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PubMed2005

Predictors of operative death after oesophagectomy for carcinoma.

BACKGROUND: Oesophagectomy for carcinoma provides a chance of cure but carries significant risk. This study defined risk factors for death after oesophageal resection for malignant disease. METHODS: Between 1990 and 2003, 773 oesophagectomies for oesophageal cancer were performed. Continuous variables were categorized into quartiles for analysis. Predictors of operative mortality were identified by univariate and multiple logistic regression analysis. RESULTS: The operative mortality rate was 4.8 per cent (37 of 773). In univariate analysis, advanced age, reduced forced expiratory volume in 1 s (FEV1), reduced forced vital capacity, presence of diabetes and tumour located in the upper third of the oesophagus were associated with a higher mortality rate. Multivariate analysis identified age (highest relative to lowest quartile, odds ratio (OR) 4.87 (95 per cent confidence interval (c.i.) 1.35 to 17.55); P = 0.009), tumour position (upper third relative to other locations, OR 4.23 (95 per cent c.i. 1.06 to 16.86); P = 0.041) and FEV1 (lowest relative to highest quartile, OR 4.72 (95 per cent c.i. 1.01 to 21.99); P = 0.018) as independent predictors of death. CONCLUSION: Advanced age, impaired preoperative respiratory function and a tumour high in the oesophagus are associated with a significantly increased risk of death after oesophagectomy for carcinoma.

Adult↗

PubMed2005

C-terminal region of Bfl-1 induces cell death that accompanies caspase activation when fused with GFP.

Previously, we reported that anti-apoptotic Bfl-1 is converted to a pro-apoptotic protein following fusion at its N-terminus with green fluorescent protein (GFP) (GFP-Bfl-1). In this study, we performed a Bfl-1 deletion study in order to elucidate the underlying mechanism of GFP-Bfl-1-induced cell death. We found that the Bcl-2 homology (BH) domains in Bfl-1 are dispensable with respect to cell death and that GFP fusion with the 29 amino acids of the C-terminal region of Bfl-1 (GFP-BC) is sufficient to induce cell death. Moreover, when BC was fused with other tagging partners like GST or MBP, little cell death was observed, implying that the GFP region is as important as the BC region for GFP-BC-induced cell death. Further deletion analysis defined a region of GFP as a determinant of GFP-BC-induced cell death. Confocal microscopic analysis showed that GFP-chimeras containing the BC region of Bfl-1 are located mainly in mitochondria. The GFP-BC-induced cell death accompanied cellular caspase activation, and treatment with the pan-caspase inhibitor, Boc-D-FMK, partially inhibited GFP-BC-induced cell death. However, the over-expression of anti-apoptotic molecules, such as Bcl-x(L) and CrmA, did not block GFP-BC-induced cell death. In summary, GFP-BC induces cell death with caspase activation through mitochondria dependent process.

Apoptosis↗

PubMed1999

Modes of L929 cell death induced by TNF-alpha and other cytotoxic agents.

Recent studies have variably reported that tumour necrosis factor alpha (TNF-alpha) induces either necrosis or apoptosis in L929 cells. This study was undertaken to better characterize the mode of death induced in L929 cells by this agent. We determined the effects of exposure to TNF-alpha and other cytotoxic agents on cell size and morphology, cell membrane permeability, exposure of phosphatidylserine at the cell surface, nuclear morphology and fragmentation of DNA. Our results suggest that L929 cells treated with TNF-alpha alone show nuclear changes and a pattern of DNA fragmentation that are atypical of apoptosis. In contrast, our results demonstrate that, when augmented with actinomycin D, TNF-alpha induces classical apoptosis in L929 cells. We also provide the first report that, in L929 cells, staurosporine induces classical apoptosis and colchicine induces a form of apoptosis lacking internucleosomal DNA fragmentation. Previous studies of TNF-alpha-induced death in L929 cells relied on measurements of only one or two parameters to define the mode of death. Overall, our results suggest that in future cellular or biochemical studies of the effects of TNF-alpha on L929 cells it will be prudent to characterize the mode of death in each case using a multi-parameter approach, as done here.

Animals↗

PubMed2002

Comparative biology and pathology of oxidative stress in Alzheimer and other neurodegenerative diseases: beyond damage and response.

In this review, we consider comparative aspects of the biology and pathology of oxygen radicals in neurodegenerative disease and how these findings have influenced our concept of oxidative stress. The common definition of oxidative stress is a breach of antioxidant defenses by oxygen radicals leading to damage to critical molecules and disrupted physiology. Inherent in this definition is that oxidative stress is an unstable situation, for if there is net damage, viability of the system decreases with time, leading to disequilibria and death. While this circumstance defines acute conditions, such as stroke and head trauma which result in dysfunction and death, it does not fit physiological situations or chronic diseases closely aligned to normal physiology. Therefore, we propose that oxidative modifications in Alzheimer disease may actually serve as a homeostatic response to stress resulting in a shift of neuronal priority from normal function to basic survival. This phenomenon is comparable to normal physiological conditions of metabolic decrease, such as those seen in hibernation and estivation. Thus, Alzheimer disease could be seen as part of normal aging that includes additional pathology due to inadequate homeostatic response.

Alzheimer Disease↗

PubMed2002

Secretory phospholipase A2-mediated neuronal cell death involves glutamate ionotropic receptors.

To define the significance of glutamate ionotropic receptors in sPLA -mediated neuronal cell death we used the NMDA receptor antagonist MK-801 and the AMPA receptor antagonist PNQX. In primary neuronal cell cultures both MK-801 and PNQX inhibited sPLA - and glutamate-induced neuronal death. [ H]Arachidonic acid release induced by both sPLA and glutamate was partially blocked by MK-801, indicating that the glutamate-NMDA-cPLA pathway contributes to sPLA -induced arachidonic acid release. Systemic administration of MK-801 to rats that had sPLA injected into the right striatum significantly decreased neuronal cell death. We conclude that glutamatergic synaptic activity modulates sPLA -induced neuronal cell death.

Animals↗

PubMed2000

Early morphologic alterations in trophically deprived neuronal death in vitro occur without alterations in cytoplasmic Ca(2+).

Morphologic and functional parameters altered during neuronal death were investigated in chick ciliary ganglion (CG) neurons in vitro isolated from embryonic day 8 (E8, stage 34). Neurons were separated from nonneuronal cells to investigate their inherent cell death program and were cultured with or without trophic support (choroid, iris, pigment epithelium) from their appropriate target tissue. The cell death process was characterized with investigations focused on the earliest events at the onset of commitment to cell death at 11 hours after plating. Initial morphologic changes in the process of cell death were cytoplasmic; swelling, dendritic retraction, blebbing, vacuolization, which are all characteristics of necrosis. Later, nuclear chromatin condensation occurred, a characteristic of apoptosis. An increase in membrane permeability was measured earlier at 8 hours. During these alterations (associated with the initiation of cell death) single cell analysis was performed to evaluate mobile Ca(2+) changes in the same trophically deprived neurons during the course of the death process; Ca(2+) levels remained at 50 nM. Transient Ca(2+) entry was buffered in control and deprived cells at 13 hours but with different parameters. During the execution stage of death mobile Ca(2+) levels were variable. In this final stage of cell death, neurons demonstrated nuclear damage, cytosol disintegration, or morphology sharing both characteristics. These observations define embryonic CG cell death in vitro as neither purely apoptotic nor necrotic but a form of that exhibits features of both. These results also demonstrate a disassociation of changes in cytosolic Ca(2+) from both CG neuronal survival and trophically deprived cell death in vitro.

Animals↗

PubMed2000

Setting priorities for waiting lists: defining our terms. Steering Committee of the Western Canada Waiting List Project.

In order to develop standardized measures to assess patients' relative priority for services for which there are waiting lists, it is essential that key terms be clearly defined. We propose that severity be defined as the degree or extent of suffering, limits to activities or risk of death; that urgency be defined as severity combined with considerations of the expected benefit and the natural history of the condition; that need be considered equivalent to urgency; and that priority be defined in terms of urgency (or need) with or without consideration of social factors.

Disease Progression↗

PubMed2002

A good death: a qualitative study of patients with advanced AIDS.

The objective of this study was to identify and describe the domains that define a "good" versus "bad" death from the perspective of patients with advanced AIDS. We analyzed qualitative data from face-to-face interviews with 35 patients with C3 AIDS. An experienced research interviewer asked the patients to describe a good and bad death. Investigators used the principles of grounded theory to analyze the interview transcripts and identify the major domains defining a "good" versus a "bad" death. We identified 15 domains, of which 12 were mentioned by at least two participants. The 12 domains include: symptoms, quality of life, people present, dying process, location, a sense of resolution, patient control of treatment, issues of spirituality, death scene, physician-assisted suicide, aspects of medical care, and acceptance of death. Within these, we identified 38 sub-categories representing specific aspects of the domains that shape a "good" versus "bad" death for the patients in this study. The identified 12 major domains encompass the major determinants of a "good" versus "bad" death from the perspective of patients with advanced AIDS. A better understanding of these domains may enable clinicians to more fully appreciate the experiences of their dying patients and identify ways to improve the care they provide at the end of life.

Acquired Immunodeficiency Syndrome↗

PubMed1996

Mode of death in chronic heart failure. A request and proposition for more accurate classification.

The proportion of patients reported to die suddenly or from progressive circulatory failure is not consistent among studies of heart failure. Lack of an adequate or consistent classification of how patients die contributes to the current confusion over the mode of death in heart failure. Defining how patients with heart failure die could be important in developing strategies to reduce the continuing high mortality associated with this condition. We identified 27 studies that reported 50 or more deaths among patients with heart failure to ascertain how death was classified. Definitions of sudden death appeared heterogeneous and the majority of studies failed to publish or make reference to how circulatory failure was defined. A framework for the classification of the mode of death has been developed in which clear separation of the activity and place at the time of death, cause of death, mode of death, and events prior to death is made (ACME: Activity, Cause, Mode and Event). This mode of classifying death has been successfully piloted in two mortality studies; AIRE and NETWORK. Classifying mortality in this way will help identify pathways leading to death and hence suggest therapies and strategies to reduce mortality in patients with heart failure, a group of patients whose prognosis remains poor.

Adult↗

PubMed1998

The hypersensitive response. A programmed cell death associated with plant resistance.

In plants, the hypersensitive response (HR) is defined as a rapid cell death occurring in response to pathogen attack, and is closely related to active resistance. Initiation of the HR process begins with the recognition of the pathogen by the plant, which is mediated mainly by the pathogen avirulence genes and the plant resistance genes. Then, complex signal transduction pathways intervene, involving changes in protein phosphorylation, production of reactive oxygen species and modification of ion fluxes. Components required for the regulation of the HR cell death are now being identified genetically by the isolation of mutants, in contrast to those involved in the execution of the cell death programme, which are still largely unknown. Further genetic and biochemical analyses will undoubtedly answer the question as to whether this form of programmed cell death (PCD) can be compared with other forms of PCD in plants and with apoptosis in animals.

Apoptosis↗

PubMed1985

Ischaemic heart disease and prodromes of sudden cardiac death. Is it possible to identify high risk groups for sudden cardiac death?

A study was carried out to determine the incidence of sudden cardiac death in a well defined population in relation to prodromes, medical history, and previous medical consultations before sudden cardiac death. In Frederiksborg county, Denmark (population 332 000), of 1309 consecutive deaths in a six month period, 166 were due to sudden cardiac death; among men aged 50-69, 22% of all deaths were due to sudden cardiac death. The incidence per 1000 population per year by age group (less than 50, 50-69, greater than or equal to 70 years) was 0.19, 3.6, 11.4 in men and 0.12, 1.0, and 6.4 in women. The increasing incidence with age was significant. Ischaemic heart disease or hypertension had been recorded in 75% (124/166) of patients. Prodromes were reported in 54% (38/71) of patients with angina, and in 26% (25/95) without. Nineteen per cent (32/166) had neither prodromes nor overt heart disease. Forty six per cent of patients with known ischaemic heart disease and 24% without had consulted a doctor less than four weeks before death. Eight per cent had had a myocardial infarction within a year of death.

Adult↗

PubMedDate not supplied

[Populational study of investigation of perinatal and infant deaths: methodology, validity of diagnosis and under-registration].

OBJECTIVE: The main objectives of the present study were to evaluate the percentage of under-registration of infant mortality in 1993 and compare it with the ones found 1982; to analyze the agreement between the official death certificates and the ones made by the referees. METHODS: The infant mortality of all children born in Pelotas, in 1993, was monitored through daily visits to hospitals, as it was done in 1982; monthly, cemeteries and public registration offices were visited to detect any deaths outside the hospitals. Besides the official death certificates, two independent referees established the underlying cause of death based on information from pediatricians, case-notes, autopsies and through a home visit to the parents of the children. RESULTS: The percentage of under-registration fell substantially from 24%, in 1982, to 5.4%, in 1993. The agreement between the official death certificates and the ones made by the referees showed satisfactory Kappas, unless for ill defined diseases such as sudden infant death, where the agreement was null. CONCLUSIONS: The authors conclude that there was a significant fell of the under-registration for infant death in Pelotas, and the ill defined causes such as sudden infant death have been hidden by the diagnosis of pneumonia.

English Abstract↗

PubMed2005

Impact of newly available drugs on clinical progression in patients with virological failure after exposure to three classes of antiretrovirals.

OBJECTIVE: To study the prognosis of HIV-infected patients with virological failure after exposure to three classes of antiretroviral drugs (ARVs). DESIGN: Cohort study. SETTING: French Hospital Database on HIV. PATIENTS: Patients previously exposed to at least two nucleoside reverse transcriptase inhibitors (NRTIs), two protease inhibitors and one non-NRTI, with viral load (/L) values of > 5000 copies/ml after the exposure criteria were met and a new treatment initiated between 1998 and 2001 with VL > 5000 copies/ml. MAIN OUTCOME MEASURES: Risk of new AIDS-defining-events (ADEs) or death from first introduction of a drug never used before occurring between 1998 and 2001 defined as baseline. RESULTS: The main baseline characteristics of the 1092 patients were: previous ADE in 49% of cases, median CD4 cell count 181 microl, median VL 4.9 log10 copies/ml, median duration of ARV therapy 5.0 years and previous exposure to a median of nine ARVs. The crude progression rates were 20.1/100 patient-years among patients included in 1998, 15.1 in 1999, 11.1 in 2000 and 8.6 in 2001. After adjustment for baseline characteristics, the calendar year of inclusion was associated with the risk of clinical progression (P < 0.001). When the types of newly available drugs used at baseline or during follow-up were introduced into the model, year of inclusion was no longer associated with the risk of clinical progression (P = 0.42), while exposure to amprenavir/r, lopinavir/r, abacavir or tenofovir was associated with a lower risk. CONCLUSIONS: The clinical prognosis of heavily pretreated patients experiencing virological failure improved between 1998 and 2001, mainly thanks to the use of newly available drugs with more favourable resistance profiles.

Adult↗

PubMed2002

Adverse events and complications among patients admitted to hospital in the home directly from the emergency department.

INTRODUCTION: The nature and incidence of adverse events and complications among patients admitted from the emergency department to hospital in the home has not been investigated. This study aimed to investigate this problem and make recommendations for prevention strategies. METHODS: This was an explicit retrospective chart review of patients admitted from the emergency department directly to hospital in the home between 22 February 1995 and 1 September 2000. A data extraction document was designed specifically for the study and used to extract data relating to patient demographics, diagnosis, past medical history and outcome. The outcomes of interest include adverse events, complications and death. An adverse effect is defined as an unintended injury or complication that results in disability, death or prolonged hospital stay and is caused by health care management. These adverse events may occur prior to or during the index admission and may be noted during or after the index admission. A complication is defined as an undesirable outcome that occurs during the management but not causing disability, death or prolonged hospital stay. RESULTS: Three hundred and fifty-seven patients were enrolled (51.3% male; median age 52 years, range 16-96 years). Fifty-five adverse events were identified: 49 adverse events (89%) were due to management prior to hospital in the home admission and six adverse events (10.9%) were directly attributable to hospital in the home management. This represents a rate of 1.7 adverse events per 100 hospital in the home admissions directly attributable to hospital in the home management. One hundred and eighteen complications were identified. Most complications were easily managed. Thirty-one patients had unplanned re-admissions and two patients died within 28 days of hospital in the home admission. CONCLUSION: Most patients admitted to hospital in the home from the emergency department were managed successfully. Few adverse events arose from hospital in the home treatment. Complications were common but minor in nature. Strategies for the prevention of phlebitis and constipation are recommended.

Adolescent↗

PubMed2005

Myofiberbreak-up: a marker of ventricular fibrillation in sudden cardiac death.

BACKGROUND: Electrophysiologically, ventricular fibrillation is defined as a "chaotic, random, asynchronous electrical activity of the ventricles due to repetitive re-entrant excitation and/or rapid focal discharge". To this point its morphological equivalent has not been defined. MATERIAL AND METHOD: Several groups of different diseases and types of accidental death in normal subjects were studied. A complete autopsy was performed and the hearts were examined in 432 cases. A total of 16 myocardial samples per heart were processed for histological examination and sections were stained by haematoxylin and eosin or by specific stains. The frequency, location and extent of myocellular segmentation (stretching and/or rupture) of intercalated discs and associated changes of myocardial bundles and single myocells were investigated. A quantitative analysis was performed and the data were processed for statistical evaluation. RESULTS: The frequency of MFB was maximal in coronary (88%) and Chagas (76%) groups followed by the intracranial brain haemorrhage group (52%). The extent of myofiberbreak-up was maximal in coronary/Chagas groups followed by intracranial haemorrhage and transplant groups. CONCLUSIONS: No correlation was seen between gender, age, heart weight, degree of coronary atherosclerosis, myocardial fibrosis, survival and MFB. If our postulate is correct, finding MFB in the myocardium might allow the diagnosis of a malignant arrhythmia followed by cardiac arrest due to ventricular fibrillation even in the absence of clinical information (sudden death out-of-hospital).

Adult↗

PubMed2006

Fetal growth risk curves: defining levels of fetal growth restriction by neonatal death risk.

OBJECTIVE: We developed a fetal growth risk curve that delineates the birth weight values for gestational age that reflect a 2-, 2.5-, and 3-fold neonatal death risk relative to infants with normal fetal growth. STUDY DESIGN: We analyzed 18,085,052 single gestation infants (25-42 weeks) who were born to US resident mothers from 1996 to 2000. Multivariate models were used to predict the relationship between neonatal death and birth weight percentile. Fetal risk curves were derived on the basis of birth weight percentile-specific neonatal mortality rates that were relative to an average rate of neonatal death for a comparison group that was representative of typical growth (ie, infants between 45th-55th birth weight percentiles for gestational age). RESULTS: The 10th percentile of birth weight for gestational age is associated with an increased but variable risk of neonatal death relative to the comparison group across the spectrum of gestational ages. At 26 weeks of gestation, infants at the 10th percentile experienced a 3-fold risk of dying within the first 28 days of life (relative to the comparison group); whereas at 40 weeks, the risk was 1.13. CONCLUSION: Fetal growth risk curves facilitate the identification of populations of infants whose risk of death are deemed excessive compared with that of infants at the norm of fetal growth and may be useful for counseling pregnant women.

Birth Weight↗

PubMed2006

Naive regulatory T cells: a novel subpopulation defined by resistance toward CD95L-mediated cell death.

Most CD4(+)CD25(hi)FOXP3(+) regulatory T cells (T(regs)) from adult peripheral blood express high levels of CD45RO and CD95 and are prone to CD95L-mediated apoptosis in contrast to conventional T cells (T(convs)). However, a T(reg) subpopulation remained consistently apoptosis resistant. Gene microarray and 6-color flow cytometry analysis including FOXP3 revealed an increase in naive T-cell markers on the CD95L-resistant T(regs) compared with most T(regs). In contrast to T(regs) found in adult humans, most CD4(+)CD25(+)FOXP3(+) T cells found in cord blood are naive and exhibit low CD95 expression. Furthermore, most of these newborn T(regs) are not sensitive toward CD95L similar to naive T(regs) from adult individuals. After short stimulation with anti-CD3/CD28 monoclonal antibodies (mAbs), cord blood T(regs) strongly up-regulated CD95 and were sensitized toward CD95L. This functional change was paralleled by a rapid up-regulation of memory T-cell markers on cord blood T(regs) that are frequently found on adult memory T(regs). In summary, we show a clear functional difference between naive and memory T(regs) that could result in different survival rates of those 2 cell populations in vivo. This new observation could be crucial for the planning of therapeutic application of T(regs).

Apoptosis↗

PubMed2000

When does a worker's death become murder?

During the past 2 decades, a growing number of manslaughter and even murder charges have been brought against employers in cases involving the death of workers on the job. In this commentary, the author reviews some of these recent cases and looks at other periods in American history when workers' deaths were considered a form of homicide. He examines the social forces that shape how we define a worker's death: as an accidental, chance occurrence for which no individual is responsible, or as a predictable result of gross indifference to human life for which management bears criminal responsibility. He asks whether there is a parallel between the conditions of 19th-century laissez-faire capitalism that led to popular movements promoting workplace safety and the move in recent decades toward deregulation and fewer restraints on industry that has led state and local prosecutors to criminalize some workplace accidents. Despite an increased federal presence, the activities of state and local district attorneys perhaps signal a redefinition of the popular understanding of employers' responsibility in maintaining a safe workplace.

Accidents, Occupational↗