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PubMed1977

Newcastle survey of deaths in early childhood 1974/76, with special reference to sudden unexpected deaths. Working party for early childhood deaths in Newcastle.

All early childhood deaths within a total population of 297 000 were studied by prospective methods. 70 deaths of children aged 1 week to 5 years occurred during a 27-month period; 36 died at home, 29 suddenly and unexpectedly. An extensive standardized necropsy showed a disease process clearly or probably related to death in half the sudden unexpected deaths; in the remainder no recognized disease process was identified. The events preceding sudden unexpected death, and the child's environment, were investigated by a controlled parental interview. Symptoms of serious illness within 24 hours of death were identified in 9 of the 29 children, but in the majority symptoms were thought to have been absent or no more severe than those of the control children. Most children with major symptoms had been seen by a doctor within a few days of death. The two most striking social findings were that 16 of the 29 sudden unexpected deaths occurred at a weekend or bank holiday, and that 45% occurred in three adjacent city wards which contain only 13% of the under-five study population. The additional support and explanation provided during the home visits was greatly appreciated by the bereaved families.

Age Factors↗
PubMed2005

A comparison of death certificate out-of-hospital coronary heart disease death with physician-adjudicated sudden cardiac death.

The number of deaths due to out-of-hospital coronary heart disease as determined by death certificates was compared with the number physician-adjudicated sudden cardiac deaths in the Framingham Heart Study from 1950 to 1999. Out-of-hospital coronary heart disease deaths overestimated sudden cardiac death by 47%, suggesting that out-of-hospital coronary heart disease death rates derived from death certificates should be interpreted with caution.

Aged↗
PubMed1998

"Brainstem death," "brain death" and death: a critical re-evaluation of the purported equivalence.

The author challenges brain-based diagnoses of death by re-examining the concept of death, its definition, the anatomical criterion, and the clinical signs or tests. Dr. Shewmon challenges the fundamental assumptions underlying brain death: (1) that the brain is the body's "critical system"; and (2) that the body even has a localized "critical system." He does not redefine death, but shifts the anatomical criterion from a single focus (the brain) to the entire body. The clinical tests correspondingly shift from those implying loss of brain function to those implying thermodynamically supracritical microstructural damage diffusely throughout the body. He concludes that the notion of "brain death" as bodily death is logically and physiologically incoherent, and that its replacement by something scientifically more credible would promote not only the sanctity of life, but ironically even transplantation as well.

Age Factors↗
PubMed1995

Sudden infant death syndrome in Sweden, 1983-1990: season at death, age at death, and maternal smoking.

Several risk factors for sudden infant death syndrome (SIDS) have been consistently reported, while results regarding seasonality and age at death of SIDS victims are conflicting. In the present population-based cohort study, single births in Sweden from 1983 through 1990 were used to estimate the relative and absolute risks for SIDS associated with season at death, age at death, and maternal smoking. In the winter period, 283 SIDS deaths occurred, while only 98 infants died during summer (winter/summer ratio = 2.9). Taking person-time at risk into account and restricting the analysis to infants aged 7-180 days, the authors determined the relative risk for SIDS to be 3.5 times higher in winter than in summer. When comparing incidence rate differences, they found a more noticeable seasonal variation for early SIDS (7-90 days at death) than for late SIDS (91-180 days at death). For early SIDS, the incidence rate was 0.6 cases per 100,000 person-days higher among smokers than among nonsmokers; for late SIDS, the corresponding difference was 0.3. The effect of smoking on SIDS was not associated with seasonality. Since exposure to passive smoking is likely to vary by season, the results suggest that the effect of smoking on SIDS is prenatal rather than the result of passive smoking after birth.

Adolescent↗
PubMed1975

Coronary atherosclerosis in cases of coronary death as compared with that occurring in the populatiom. A study of a medico-legal autopsy series of coronary deaths and violent deaths.

The severity of coronary atherosclerosis at autopsy was studied in two series comprising 169 cases of coronary death and 231 people who died of violent causes. In the former the fatal attack lasted less than 24 hours from the onset of symptoms in 70% of cases. In only three men did the terminal attack last more than 24 hours, while in the remaining 28% of cases, although death was not witnessed these were also likely to have been sudden deaths. A recent infarct with or without an old myocardial infarct was found at autopsy in 47% of cases and an old infarct alone in 34%. In 19% of coronary deaths no recent or old infarct was detected. The surface areas of the atherosclerotic lesions were assessed in arterial specimens by pointcounting. The degree of stenosis was estimated visually. The mean extent of raised lesions and clacification and the median value of stenosis score, which expressed the degree of stensosi in the coronary arterial tree, were significantly higher in all age groups in persons who died of coronary heart disease than in those who died violently. A marked overlapping between the individuals in the two series was, however, found in both for the exent of raised lesions and the severity of stenosis score. Raised lesions in coronary patients were calcified to about the same extent as those in persons ten years older in the series of violent deaths. Coronary atherosclerosis was most severe in coronary patients who had had symptomatic heart disease and had an old myocardial infarct and least severe in those in whome sudden death was the first manifestation of coronary heart disease from violent deaths as regards the extent of the raised lesions or prevalence of occlusion. The degree of coronary stenosis in coronary patients was closely related to the total extent of advanced coronary atherosclerosis.

Adult↗
PubMed1995

Induction of cell death by myristylated death domain of p55 TNF receptor is not abolished by Iprcg-like point mutation in death domain.

We transiently expressed the intracellular domains of p55 TNF receptor (TNFR1) as either a cytosolic- or a membrane-associated form and examined their effects on the endogenous receptor-mediated gene expression as well as on cell viability. We found that gene expression as measured by luciferase activity under NF-kappa B-controlling elements was blocked by all forms of the intracellular domain of TNFR1. The blockade of reporter gene expression was due to the cell death induced by the intracellular domain of TNFR1 per se. The killing mechanism of the intracellular domain peptides appeared to be apoptotic. Interestingly, myristylated form of the intracellular domain, consisting of mainly death domain showed the most potent cell-killing activity. Moreover, this myristylated death domain could still induce cell death even if lprcg-like point mutation (Leu351 to Ala), which has been reported to abrogate TNF-induced cytotoxicity, was introduced. This result suggests that the myristylated death domain activates an additional death signaling pathway which is not involved in TNF-induced cell death.

Apoptosis↗
PubMed1993

Sudden natural death in childhood. A review of forensic autopsy protocols in cases of sudden death between the ages of one and five years, 1982-1991, with a special view to sudden unexplained death.

All cases of sudden death of individuals between the ages of one and five years examined at the Forensic Institute, Copenhagen, in a 10-year period were identified to assess the impact of sudden unexplained death in this age group. Of a total of 68 cases, 27 cases were due to accidents, there were 13 cases of homicide, 27 cases were sudden natural deaths and in 1 case the manner of death was uncertain. The autopsy records and histological sections in the 27 cases of natural death were reviewed; the cause of death was not explained in 11 of these cases (40%). Seven cases were previously considered to be caused by infectious disease or aspiration. Criteria for classification are discussed.

Accidents↗
PubMed1999

[Sudden death (III). The causes of sudden death. Problems at the time of establishing and classifying the types of death].

Sudden cardiac death is one of the main causes of death in Western countries. Identification of possible causes and their intrinsic mechanisms, is directed to achieve a better risk stratification, which permits the obtention of a more effective primary and secondary prevention. In the last two decades, important advances in the field of arrhythmia treatment have been obtained, which could have an important impact on the incidence of sudden death in the highest risk groups. However, the low positive predictive value of the diagnostic tools available nowadays, as well as the high number of patients who have sudden death as the first initial symptom of their disease, represent an important limitation for the primary prevention on the whole of the general population. In this article we review different diseases associated with sudden death, with special focus on the subgroup of patients with higher risk within each disease group, as well as the problems in establishing an accurate definition of sudden death.

Cause of Death↗
PubMed1998

Are elevated cerebrospinal fluid levels of IL-6 in sudden unexplained deaths, infectious deaths and deaths due to heart/lung disease in infants and children due to hypoxia?

Many SIDS cases probably die after periods of hypoxia and it has been shown that hypoxia may stimulate IL-6 production. The purpose of this paper was to examine if there were any correlations between hypoxanthine in vitreous humour and IL-6 in CSF. The concentration of IL-6, IL-1beta and TNFalpha in cerebrospinal fluid of 50 Sudden Infant Death syndrome (SIDS) cases, 9 borderline SIDS cases, 18 infectious deaths, 8 violent deaths and 22 cases with heart/lung disease were measured by ELISA. The hypoxanthine (Hx) vitreous humour concentrations in the same groups were determined by high performance liquid chromatography. The IL-6 levels in cases of infectious death, heart/lung disease and borderline cases were significantly higher than in the SIDS cases (p < 0.01). The Hx levels were in the same range in cases of SIDS, borderline SIDS and infectious death, and they were significantly higher than the levels in cases of violent death and heart/lung disease (p < 0.01). There was no correlation between hypoxanthine and IL-6 in any of the groups. In the cases studied IL-6 elevation is probably not induced by hypoxia, but is rather a result of immunological stimulation.

Biomarkers↗
PubMed2006

Purkinje cell death: differences between developmental cell death and neurodegenerative death in mutant mice.

This review is devoted to Purkinje cell death occurring during development and in spontaneous cerebellar mutations of the mouse. We first present evidence in favor of an apoptotic developmental Purkinje cell death. Then, the different types of Purkinje cell degeneration occurring in mutant mice primarily affecting this neuronal population (nervous, purkinje cell degeneration, Lurcher, toppler, and woozy) are described and discussed. In addition, we show, by reporting new data, that cell death in tambaleante mutant mice can be related to autophagy. Last, we discuss the fact that the cell death pathways in mutant mice are more complex than the three types of developmental death generally described (apoptosis, autophagy, necrosis), since they share often characteristics of more than one type of these developmental cell deaths, particularly autophagy and apoptosis.

Animals↗
PubMed1987

High death rates: more deaths or earlier deaths?

In the analysis of mortality statistics high age-specific death rates could be interpreted as meaning more deaths (more disease), but they could equally well be interpreted as meaning earlier deaths (death at younger age). The distinction markedly affects the choice of hypotheses that may be advanced to explain variations in person, time and place and the design of subsequent, more detailed field studies to test the hypotheses. Furthermore, the majority of descriptive papers make no comparisons with a control disease and thereby break one of the ground rules of epidemiology. This paper shows how, in the example of the geographical variations within England and Wales of ischaemic heart disease, a control may be simply introduced and that much of the observed variation is not in the proportion who suffer heart disease deaths but is in the age at which deaths occur.

Adult↗
PubMed2002

Death effector domain-only polypeptides of caspase-8 and -10 specifically inhibit death receptor-induced cell death.

Caspase-8 and -10 are thought to be involved in a signaling pathway leading to death receptor-mediated apoptosis. The prodomains of these caspases are known to form fibrous structures in the perinuclear region when overexpressed, though the meaning of the structures remains unclear. In a previous study we showed that the overexpressed caspase-8 or -10 prodomain (PDCasp8 or PDCasp10) did not induce cell death, and we hypothesized that these prodomains interfere with the receptor-mediated cell death signaling pathway. Indeed, in 293, HeLa and Jurkat cells, cell death mediated by agonistic anti-Fas antibody, TRAIL or overexpression of full-length caspase-8 was significantly inhibited by overexpression of PDCasp8 or PDCasp10 which colocalized with the Golgi complex and with overexpressed FADD. However, when about 20 amino acid residues were deleted from either terminus of the caspase-10 prodomain (amino acid residue 1 to 219), the ability to inhibit Fas-mediated cell death was lost. Interestingly, these deletion mutants also lost the ability to make fibrous structures and to bind FADD, suggesting that FADD binding is important for their function, and that PDCasp8 and PDCasp10 act as dominant-negative inhibitors.

Adaptor Proteins, Signal Transducing↗
PubMed2001

alpha-Toxin is a mediator of Staphylococcus aureus-induced cell death and activates caspases via the intrinsic death pathway independently of death receptor signaling.

Infections with Staphylococcus aureus, a common inducer of septic and toxic shock, often result in tissue damage and death of various cell types. Although S. aureus was suggested to induce apoptosis, the underlying signal transduction pathways remained elusive. We show that caspase activation and DNA fragmentation were induced not only when Jurkat T cells were infected with intact bacteria, but also after treatment with supernatants of various S. aureus strains. We also demonstrate that S. aureus-induced cell death and caspase activation were mediated by alpha-toxin, a major cytotoxin of S. aureus, since both events were abrogated by two different anti-alpha-toxin antibodies and could not be induced with supernatants of an alpha-toxin-deficient S. aureus strain. Furthermore, alpha-toxin-induced caspase activation in CD95-resistant Jurkat sublines lacking CD95, Fas-activated death domain, or caspase-8 but not in cells stably expressing the antiapoptotic protein Bcl-2. Together with our finding that alpha-toxin induces cytochrome c release in intact cells and, interestingly, also from isolated mitochondria in a Bcl-2-controlled manner, our results demonstrate that S. aureus alpha-toxin triggers caspase activation via the intrinsic death pathway independently of death receptors. Hence, our findings clearly define a signaling pathway used in S. aureus-induced cytotoxicity and may provide a molecular rationale for future therapeutic interventions in bacterial infections.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Photoreceptor death: spatiotemporal patterns arising from one-hit death kinetics and a diffusible cell death factor.

Retinitis pigmentosa (RP) is an inherited disease affecting approximately 1:4000 individuals in North America. It is characterized clinically by the gradual apoptotic death of photoreceptor cells that occurs nonuniformly across the surface of the retina. Recently, it has been demonstrated that the time of death of many individual photoreceptors is random, a fact that must be reconciled with the spatiotemporal patterns of photoreceptor degeneration that are observed in patients with RP. One possible explanation is that a diffusible toxic factor is released by dying photoreceptors and induces adjacent cells to likewise undergo apoptosis. To determine if such a mechanism can result in patchy distributions of photoreceptor death, as frequently observed in RP patients, we studied cell attrition produced by a bistable biochemical switch in an idealized one-dimensional retina. We found that with a reasonable choice of parameter values, our model was able to produce patterns of cell death resembling those observed in RP. In the context of this model, patches on the order of histologically observable size could develop from a single release event, but their rates of formation were independent of the concentration of toxic factor released. Instead, factor concentration affected the overall rate of cell death, the number of degenerating patches, and their distribution across the retina.

Apoptosis↗