence of fructose and cyanide, oligomycin protected cells against CCCP-induced ATP depletion and cell death but did not prevent mitochondrial depolarization. In every instance, cell killing was associated with ATP depletion, whereas protection against lethal cell injury was associated with preservation of ATP. In conclusion, protection by fructose against toxicity of cyanide, oligomycin, and CCCP was mediated by glycolytic ATP formation rather than by preservation of the mitochondrial membrane potential. These findings support the hypothesis that inhibition of cellular ATP formation is a crucial event in the progression of irreversible cell injury.
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Terenghi, G., A. Hart, and M. Wiberg. "The nerve injury and the dying neurons: diagnosis and prevention." Journal of Hand Surgery (European Volume) 36, no. 9 (November 2011): 730–34. http://dx.doi.org/10.1177/1753193411422202.
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Following distal nerve injury significant sensory neuronal cell death occurs in the dorsal root ganglia, while after a more proximal injury, such as brachial plexus injury, a sizeable proportion of spinal motoneurons also undergo cell death. This phenomenon has been undervalued for a long time, but it has a significant role in the lack of functional recuperation, as neuronal cells cannot divide and be replaced, hence the resulting nerve regeneration is usually suboptimal. It is now accepted that this cell death is due to apoptosis, as indicated by analysis of specific genes involved in the apoptotic signalling cascade. Immediate nerve repair, either by direct suturing or nerve grafting, gives a degree of neuroprotection, but this approach does not fully prevent neuronal cell death and importantly it is not always possible. Our work has shown that pharmacological intervention using either acetyl-L-carnitine (ALCAR) or N-acetyl-cysteine (NAC) give complete neuroprotection in different types of peripheral nerve injury. Both compounds are clinically safe and experimental work has defined the best dose, timing after injury and duration of administration. The efficacy of neuroprotection of ALCAR and NAC can be monitored non-invasively using MRI, as demonstrated experimentally and more recently by clinical studies of the volume of dorsal root ganglia. Translation to patients of this pharmacological intervention requires further work, but the available results indicate that this approach will help to secure a better functional outcome following peripheral nerve injury and repair.
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Bayley, Jeppe Seamus, Christian Bak Winther, Mads Kuhlmann Andersen, Camilla Grønkjær, Ole Bækgaard Nielsen, Thomas Holm Pedersen, and Johannes Overgaard. "Cold exposure causes cell death by depolarization-mediated Ca2+ overload in a chill-susceptible insect." Proceedings of the National Academy of Sciences 115, no. 41 (September 25, 2018): E9737—E9744. http://dx.doi.org/10.1073/pnas.1813532115.
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Cold tolerance of insects is arguably among the most important traits defining their geographical distribution. Even so, very little is known regarding the causes of cold injury in this species-rich group. In many insects it has been observed that cold injury coincides with a cellular depolarization caused by hypothermia and hyperkalemia that develop during chronic cold exposure. However, prior studies have been unable to determine if cold injury is caused by direct effects of hypothermia, by toxic effects of hyperkalemia, or by the depolarization that is associated with these perturbations. Here we use a fluorescent DNA-staining method to estimate cell viability of muscle and hindgut tissue from Locusta migratoria and show that the cellular injury is independent of the direct effects of hypothermia or toxic effects of hyperkalemia. Instead, we show that chill injury develops due to the associated cellular depolarization. We further hypothesized that the depolarization-induced injury was caused by opening of voltage-sensitive Ca2+ channels, causing a Ca2+ overload that triggers apoptotic/necrotic pathways. In accordance with this hypothesis, we show that hyperkalemic depolarization causes a marked increase in intracellular Ca2+ levels. Furthermore, using pharmacological manipulation of intra- and extracellular Ca2+ concentrations as well as Ca2+ channel conductance, we demonstrate that injury is prevented if transmembrane Ca2+ flux is prevented by removing extracellular Ca2+ or blocking Ca2+ influx. Together these findings demonstrate a causal relationship between cold-induced hyperkalemia, depolarization, and the development of chill injury through Ca2+-mediated necrosis/apoptosis.
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Prasad, Arun, Lokesh Tiwari, Pradeep Kumar, and N. Yankappa. "Accidental partial hanging by door curtain causing ischemic encephalopathy in a child: a rare case report." International Journal of Contemporary Pediatrics 7, no. 10 (September 21, 2020): 2061. http://dx.doi.org/10.18203/2349-3291.ijcp20204024.
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Accidental strangulation is an uncommon injury in children, however it may lead to neurological disability or death. Various modes of injuries have been reported in such accidents. Children might get strangulated while playing if they are wrapping any cord or cloth like material around their neck. Caregivers of the children should be aware of the potential sources around and mechanisms of such injuries to avoid such accidents.
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Chen, Guang-Xiang, and David E. Fosbroke. "Work-Related Fatal-Injury Risk of Construction Workers by Occupation and Cause of Death." Human and Ecological Risk Assessment: An International Journal 4, no. 6 (December 1998): 1371–90. http://dx.doi.org/10.1080/10807039891284721.
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Shah, Shenil, Bimal Padaliya, and Sri Krishna Madan Mohan. "Noninfiltrating Adenocarcinoma of the Lung Causing ST-Segment Elevation." Texas Heart Institute Journal 42, no. 4 (August 1, 2015): 381–84. http://dx.doi.org/10.14503/thij-14-4268.
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ST-segment-elevation myocardial infarction is a leading cause of cardiovascular morbidity and death. We describe the case of a 51-year-old woman with advanced adenocarcinoma of the lung who presented with ST-segment elevation in the presence of an extracardiac lung mass but no objective evidence of myocardial ischemia or pericardial involvement. After the patient died of hypoxic respiratory failure, autopsy findings confirmed normal-appearing pericardium and myocardium, and mild-to-moderate atherosclerosis in the coronary arteries. A 4.5 × 4-cm extracardiac left hilar lung mass was confirmed to be poorly differentiated adenocarcinoma of the lung adjacent to the myocardium. The persistent current of injury that had been detected electrocardiographically was thought to occur from direct myocardial compression. ST-segment elevations secondary to direct mass contact on the myocardium should be considered in patients who have a malignancy and ST-segment elevation.
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Mangus, Barry E., Luke Y. Shen, Stephen D. Helmer, Janae Maher, and R. Stephen Smith. "Taser and Taser Associated Injuries: A Case Series." American Surgeon 74, no. 9 (September 2008): 862–65. http://dx.doi.org/10.1177/000313480807400920.
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Taser devices were introduced in 1974 and are increasingly used by law enforcement agencies. Taser use theoretically reduces the risk of injury and death by decreasing the use of lethal force. We report a spectrum of injuries sustained by four patients subdued with Taser devices. Injuries identified in our review included: 1) a basilar skull fracture, right subarachnoid hemorrhage, and left-sided epidural hemorrhage necessitating craniotomy; 2) a concussion, facial laceration, comminuted nasal fracture, and orbital floor fracture; 3) penetration of the outer table and cortex of the cranium by a Taser probe with seizure-like activity reported by the officer when the Taser was activated; and 4) a forehead hematoma and laceration. The Taser operator's manual states that these devices are designed to incapacitate a target from a safe distance without causing death or permanent injury. However, individuals may be exposed to the potential for significant injury. These devices represent a new mechanism for potential injury. Trauma surgeons and law enforcement agencies should be aware of the potential danger of significant head injuries as a result of loss of neuromuscular control.
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Redecha, Patricia, Nico van Rooijen, Donald Torry, and Guillermina Girardi. "Pravastatin prevents miscarriages in mice: role of tissue factor in placental and fetal injury." Blood 113, no. 17 (April 23, 2009): 4101–9. http://dx.doi.org/10.1182/blood-2008-12-194258.
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Abstract Pregnancy loss and intrauterine growth restriction (IUGR) are serious pregnancy complications, and the triggers and mediators of placental and fetal damage are not completely understood. Using a mouse model of recurrent spontaneous miscarriages (DBA/2-mated CBA/J mice) that shares features with human recurrent miscarriage and fetal growth restriction, we identified tissue factor (TF) as an essential participating factor in placental and fetal injury. We have previously shown that C5a releases antiangiogenic molecule sFlt-1 in monocytes that causes defective placental development and fetal death in DBA/2-mated CBA/J mice. In this study, we found that TF not only activates the coagulation pathway, but it also mediates sFlt-1 release in monocytes causing defective placental development and fetal death. Blockade of TF with a monoclonal antibody inhibited sFlt-1 release, prevented the pathological activation of the coagulation pathway, restored placental blood flow, prevented placental oxidative stress, and rescued pregnancies. We also demonstrated that pravastatin, by down-regulating TF expression on monocytes and trophoblasts, prevented placental damage and protected pregnancies in DBA/2-mated CBA/J mice. These studies indicate that TF is an important mediator in fetal death and growth restriction and that statins may be a good treatment for women with recurrent miscarriages and IUGR.
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Ahmed-Bentley, Jasmine, A. Uma Chandran, A. Mark Joffe, Desiree French, Gisele Peirano, and Johann D. D. Pitout. "Gram-Negative Bacteria That Produce Carbapenemases Causing Death Attributed to Recent Foreign Hospitalization." Antimicrobial Agents and Chemotherapy 57, no. 7 (April 22, 2013): 3085–91. http://dx.doi.org/10.1128/aac.00297-13.
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ABSTRACTOverseas travel, as a risk factor for the acquisition of infections due to antimicrobial-resistant organisms, has recently been linked to carbapenemase-producing Gram-negative bacteria. MultiresistantKlebsiella pneumoniae,Escherichia coli, andAcinetobacter baumanniistrains were isolated from a wound of a Canadian patient with a recent history of hospitalization in India. This resulted in the initiation of outbreak management that included surveillance cultures. Epidemiological and molecular investigations showed that NDM-1-producingK. pneumoniaeST16 and OXA-23-producingA. baumanniiST10 strains were transmitted to 5 other patients, resulting in the colonization of 4 patients and the death of 1 patient due to septic shock caused by the OXA-23-producingA. baumanniistrain. The high rate of false positivity of the screening cultures resulted in additional workloads and increased costs for infection control and clinical laboratory work. We believe that this is the first report of an infection with carbapenemase-producing Gram-negative bacteria resulting in death attributed to a patient with recent foreign hospitalization. We recommend routine rectal and wound screening for colonization with multiresistant bacteria for patients who have recently been admitted to hospitals outside Canada.
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Held, Philip, Randy A. Boley, Niranjan S. Karnik, Mark H. Pollack, and Alyson K. Zalta. "Characteristics of veterans and military service members who endorse causing harm, injury, or death to others in the military." Psychological Trauma: Theory, Research, Practice, and Policy 10, no. 3 (May 2018): 352–59. http://dx.doi.org/10.1037/tra0000294.
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Kramer, Boris W., Susanne Kramer, Machiko Ikegami, and Alan H. Jobe. "Injury, inflammation, and remodeling in fetal sheep lung after intra-amniotic endotoxin." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 2 (August 1, 2002): L452—L459. http://dx.doi.org/10.1152/ajplung.00407.2001.
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Chorioamnionitis is frequent in preterm labor and increases the risk of bronchopulmonary dysplasia. We hypothesized that intra-amniotic endotoxin injures the lung in utero, causing a sequence of inflammation and tissue injury similar to that which occurs in the injured adult lung. Preterm lamb lungs at 125 days gestational age were evaluated for indicators of inflammation, injury, and repair 5 h, 24 h, 72 h, and 7 days after 4 mg of intra-amniotic endotoxin injection. At 5 h, the epithelial cells in large airways expressed heat shock protein 70, and alveolar interleukin-8 was increased. Surfactant protein B (SP-B) decreased in alveolar type II cells at 5 h, and SP-B in lung tissue and alveolar lavage fluid increased by 72 h. By 24 h, neutrophils were recruited into the large airways, and cell death was the highest. Alveolar type II cells decreased by 25% at 24 h, and proliferation was highest at 72 h, consistent with tissue remodeling. Intra-amniotic endotoxin caused surfactant secretion, inflammation, cell death, and remodeling as indications of lung injury. The recovery phase was accompanied by maturational changes in the fetal lung.
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Wang, Yaohui, Hailong Zhang, Zhizeng Wang, Yinxiang Wei, Mingli Wang, Meichen Liu, Xuance Wang, et al. "Blocking the death checkpoint protein TRAIL improves cardiac function after myocardial infarction in monkeys, pigs, and rats." Science Translational Medicine 12, no. 540 (April 22, 2020): eaaw3172. http://dx.doi.org/10.1126/scitranslmed.aaw3172.
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Myocardial infarction (MI) is a leading cause of death worldwide for which there is no cure. Although cardiac cell death is a well-recognized pathological mechanism of MI, therapeutic blockade of cell death to treat MI is not straightforward. Death receptor 5 (DR5) and its ligand TRAIL [tumor necrosis factor (TNF)–related apoptosis-inducing ligand] are up-regulated in MI, but their roles in pathological remodeling are unknown. Here, we report that blocking TRAIL with a soluble DR5 immunoglobulin fusion protein diminished MI by preventing cardiac cell death and inflammation in rats, pigs, and monkeys. Mechanistically, TRAIL induced the death of cardiomyocytes and recruited and activated leukocytes, directly and indirectly causing cardiac injury. Transcriptome profiling revealed increased expression of inflammatory cytokines in infarcted heart tissue, which was markedly reduced by TRAIL blockade. Together, our findings indicate that TRAIL mediates MI directly by targeting cardiomyocytes and indirectly by affecting myeloid cells, supporting TRAIL blockade as a potential therapeutic strategy for treating MI.
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Spencer, J. R., and Marie-Aimée Brajeux. "CRIMINAL LIABILITY FOR NEGLIGENCE—A LESSON FROM ACROSS THE CHANNEL?" International and Comparative Law Quarterly 59, no. 1 (January 2010): 1–24. http://dx.doi.org/10.1017/s0020589309990042.
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AbstractThis article first examines criminal liability for negligently causing death or injury in English law, which it shows to be both complex and confused. It then examines French law on the subject, which at first sight appears both simpler and more rational, but has run into a number of difficulties in practice. A third and final section considers whether the French experience provides any useful lessons for the possible reform of English law.
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Persson, H. Lennart, Tino Kurz, John W. Eaton, and Ulf T. Brunk. "Radiation-induced cell death: importance of lysosomal destabilization." Biochemical Journal 389, no. 3 (July 26, 2005): 877–84. http://dx.doi.org/10.1042/bj20050271.
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The mechanisms involved in radiation-induced cellular injury and death remain incompletely understood. In addition to the direct formation of highly reactive hydroxyl radicals (HO·) by radiolysis of water, oxidative stress events in the cytoplasm due to formation of H2O2 may also be important. Since the major pool of low-mass redox-active intracellular iron seems to reside within lysosomes, arising from the continuous intralysosomal autophagocytotic degradation of ferruginous materials, formation of H2O2 inside and outside these organelles may cause lysosomal labilization with release to the cytosol of lytic enzymes and low-mass iron. If of limited magnitude, such release may induce ‘reparative autophagocytosis’, causing additional accumulation of redox-active iron within the lysosomal compartment. We have used radio-resistant histiocytic lymphoma (J774) cells to assess the importance of intralysosomal iron and lysosomal rupture in radiation-induced cellular injury. We found that a 40 Gy radiation dose increased the ‘loose’ iron content of the (still viable) cells approx. 5-fold when assayed 24 h later. Cytochemical staining revealed that most redox-active iron was within the lysosomes. The increase of intralysosomal iron was associated with ‘reparative autophagocytosis’, and sensitized cells to lysosomal rupture and consequent apoptotic/necrotic death following a second, much lower dose of radiation (20 Gy) 24 h after the first one. A high-molecular-mass derivative of desferrioxamine, which specifically localizes intralysosomally following endocytic uptake, added to the culture medium before either the first or the second dose of radiation, stabilized lysosomes and largely prevented cell death. These observations may provide a biological rationale for fractionated radiation.
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Pate, Rajeshwar S., Rohan C. Hire, and Mohit V. Rojekar. "Pattern of head injury in central India population." International Journal of Research in Medical Sciences 5, no. 8 (July 26, 2017): 3515. http://dx.doi.org/10.18203/2320-6012.ijrms20173553.
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Background: In India, the developing economy and growing population simultaneously made a strong impact on increase in motor vehicle population. This increase in motorization has some adverse effects such as increase in road accidents with economic and functional loss. Head injury is the most common cause of mortality in road traffic accidents. The aim of this study was to know the incidence, pattern, mechanism, mode of head injury along with its distribution in relation to site of vault fracture and intracranial hemorrhage.Methods: Total 391 post-mortem cases of head injury were enrolled during study period. The information regarding age, sex, residence, marital status, date and time of time of accident and of death was gathered from police inquest report, relatives, dead body challan and clinical details from hospital records. During autopsy, detailed examination was carried out and data regarding both external and internal injuries were carefully recorded and analyzed.Results: The peak incidence of head injury was observed in the age group of 21-30 years. Most of deceased were from early age group and the male deceased were more than females. Majority victims of head injury were from road Traffic Accidents followed by fall from height, railway accidents and assault. Fissured fracture of vault was found in almost half cases. Subdural and subarachnoid hemorrhage were the most common one we encountered.Conclusions: Head injury due to RTA is well known public health problem causing death and disability. It is required from concerned government authority to take appropriate and immediate measures for reducing the incidence of head injury.
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Jones, Timothy H. "Causation, homicide and the supply of drugs." Legal Studies 26, no. 2 (June 2006): 139–54. http://dx.doi.org/10.1111/j.1748-121x.2006.00014.x.
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This paper examines the significance of the issue of causation where a death results from the supply of an illegal drug. The characterisation of the drug user’s conduct by means of a principle of voluntary intervention, as favoured in English and Welsh law, is questioned. The customary academic reliance upon the work of Hart and Honoré is doubted. The possibility of a new statutory offence of causing death by the supply of a controlled drug is considered.
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Brickler, Thomas, Kisha Gresham, Armand Meza, Sheryl Coutermarsh-Ott, Tere M. Williams, Daniel E. Rothschild, Irving C. Allen, and Michelle H. Theus. "Nonessential Role for the NLRP1 Inflammasome Complex in a Murine Model of Traumatic Brain Injury." Mediators of Inflammation 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/6373506.
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Traumatic brain injury (TBI) elicits the immediate production of proinflammatory cytokines which participate in regulating the immune response. While the mechanisms of adaptive immunity in secondary injury are well characterized, the role of the innate response is unclear. Recently, the NLR inflammasome has been shown to become activated following TBI, causing processing and release of interleukin-1β(IL-1β). The inflammasome is a multiprotein complex consisting of nucleotide-binding domain and leucine-rich repeat containing proteins (NLR), caspase-1, and apoptosis-associated speck-like protein (ASC). ASC is upregulated after TBI and is critical in coupling the proteins during complex formation resulting in IL-1βcleavage. To directly test whether inflammasome activation contributes to acute TBI-induced damage, we assessed IL-1β, IL-18, and IL-6 expression, contusion volume, hippocampal cell death, and motor behavior recovery inNlrp1−/−,Asc−/−, and wild type mice after moderate controlled cortical impact (CCI) injury. Although IL-1βexpression is significantly attenuated in the cortex ofNlrp1−/−andAsc−/−mice following CCI injury, no difference in motor recovery, cell death, or contusion volume is observed compared to wild type. These findings indicate that inflammasome activation does not significantly contribute to acute neural injury in the murine model of moderate CCI injury.
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Herold, Susanne, Christin Becker, Karen M. Ridge, and G. R. Scott Budinger. "Influenza virus-induced lung injury: pathogenesis and implications for treatment." European Respiratory Journal 45, no. 5 (March 18, 2015): 1463–78. http://dx.doi.org/10.1183/09031936.00186214.
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The influenza viruses are some of the most important human pathogens, causing substantial seasonal and pandemic morbidity and mortality. In humans, infection of the lower respiratory tract of can result in flooding of the alveolar compartment, development of acute respiratory distress syndrome and death from respiratory failure. Influenza-mediated damage of the airway, alveolar epithelium and alveolar endothelium results from a combination of: 1) intrinsic viral pathogenicity, attributable to its tropism for host airway and alveolar epithelial cells; and 2) a robust host innate immune response, which, while contributing to viral clearance, can worsen the severity of lung injury. In this review, we summarise the molecular events at the virus–host interface during influenza virus infection, highlighting some of the important cellular responses. We discuss immune-mediated viral clearance, the mechanisms promoting or perpetuating lung injury, lung regeneration after influenza-induced injury, and recent advances in influenza prevention and therapy.