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PubMed2005

Beyond apoptosis: nonapoptotic cell death in physiology and disease.

Apoptosis is a morphologically defined form of programmed cell death (PCD) that is mediated by the activation of members of the caspase family. Analysis of death-receptor signaling in lymphocytes has revealed that caspase-dependent signaling pathways are also linked to cell death by nonapoptotic mechanisms, indicating that apoptosis is not the only form of PCD. Under physiological and pathological conditions, cells demonstrate a high degree of flexibility in cell-death responses, as is reflected in the existence of a variety of mechanisms, including necrosis-like PCD, autophagy (or type II PCD), and accidental necrosis. In this review, we discuss recent data suggesting that canonical apoptotic pathways, including death-receptor signaling, control caspase-dependent and -independent cell-death pathways.

Animals↗

PubMed1990

Diagnostic open-lung biopsy after bone marrow transplantation.

The development of pulmonary infiltrates is an ominous sign in the immunocompromised host (ICH). Selection of the best diagnostic and therapeutic approach is often difficult, and in part depends on the risk-to-benefit ratio of various diagnostic modalities, such as bronchoscopy, bronchioalveolar lavage, percutaneous needle biopsy, and open-lung biopsy (OLB). We reviewed our experience with OLB and bronchoscopy in a predominantly pediatric bone marrow transplantation population, and attempted to assess the frequency with which OLB results directed a therapeutic change, as well as the clinical results of any such therapeutic alteration. A retrospective chart review was conducted of 87 bone marrow transplantation recipients undergoing diagnostic OLB from 1975 to 1986. Bronchoscopic and OLB cultures, histopathologic studies, serological data, and autopsy results were all carefully examined. An assessment of therapeutic alteration as a result of OLB was made, and clinical changes attributable to an OLB-directed therapeutic alteration were sought. Ninety-four OLBs and 37 bronchoscopic examinations were performed in 87 patients. All patients had undergone bone marrow transplantation, most often for leukemia (58/87) or aplastic anemia (13/87). The mean interval from bone marrow transplantation to OLB was 106 days. There were no intraoperative complications, but minor postoperative surgical complications were frequent (incidence, 21%). Postoperative mortality, defined as a death occurring within 30 days of surgery, was 45% (39/87). Seventy-four percent of the patients (64/87) died during the course of the study, at a mean of 43 days after OLB. Most OLBs (60%) yielded a specific diagnosis, defined as the establishment of a precise cause for the infiltrate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1998

Intensive care, old age, and the problem of death in America.

This article, part of a larger anthropological investigation of how death occurs in the hospital, explores the relationship of elderly deaths in the intensive care unit to the cultural conversation about the desire for "death with dignity." Based on participant observation, it provides three case studies that focus on the unfolding of events surrounding patient treatment, decision making, and family involvement. The cases are interpreted in the context of four sources of the culturally defined "problem" of death: (a) how medicine operates as the dominant conceptual framework for understanding both old age and death; (b) the power of the technological imperative to determine events; (c) ambivalence regarding end-of-life goals; and (d) the incommensurability of lay and medical knowledge.

Aged↗

PubMed2003

Ceramide and glutathione define two independently regulated pathways of cell death initiated by p53 in Molt-4 leukaemia cells.

The tumour suppressor p53 induces cell death by launching several pathways that are either dependent on or independent of gene transcription. Accumulation of the sphingolipid ceramide and reactive oxygen species are among these pathways. Crossregulation of these two pathways is possible owing to the demonstrated inhibition of neutral sphingomyelinase by glutathione, the predominant cellular antioxidant, and has been observed in some cytokine-dependent cell-death models. In a model of irradiation-induced cell death of Molt-4 leukaemia cells, it was found that ceramide accumulation and glutathione depletion were dependent on p53 up-regulation. The loss of p53 owing to expression of the papilloma virus E6 protein inhibited both pathways after irradiation. However, in this model, these two pathways appeared to be independently regulated on the basis of the following observations: (1) glutathione supplementation or depletion did not alter irradiation-induced ceramide accumulation, (2) exogenous ceramide treatment did not induce glutathione depletion, (3) glutathione depletion was dependent on new protein synthesis, whereas ceramide accumulation was independent of it and (4) caspase activation was required for ceramide accumulation but not for glutathione depletion. Furthermore, caspase 9 activation, which is dependent on the release of mitochondrial cytochrome c, was not required for ceramide accumulation. This suggested that a caspase, other than caspase 9, was necessary for ceramide accumulation. Interestingly, Bcl-2 expression inhibited these pathways, indicating a possible role for mitochondria in regulating both pathways. These findings indicate that these two pathways exhibit cross-regulation in cytokine-dependent, but not in p53-dependent, cell-death models.

Apoptosis↗

PubMed2001

Caspase-3 gene knockout defines cell lineage specificity for programmed cell death signaling in the ovary.

Previous studies have proposed the involvement of caspase-3, a downstream executioner enzyme common to many paradigms of programmed cell death (PCD), in mediating the apoptosis of both germ and somatic cells in the ovary. Herein we used caspase-3 gene knockout mice to directly test for the functional requirement of this protease in oocyte and/or granulosa cell demise. Using both in vivo and in vitro approaches, we determined that oocyte death initiated as a result of either developmental cues or pathological insults was unaffected by the absence of caspase-3. However, granulosa cells of degenerating antral follicles in both mouse and human ovaries showed a strong immunoreaction using an antibody raised against the cleaved (activated) form of caspase-3. Furthermore, caspase-3 mutant female mice possessed aberrant atretic follicles containing granulosa cells that failed to be eliminated by apoptosis, as confirmed by TUNEL (terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling) analysis of DNA cleavage and 4',6-diamidino-2-phenylindole staining of nuclear morphology (pyknosis). These in vivo results were supported by findings from in vitro cultures of wild-type and caspase-3-deficient antral follicles or isolated granulosa cells. Contrasting the serum starvation-induced occurrence of apoptosis in wild-type granulosa cells, caspase-3-null granulosa cells deprived of hormonal support were TUNEL-negative, showed attenuated chromatin condensation by 4',6-diamidino-2-phenylindole staining and exhibited delayed internucleosomal DNA cleavage. Such ex vivo findings underscore the existence of a cell autonomous (granulosa cell intrinsic) defect in apoptosis execution resulting from caspase-3 deficiency. We conclude that caspase-3 is functionally required for granulosa cell apoptosis during follicular atresia, but that the enzyme is dispensable for germ cell apoptosis in the female.

Animals↗

PubMed1984

Comparison of programmed electrical stimulation and ambulatory electrocardiographic (Holter) monitoring in the management of ventricular tachycardia and ventricular fibrillation.

Forty-four patients with primary ventricular fibrillation or recurrent ventricular tachycardia were stabilized on an antiarrhythmic drug regimen before electrophysiologic study and 24 to 72 hours of ambulatory electrocardiographic monitoring were performed. The long-term predictive value of these two tests was then compared retrospectively for a 12 to 32 month (mean 18) follow-up period, during which all patients continued receiving the same antiarrhythmic drug regimen. Electrophysiologic testing induced ventricular tachycardia (greater than or equal to 3 beats) in 26 patients; 23 had a poor clinical outcome (positive predictive value 88%), defined as sudden death or sustained ventricular tachycardia. In 18 patients with a negative electrophysiologic test, only 1 had a poor clinical outcome (negative predictive value 94%). Ambulatory electrocardiographic monitoring accurately predicted outcome in 7 of 10 patients with a positive recording (positive predictive value 70%), defined as three or more consecutive ventricular extrasystoles, and in 17 of 34 patients with negative ambulatory monitor recordings (negative predictive value 50%). The long-term predictive accuracy of the electrophysiologic study was significantly higher than that of the ambulatory electrocardiographic monitor (p less than 0.001). Electrophysiologic studies offer advantages over ambulatory electrocardiographic monitoring in this high risk patient group, providing a high degree of accuracy in predicting the long-term clinical response to antiarrhythmic drugs for at least 18 months.

Adult↗

PubMed1998

Severity and prognosis of acute human immunodeficiency virus type 1 illness: a dose-response relationship.

This study examined the relationship between the severity of acute human immunodeficiency virus type 1 (HIV-1) illness and disease progression and death. The population included 218 patients with acute HIV-1 illness and 41 asymptomatic patients who underwent HIV-1 seroconversion; the patients were followed up prospectively. We analyzed progression to Centers for Disease Control and Prevention clinical categories B and C (AIDS-defining conditions) and death according to an additive clinical score (CS) based on six predictive clinical features at the time of acute HIV-1 infection. Compared with patients with a CS of 0 (asymptomatic patients), those with a CS of 3-4 and 5-6 had faster progression to category B disease (adjusted hazard ratio [HR], 1.39; 95% confidence interval [CI], 1.01-1.92; and HR, 1.80; 95% CI, 1.34-2.40; respectively); those with a CS of 5-6 had faster progression to category C disease (HR, 1.37; 95% CI, 1.01-1.89) and death (HR, 2.05; 95% CI, 1.27-3.32). Thus, the number of symptoms and signs at the time of acute HIV-1 illness affects disease progression and survival, even in symptomatic patients who have undergone seroconversion.

Acute Disease↗

PubMed2004

Cyclic antidepressants and the risk of sudden cardiac death.

BACKGROUND: Tricyclic and other related cyclic antidepressants (TCAs), used frequently for the treatment of depression and several other indications, have cardiovascular effects that may increase the risk of sudden cardiac death. We thus sought to quantify the risk of sudden cardiac death among TCA users, according to dose, as well as among users of selective serotonin reuptake inhibitors (SSRIs). METHODS: We conducted a retrospective cohort study in Tennessee Medicaid, from Jan 1, 1988, through Dec 31, 1993, which included large numbers of antidepressant users and computer files describing medication use and comorbidity. The cohort included 1,282,091 person-years of follow-up for persons aged 15 to 84 years who were not in a nursing home and were free of life-threatening noncardiac illness. This included 58,956 person-years for current use of TCAs alone, 6291 person-years for SSRIs only, and 96,220 person-years for former use. RESULTS: The cohort included 1487 confirmed sudden cardiac deaths occurring in the community. When compared with nonusers of antidepressants, current users of TCAs had a dose-related increase in the risk of sudden cardiac death. Rate ratios increased from 0.97 (95% confidence interval [CI], 0.72-1.29) for doses lower than 100 mg (amitriptyline or its equivalent) to 2.53 (95% CI, 1.04-6.12) for doses of 300 mg or more (P =.03, test for dose-response). The rate ratio for SSRIs was 0.95 (95% CI, 0.42-2.15). There was no evidence that TCA doses lower than 100 mg increased the risk of sudden cardiac death in subgroups defined by pre-existing cardiovascular disease, female sex, age 65 years or older, or use of amitriptyline. CONCLUSIONS: Our data suggest that SSRI antidepressants and TCAs in doses of less than 100 mg (amitriptyline equivalents) did not increase the risk of sudden cardiac death. However, higher doses of TCAs were associated with increased relative risk, which suggests that such doses should be used cautiously, particularly in patients with an elevated baseline risk of sudden death.

Adolescent↗

PubMed2005

The risk of congestive heart failure in rheumatoid arthritis: a population-based study over 46 years.

OBJECTIVE: It is hypothesized that the systemic inflammation associated with rheumatoid arthritis (RA) promotes an increased risk of cardiovascular (CV) morbidity and mortality. We examined the risk and determinants of congestive heart failure (CHF) in patients with RA. METHODS: We assembled a population-based, retrospective incidence cohort from among all individuals living in Rochester, Minnesota, in whom RA (defined according to the American College of Rheumatology 1987 criteria) was first diagnosed between 1955 and 1995, and an age- and sex-matched non-RA cohort. After excluding patients in whom CHF occurred before the RA index date, all subjects were followed up until either death, incident CHF (defined according to the Framingham Heart Study criteria), migration from the county, or until January 1, 2001. Detailed information from the complete medical records (including all inpatient and outpatient care provided by all local providers) regarding RA, ischemic heart disease, and traditional CV risk factors was collected. Cox models were used to estimate the effect of RA on the development of CHF, adjusting for CV risk factors and/or ischemic heart disease. RESULTS: The study population included 575 patients with RA and 583 subjects without RA. The CHF incidence rates were 1.99 and 1.16 cases per 100 person-years in patients with RA and in non-RA subjects, respectively (rate ratio 1.7, 95% confidence interval [95% CI] 1.3-2.1). After 30 years of followup, the cumulative incidence of CHF was 34.0% in patients with RA and 25.2% in non-RA subjects (P< 0.001). RA conferred a significant excess risk of CHF (hazard ratio [HR] 1.87, 95% CI 1.47-2.39) after adjusting for demographics, ischemic heart disease, and CV risk factors. The risk was higher among patients with RA who were rheumatoid factor (RF) positive (HR 2.59, 95% CI 1.95-3.43) than among those who were RF negative (HR 1.28, 95% CI 0.93-1.78). CONCLUSION: Compared with persons without RA, patients with RA have twice the risk of developing CHF. This excess risk is not explained by traditional CV risk factors and/or clinical ischemic heart disease.

Arthritis, Rheumatoid↗

PubMed1999

Application of transcranial doppler ultrasonography for the diagnosis of brain death.

OBJECTIVE: To determine the clinical validity of transcranial Doppler ultrasonographic (TCD) signs of total cerebral circulatory arrest for confirmation of brain death and to define the test protocol. DESIGN: Study of a diagnostic test. SETTING: General and neurosurgery intensive care units. PATIENTS: 137 patients in a coma (Glasgow Coma Score 3-5), caused by various pathological conditions, observed from January 1992 to July 1998. 84 patients met the clinical criteria of brain death; 43 patients out of 137 received sedative drug therapy and 31 of these developed brain death. RESULTS: Total cerebral circulatory arrest was demonstrated by TCD in 81 patients. All of them proved to be brain dead according to subsequent clinical examination In 29 of 31 patients who had received sedative drug therapy TCD examination showed total cerebral circulatory arrest 12-48 h before the formal confirmation of the diagnosis. In 1 out of 84 clinically brain dead patients a false negative result was obtained. In 2 of 84 cases, no clear signals from intracranial vessels were obtainable. Fifty-three patients who did not meet the clinical criteria for brain death showed no TCD signs of total cerebral circulatory arrest. The specificity of the TCD test for confirmation of brain death was 100 % and the sensitivity 96.5 %. CONCLUSIONS: In agreement with previously published data, we conclude that TCD ultrasonography is a highly specific and sensitive confirmatory test and should be included as an additional test in the protocol for the assessment of brain death.

Adolescent↗

PubMedDate not supplied

Many ways to die: passive and active cell death styles.

In multicellular organisms, cells may undergo passive, pathological death in response to various environmental injuries, or actively decide to self-destroy in order to ensure proper physiological morphogenesis, preserve tissue homeostasis and eliminate abnormal cells. While the passive cell demise occurs in an accidental, violent and chaotic way, corresponding to "necrosis", the active auto-elimination, defined "programmed cell death" (PCD), is executed in planned modalities. Different PCD pathways have been described, such as apoptosis, autophagic death, para-apoptosis and programmed necrosis. However, death patterns may overlap or integrate, providing a variety of cellular responses to various circumstances or stimuli. The consequences for the whole organism of necrosis and PCD are quite different. In the case of classical necrosis, cytosolic constituents chaotically spill into extracellular space through damaged plasma membrane and provoke an inflammatory response, while in most PCDs the cellular components are safely isolated by membranes, and then consumed by adjacent parenchymal cells and/or resident phagocytes without inflammation. Thus, whereas the necrotic cell removal induces and amplifies pathological processes, the elimination of PCD debris may remain virtually unnoticed by the body. Otherwise, alterations of PCD controls may be involved in human diseases, such as developmental abnormalities, or neurodegenerative, autoimmune and neoplastic affections, whose treatment implies the complete understanding of cell suicide processes. In this review, the cellular death patterns are focused and their significance discussed.

Cell Death↗

PubMed1994

Serial neurologic examinations after near drowning and outcome.

OBJECTIVE: We evaluated serial neurologic examinations after warm water near drowning to determine how rapidly survivors with poor neurologic outcome could be identified. RESEARCH DESIGN: Retrospective chart review. SETTING: University-affiliated pediatric hospital. PATIENTS: Forty-four children admitted to the pediatric intensive care unit with an abnormal mental status after near drowning during a 5-year period. Follow-up was a minimum of 6 months. INTERVENTIONS: None. MEASUREMENTS: A 14-point coma scale was used to evaluate both cortical and brain-stem function at the time of hospital admission and then daily afterward. The Mann-Whitney U Test was used to compare patients grouped as having satisfactory outcomes (those who returned to their presubmersion baseline or had very mild deficits) and unsatisfactory outcomes (total custodial care or death). Significance was defined as P < .05. CONCLUSION: All satisfactory survivors were sufficiently awake to have spontaneous, purposeful movements 24 hours after near drowning and had normal brain-stem function. All children without spontaneous, purposeful movements and normal brain-stem function 24 hours after near drowning suffered severe neurologic deficits or death. In this retrospective investigation of 44 children, the cortical examination 24 hours after warm water near drowning distinguished satisfactory survivors from children who required total custodial care or died.

Adolescent↗

PubMed2006

[Management of in utero foetal death: Which assessment to undertake?].

OBJECTIVE: To assess the value of para-clinical exams prescribed in case of in utero foetal death, to result in the establishment of a new algorithm of diagnostic tests. MATERIALS AND METHODS: A retrospective analysis on a series of 106 stillbirths gathered between September 1989 and December 1998 in the obstetrical and gynaecological department of the Lausanne University Hospital which is a tertiary centre. Stillbirth was defined as foetal death occurring as from the date of foetal viability. Thus, only pregnancies from 24 weeks and onwards were included in this series. We excluded all stillbirths occurring during medical termination of pregnancy and cases with incomplete data files. The Fretts' classification was used. The different exams asked by the physician were screened and we analysed their pertinence to determine the aetiological diagnosis for each case. The search for significant risk factors was also taken into account. We compared our management of in utero foetal death with data from the literature to propose a new algorithm. RESULTS: The aetiology of in utero foetal death could be attributed in ninety percent of the cases. The principal causes were in utero growth retardation (19.8%), foetal congenital and chromosomal anomalies (18.9%), infections (15.1%), placental abruption (7.5%), preeclampsia (5.6%), maternal diabetes (3.8%). The remaining 18.9% are divided in to miscellaneous causes. In 10.4% of the cases we could not find any explanation to the death of the foetus. The exams that yielded the most information when done were: foetal autopsy which was abnormal in 92.7%, placental investigation which was abnormal in 93% and the babygramme (X-ray of the foetal skeleton) which was abnormal in 53%. Maternal serology for infections was informative in 6.6% of the cases. CONCLUSION: We present here a protocol for the diagnostic management of stillbirth which is differentiated according to the circumstances surrounding the event. This should prove useful to reduce superfluous tests.

Abruptio Placentae↗

PubMed2001

Differences in HIV disease progression by injection drug use and by sex in the era of highly active antiretroviral therapy.

BACKGROUND: The advent of highly active antiretroviral therapy (HAART) has reduced the incidence of most AIDS-related opportunistic illnesses (OI) and death in HIV-infected individuals. We investigated whether there are demographic disparities in HIV disease progression in the HAART era compared with before. METHODS: HIV-infected patients in an urban HIV clinical practice in the USA were compared using survival methods for time to a new AIDS-defining OI or death in therapeutic era 1 (monotherapy and combination therapy; 1990--1995; n = 2016) versus era 2 (HAART; 1996--1999; n = 2165). RESULTS: A total of 1037 (51.4%) events occurred in era 1; 666 (30.8%) events occurred in era 2. In women, the median disease-free survival time increased by 14% (CD4 cell counts > 200 cells/mm(3) at baseline) and 34% (CD4 cell counts < or = 200) in era 2 compared with era 1, whereas for men it increased by 43 and 100%. The relative hazard (RH) of progression for women compared with men in era 2 compared with era 1 was 1.34. For injecting drug use (IDU), disease-free survival time increased by 16% and 34% in era 2 compared with era 1, whereas non-IDU improved by 65 and 135%. The RH of progression for IDU compared with non-IDU in era 2 compared with era 1 was 1.39. No significant differences were detected by race or other HIV transmission risk group. CONCLUSION: Disease-free survival time was extended with the use of HAART, but these gains were not equally distributed by sex and IDU in our cohort.

Adult↗

PubMed1991

Birthdate and mortality: an evaluation of the death-dip/death-rise.

The effect on mortality of socially significant events is examined using birth date as the criterion date for a large sample from official state mortality records for Ohio. The sample consisted of all deaths from natural causes for 1979-1981. "The findings show that there is a greater tendency for persons to die within thirty days after the date of birth than before. More specifically, there was a statistically significant pattern of increased mortality for those who were never married and for ill-defined causes of death. A theoretical foundation and a brief interpretation of these findings is offered."

Americas↗

PubMed2002

Increased atrial fibrillation mortality: United States, 1980-1998.

The authors used death certificate data to evaluate national trends in the reporting of atrial fibrillation as an underlying or contributory cause of death for groups defined by age (45 years or older), sex, and race (Black vs. White) and to examine comorbidity. The multiple-causes mortality files from 1980 through 1998 were analyzed for decedents, with atrial fibrillation (International Classification of Diseases, Ninth Revision, code 427.3) listed as one of up to 20 conditions causing death. The number of decedents with atrial fibrillation increased from 18,947 in 1980 to 61,946 in 1998, and the proportion with atrial fibrillation reported as the underlying cause of death rose from 8.3% in 1980 to 11.6% in 1998. Age-standardized death rates from 1980 to 1998 were consistently highest among White men, followed (in descending order) by White women, Black men, and Black women. Overall, the age-standardized rate (per 100,000) increased from 27.6 in 1980 to 69.8 in 1998 (an average annual increase of 5.4%, p < 0.0001). Ischemic heart disease was the most frequent underlying cause of death among decedents with atrial fibrillation (26.8%). These findings emphasize the need for increased application of proven prevention and control measures to decrease associated cardiovascular morbidity and mortality.

Black or African American↗

PubMed2001

Trends in the risk of mortality due to cardiovascular diseases in five Brazilian geographic regions from 1979 to 1996.

OBJECTIVE - To analyze the trends in risk of death due to cardiovascular diseases in the northern, northeastern, southern, southeastern, and central western Brazilian geographic regions from 1979 to 1996. METHODS - Data on mortality due to cardiovascular, cardiac ischemic, and cerebrovascular diseases in 5 Brazilian geographic regions were obtained from the Ministry of Health. Population estimates for the time period from 1978 to 1996 in the 5 Brazilian geographic regions were calculated by interpolation with the Lagrange method, based on the census data from 1970, 1980, 1991, and the population count of 1996, for each age bracket and sex. Trends were analyzed with the multiple linear regression model. RESULTS - Cardiovascular diseases showed a declining trend in the southern, southeastern, and northern Brazilian geographic regions in all age brackets and for both sexes. In the northeastern and central western regions, an increasing trend in the risk of death due to cardiovascular diseases occurred, except for the age bracket from 30 to 39 years, which showed a slight reduction. This resulted from the trends of cardiac ischemic and cerebrovascular diseases. The analysis of the trend in the northeastern and northern regions was impaired by the great proportion of poorly defined causes of death. CONCLUSION - The risk of death due to cardiovascular, cerebrovascular, and cardiac ischemic diseases decreased in the southern and southeastern regions, which are the most developed regions in the country, and increased in the least developed regions, mainly in the central western region.

Adult↗

PubMed1981

The sudden infant death syndrome.

Recent research has defined a group of infants with certain characteristics who may be prone to sudden unexpected death, but no single criterion has yet been found that can be used to identify the victim before or after death. Although the aetiology of SIDS remains a mystery, it seems likely that certain stresses such as infection, overheating, and environmental or nutritional deprivation in a vulnerable group of infants may combine at a critical period of development to cause death by respiratory arrest. Some of these deaths may be prevented by raising the general standard of care for the whole infant population, improving health education, and increasing the surveillance of high risk groups. There remains a hard core of infants for whom the stresses appear minimal and the environment optimal but in the present state of our knowledge their death seems unavoidable.

Adult↗