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PubMed1992

Inhibition of programmed cell death by cyclosporin A; preferential blocking of cell death induced by signals via TCR/CD3 complex and its mode of action.

Cyclosporin A (CsA) is reported to inhibit programmed cell death. We confirmed this by using T-cell hybridomas which are inducible to programmed cell death by activation with immobilized anti-CD3 antibody or with anti-Thy 1.2 antibody. Cell death and DNA fragmentation, characteristic features of programmed cell death, were almost completely blocked by CsA or FK506. To investigate whether CsA inhibits only the cell death through the signals via the TCR/CD3 complex or all of the programmed cell death induced by various reagents, we further established CD4+8+ thymic lymphomas which result in programmed cell death after activation with calcium ionophore, dexamethasone, cyclic AMP or anti-CD3 antibody. It was revealed that CsA could block only the cell death mediated by the TCR/CD3 complex. For the clarification of the site of action of CsA, Ca2+ influx and endocytosis of receptors after stimulation with anti-CD3 antibody were monitored in the presence of CsA, and no significant effects of CsA were observed. Furthermore, prevention of cell death was examined by adding CsA at various periods of time after initiation of culture. CsA was found to exert its effect even when added after 4 h of cultivation, and the kinetic pattern of suppression was similar to that of the suppressive effect on IL-2 production. These observations indicate that in the events of programmed cell death, the major site of action of CsA will not be the inhibition of the immediate membrane events after activation of the TCR/CD3 complex but rather the interference in the function of molecules that transmit signals between membrane events and the activation of genes in the nucleus.

Animals↗
PubMedDate not supplied

Temporal correlation between opiate seizures in East/Southeast Asia and B.C. heroin deaths: a transoceanic model of heroin death risk.

BACKGROUND: Because heroin supply changes cannot be measured directly, their impact on populations is poorly understood. British Columbia has experienced an injection drug use epidemic since the 1980s that resulted in 2,590 illicit drug deaths from 1990-1999. Since previous work indicates heroin seizures can correlate with supply and B.C. receives heroin only from Southeast Asia, this study examined B.C. heroin deaths against opiate seizures in East/Southeast Asia. METHODS: Opiate seizures in East/Southeast Asia and data from two B.C. mortality datasets containing heroin deaths were examined. The Pearson correlation coefficient for seizures against each mortality dataset was determined. RESULTS: Opiate seizures, all illicit drug deaths and all opiate deaths concurrently increased twice and decreased twice from 1989-1999, and all reached new peak values in 1993. Three B.C. sub-regions exhibited illicit drug deaths rate trends concurrent with the three principal datasets studied. The Pearson correlation coefficient for opiate-induced deaths against opiate seizures from 1980-1999 was R=0.915 (p<0.0001), and for illicit drug deaths against opiate seizures from 1987-1999 was R=0.896 (p<0.0001). CONCLUSIONS: From 1980-1999, opiate seizures in East/Southeast Asia were very strongly correlated with B.C. opiate and illicit drug deaths. The number of B.C. heroin-related deaths may be strongly linked to heroin supply. Enforcement services are not effective in preventing harm caused by heroin in B.C.; therefore, Canada should examine other methods to prevent harm. The case for harm reduction is strengthened by the ineffectiveness of enforcement and the unlikelihood of imminent eradication of heroin production in Southeast Asia.

Asia, Southeastern↗
PubMed1993

Diversification in the concept of "birth and death": the controversy about "brain death and organ transplantation" in Japan.

There is a lot of hesitation in Japan in defining brain death as the death of the individual and in proceeding to organ transplantation. Regarding the diagnostic criteria of brain death, those issued by the Japanese Ministry of Health and Welfare in 1985 are sufficient for judgment of brain death. Many people, however, do not accept brain death as death of the individual, and even those who admit brain death as death of the individual hesitate to approve of the actual removal of organs from brain dead patients. Thus, the controversy about brain death in Japan appears to be separated from the objective of organ transplantation.

Brain Death↗
PubMed1995

Preventable factors and death certification in death due to asthma.

A 2 yr District-wide study was carried out to assess whether there were preventable factors in the management of patients dying from asthma, and also to assess the accuracy of death certification of asthma. Eighteen deaths occurred in which asthma was the certified cause of death. In 10, asthma was the actual cause of death. Due to inaccuracies of death certification, death was due to other causes in seven cases. In the remaining case it was not possible to differentiate between asthma and chronic obstructive airways disease. Among the 10 deaths from asthma the condition was considered to be mild in three. In three, death occurred too rapidly for help to have been available. Preventable factors were present in four cases. In three, either the patient, the doctor or both failed to appreciate the severity of the condition and the need for urgent help or hospitalization. The fourth patient had failed to seek any medical care. Many lives might be saved if patients and doctors treated severe breathlessness due to asthma with the same sense of urgency that chest pain suspicious of myocardial infarction is treated. Education is needed to improve both the clinical and post mortem accuracy of death certification. Both this and the management of asthma should be the subject of ongoing local audits.

Adult↗
PubMed2003

Cause-of-death query in validation of death certification by expert panel; effects on mortality statistics in Finland, 1995.

The correctness of selection, coding and registration of underlying cause-of-death is important for the quality of mortality statistics. One measure to improve quality is the query to the certifier for verification of the underlying cause-of-death. In Finland, 3478 death certificates, 7.1% of total 49074 certifications in 1995, were considered questionable by statisticians. The expert panel at Statistics Finland was able to resolve 2813 (80.9%) of them. However, 665 (19.1%) certificates needed to be further queried from the certifier. Of these, 318 (47.8%) were re-assigned to another ICD-9 category or to the applicable three-digit category within the main category of heart and vascular diseases, resulting in changes from a 17.00-fold increase in rheumatic heart diseases (ICD-9 codes 390-398) to a decrease of about one-half (0.45-fold change) in unspecified neoplasms (codes 235-239). However, a statistically significant impact on national mortality statistics was not observed in any of applied ICD categories. Among all questionable death certificates, most prone to query of the certifier, and with a statistical significance of P<0.05, were those with no cause-of-death specified, those stating underlying cause-of-death as non-specified neoplasms (with a observed/expected ratio, O/E, of 1.69), and heart and vascular diseases (1.45), with its subcategories of ischaemic heart diseases (1.33) and other heart diseases (2.92). Death certificate validation, by expert panel consultations and query to the certifiers, and the importance of estimation of the validity of cause-of-death information on death certificates are strongly pointed out in a continuous strive for correct and reliable mortality statistics.

Adolescent↗
PubMed1998

The manner of death among fatalities where dextropropoxyphene caused or contributed to death.

Dextropropoxyphene (DXP) is one of the most prescribed analgesic compounds in Sweden. To investigate the manner of death among fatalities where DXP caused or contributed to death all medico-legal autopsies performed in Sweden in 1992-1996 were analysed on the bases of toxicological analyses and death certificates. DXP in peripheral blood was found in 1782 (7.5%) of the total 23,691 blood samples. According to the death certificates 956 (54%) of the 1782 cases were classified as fatal DXP poisoning. Among these, the manner of death was classified as accidental in 49 cases (5%), suicidal in 542 cases (57%) and undetermined in 365 cases (38%). The reported manner of death differed between the six forensic medicine districts in Sweden. The accident rate differed significantly between the district with the highest rate (9%) and the districts with the lowest rate (1%). One district had a significantly higher incidence of suicide (73%) than four of the other districts, while another district had a significantly lower incidence of suicide (33%) than all the other districts. The accident classification rate among the physicians performing ten or more autopsies varied from 0% to 17%, the suicide classification rate from 25% to 83% and the rate of undetermined manner of death from 8% to 71%. A major conclusion drawn from this study is that accidental DXP fatalities may be underestimated. This may have serious consequences, as under-reporting of accidental DXP fatalities will increase the risk that knowledge of the high toxicity of DXP will not reach the population consuming this drug. Since valid death statistics concerning the manner of death at DXP fatalities are needed to provide the base for preventive actions, special attention should be paid to the classification process, in order to increase the uniformity of the assessments among the different physicians, and to avoid under-reporting of accidents.

Adolescent↗
PubMed2002

Why do we fear death? The construction and validation of the Reasons for Death Fear Scale.

Previous research has disclosed different meanings of death, varieties of death anxiety, and hundreds of factors extracted from the uni- and multi-dimensional death anxiety scales. However, there have been no empirical studies to elucidate the reasons for death fear. The Reasons for Death Fear Scale (RDFS) was constructed and validated. It consists of 18 brief items, with good reliabilities ( > .8). Four factors of the RDFS were labeled Fear of Pain and Punishment, Fear of Losing Worldly Involvements, Religious Transgressions and Failures, and Parting from Loved Ones. A high-loaded factor was extracted in which the RDFS's loading was .45, while the loadings of the scales of death anxiety, death depression, and death obsession ranged between .8 and .9. Of interest is that the correlation between the RDFS and death anxiety was higher than that with general anxiety. No gender-differences were detected with college students. It is important to note that the findings of this study were only researched through Arabic and mainly Muslim college students. The generalizability of the present results to other populations would seem to merit further investigation.

Adolescent↗
PubMed2003

Coronary heart disease death and sudden cardiac death: a 20-year population-based study.

Trends in out-of-hospital coronary heart disease (CHD) death, a surrogate for sudden cardiac death (SCD), are important for understanding the decline in CHD mortality. Little is known about out-of-hospital CHD death without prior CHD diagnosis, the definition of unexpected SCD. The authors analyzed secular trends in CHD death and unexpected SCD over a 20-year period (1979-1998) to examine the association between prior CHD and SCD and to test the hypothesis that in-hospital deaths declined more than SCDs. The yearly decline in CHD mortality rates was 5.3% for in-hospital deaths and 1.8% for out-of-hospital deaths (p = 0.001). Among all SCDs, the proportion of unexpected SCD was 49%. Mortality rates for both unexpected SCD and SCD with prior CHD declined over time, but unexpected SCD declined at a slower rate than SCD with prior CHD (p = 0.001). The relative odds of prior CHD were higher among persons with SCD than among controls, but there was a modest decline in the magnitude of the association. Thus, during the past 20 years, the decline was greater for in-hospital CHD deaths than for SCDs. Since approximately half of the SCDs were unexpected and rates of these deaths declined less over time than rates of SCD with prior CHD, primary prevention is becoming increasingly more important in sustaining the decline in CHD mortality.

Adult↗
PubMed1999

A matter of life and death: what every anesthesiologist should know about the medical, legal, and ethical aspects of declaring brain death.

Accurate criteria for death are increasingly important as it becomes more difficult for the public to distinguish between patients who are still alive from those who, through the aid of medical technology, merely look like they are alive even though they are dead. Patients and their families need to know that a clear line can be drawn between life and death, and that patients who are alive will not be unintentionally treated as though they are dead. For the public to trust the pronouncements of medical doctors as to whether a patient is dead or alive, the criteria must be unambiguous, understandable, and infallible. It is equally important to physicians that accurate, infallible criteria define death. Physicians need to know that a clear line can be drawn between life and death so that patients who are dead are not treated as though they are alive. Such criteria enable us to terminate expensive medical care to corpses. Clear criteria for death also allow us to ethically request the gift of vital organs. Clear, infallible criteria allow us to assure families and society that one living person will not be intentionally or unintentionally killed for the sake of another. The pressure of organ scarcity must not lead physicians to allow the criteria for life and death to become blurred because of the irreparable harm this would cause to the patient-physician relationship and the devastating impact it could have on organ transplantation. As the cases presented here illustrate, anesthesiologists have an important responsibility in the process of assuring that some living patients are not sacrificed to benefit others. Criteria for declaring death should be familiar to every anesthesiologist participating in organ retrieval. Before accepting the responsibility of maintaining a donor for vital organ collection, the anesthesiologist should review data supplied in the chart supporting the diagnosis of brain death and seriously question inconsistencies and inadequate testing conditions. Knowledge of brain death criteria and proper application of these criteria could have changed the course of each of the cases presented.

Adult↗
PubMed2003

Increase in deaths caused by HIV infection due to changes in rules for selecting underlying cause of death.

With implementation of the (ICD-10), for U.S. vital statistics in 1999, the criteria for selecting HIV infection as the underlying cause of death were expanded. To estimate the effect of ICD-10 rules on the number of deaths attributed to HIV infection, we applied a simplified version of ICD-10 rules to data on causes of death from all U.S. death certificates for 1998 (previously classified by rules of the 9th revision of ICD [ICD-9]) and calculated the resulting increase in deaths for which HIV infection was selected as the underlying cause. Of the 17,186 deaths in 1998 with any mention of HIV infection on the death certificate, ICD-10 rules selected HIV infection as the underlying cause for 15,145, which was 1,719 (13%) more than the 13,426 for which it had been selected by ICD-9 rules. The proportional increase differed by demographic group, being less among non-Hispanic blacks (9%) and Hispanics (13%) than among non-Hispanic whites (18%). Thus, comparison of deaths attributed to HIV infection in 1999 or later with those in 1998 or earlier should take into account the changes in ICD rules for selecting the underlying cause of death.

Adolescent↗
PubMedDate not supplied

Sudden infant death syndrome and unascertainable deaths: trends and disparities among Aboriginal and non-Aboriginal infants born in Western Australia from 1980 to 2001 inclusive.

AIM: To analyse patterns and trends in mortality from unknown causes (sudden infant death syndrome and unascertainable deaths) for all Aboriginal and non-Aboriginal infants born in Western Australia, 1980-2001. METHODS: Using total population linked data, we reviewed all post-mortem reports, including death scene investigations and final causes of death as ascertained by the coroner. Neonatal, post-neonatal and infant mortality rates attributed to unknown causes were calculated and the latter were analysed according to maternal age, geographical location, gestational age, sex and birthweight. Relative risks (95% confidence interval) for Aboriginal infants (compared with non-Aboriginal) were calculated. RESULTS: The proportion of deaths considered to be of unascertainable cause has significantly increased in recent years. In contrast to the non-Aboriginal population, there has been no significant decrease in deaths in the Aboriginal population and the overall relative risk for Aboriginal infants for the most recent years studied was 7.9 (95% confidence interval 5.1-12.2). The relative risk was significantly increased for most categories analysed. CONCLUSION: Reviewing post-mortem reports enabled identification of changes in the classification of deaths due to unknown causes. This provided a more accurate picture of the patterns and long-term trends of such deaths so that programmes can be developed to specifically target those groups most at risk. Adequately funded and evaluated education campaigns aimed at reducing the risk of sudden infant death syndrome among Aboriginal infants are required, as well as sustaining the current efforts that have been so successful for non-Aboriginal infants.

Cause of Death↗
PubMed2006

Phorbol 12-myristate 13-acetate protects against tumor necrosis factor (TNF)-induced necrotic cell death by modulating the recruitment of TNF receptor 1-associated death domain and receptor-interacting protein into the TNF receptor 1 signaling complex: Implication for the regulatory role of protein kinase C.

Protein kinase C (PKC) triggers cellular signals that regulate proliferation or death in a cell- and stimulus-specific manner. Although previous studies have demonstrated that activation of PKC with phorbol 12-myristate 13-acetate (PMA) protects cells from apoptosis induced by a number of mechanisms, including death receptor ligation, little is known about the effect or mechanism of PMA in the necrotic cell death. Here, we demonstrate that PMA-mediated activation of PKC protects against tumor necrosis factor (TNF)-induced necrosis by disrupting formation of the TNF receptor (TNFR)1 signaling complex. Pretreatment with PMA protected L929 cells from TNF-induced necrotic cell death in a PKC-dependent manner, but it did not protect against DNA-damaging agents, including doxorubicin (Adriamycin) and camptothecin. Analysis of the upstream signaling events affected by PMA revealed that it markedly inhibited the TNF-induced recruitment of TNFR1-associated death domain protein (TRADD) and receptor-interacting protein (RIP) to TNFR1, subsequently inhibiting TNF-induced activation of nuclear factor-kappaB and c-Jun NH2-terminal kinase (JNK). However, JNK inhibitors do not significantly affect TNF-induced necrosis, suggesting that the inhibition of JNK activation by PMA is not part of the antinecrotic mechanism. In addition, PMA acted as an antagonist of TNF-induced reactive oxygen species (ROS) production, thereby suppressing activation of ROS-mediated poly(ADP-ribose)polymerase (PARP), and thus inhibiting necrotic cell death. Furthermore, during TNF-induced necrosis, PARP was significantly activated in wild-type mouse embryonic fibroblast (MEF) cells but not in RIP-/- or TNFR-associated factor 2-/-MEF cells. Taken together, these results suggest that PKC activation ensures effective shutdown of the death receptor-mediated necrotic cell death pathway by modulating formation of the death receptor signaling complex.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Comparison of physician based reporting of tobacco attributable deaths and computer derived estimates of smoking attributable deaths, Oregon, 1989 to 1996.

BACKGROUND: Tobacco use prevention programmes need accurate information about smoking related mortality. Beginning in 1989, Oregon began asking physicians to report on death certificates whether tobacco use contributed to the death. OBJECTIVE: To determine the long term comparability of this method of estimating tobacco attributable mortality to estimates of smoking attributable mortality derived from a computer model. DESIGN: For the period 1989 to 1996, we compared mortality resulting from tobacco use reported by Oregon physicians to estimates of smoking attributable deaths (SADs) derived by "Smoking attributable mortality, morbidity and economic costs" software version 3.0 (SAMMEC 3.0), a widely used software program that estimates SADs on the basis of smoking prevalence and relative risks of specific diseases among current and former smokers. MAIN OUTCOME MEASURES: Numbers of deaths, age, sex, and category of disease. RESULTS: Of 212, 448 Oregon deaths during 1989-1996, SAMMEC 3.0 estimated that 42, 778 (20.1%) were attributable to cigarette smoking. For the same 27 diagnoses, physicians reported that tobacco contributed to 42, 839 (20.2%) deaths-a cumulative difference of only 61 deaths over the eight year period. The age and sex distributions of tobacco and smoking attributable deaths reported by the two systems were also similar. By category of disease, the ratio of SAMMEC 3.0 estimates to physician reported deaths was 1.11 for neoplasms, 0.88 for heart disease, and 1.04 for respiratory disease. CONCLUSIONS: Physician reporting provides comparable estimates of smoking attributable mortality and can be a valuable source of data for communicating the risks of tobacco use to the public.

Adult↗
PubMed1989

[Epidemiological study of SMON death--from the observation of death certificates during a 13-year 6-month period from July 1972].

Eight hundred and twelve vital statistics death certificates, in which either the cause of death or complications was SMON, were selected from all the death certificates filed in Japan in a 13-year 6-month period from July 1972 to December 1985. In 411, or 50.6%, of these certificates, the SMON Research Committee had records of the clinical pictures as a result of the nationwide surveys conducted earlier. The epidemiological picture presented by the death certificates and the relationship between the information in these certificates and clinical records in nationwide surveys was observed. The results are summarized as follows: 1. The male/female ratio revealed in the 812 death certificates was 0.53, which is higher than those reported in nationwide surveys (0.4). 2. Although the yearly number of certificates was more than 70 in 1974 or before, it decreased year by year. The numbers in 1984 and 1985 were less than 50. 3. The leading underlying causes of death were; SMON in 44.0% of all the certificates, heart diseases in 10.3%, cerebrovascular diseases in 9.2% and malignant neoplasm in 8.6%. 4. The presence of clinical symptoms was compared between death cases and total cases reported by the nationwide surveys. Symptoms such as visual impairment and walking incapacity were seen more frequently in death cases. 5. From these results, it was suggested that the level of the severity of the disease at onset influences the long-term prognosis of the disease, although selection bias in the death certificates observed is unavoidable.

Adult↗
PubMed1998

Comparative evaluation of underlying causes of death processed by the Automated Classification of Medical Entities and the Underlying Cause of Death Selection Systems.

INTRODUCTION: The correct identification of the underlying cause of death and its precise assignment to a code from the International Classification of Diseases are important issues to achieve accurate and universally comparable mortality statistics. These factors, among other ones, led to the development of computer software programs in order to automatically identify the underlying cause of death. OBJECTIVE: This work was conceived to compare the underlying causes of death processed respectively by the Automated Classification of Medical Entities (ACME) and the "Sistema de Seleção de Causa Básica de Morte" (SCB) programs. MATERIAL AND METHOD: The comparative evaluation of the underlying causes of death processed respectively by ACME and SCB systems was performed using the input data file for the ACME system that included deaths which occurred in the State of S. Paulo from June to December 1993, totalling 129,104 records of the corresponding death certificates. The differences between underlying causes selected by ACME and SCB systems verified in the month of June, when considered as SCB errors, were used to correct and improve SCB processing logic and its decision tables. RESULTS: The processing of the underlying causes of death by the ACME and SCB systems resulted in 3,278 differences, that were analysed and ascribed to lack of answer to dialogue boxes during processing, to deaths due to human immunodeficiency virus [HIV] disease for which there was no specific provision in any of the systems, to coding and/or keying errors and to actual problems. The detailed analysis of these latter disclosed that the majority of the underlying causes of death processed by the SCB system were correct and that different interpretations were given to the mortality coding rules by each system, that some particular problems could not be explained with the available documentation and that a smaller proportion of problems were identified as SCB errors. CONCLUSION: These results, disclosing a very low and insignificant number of actual problems, guarantees the use of the version of the SCB system for the Ninth Revision of the International Classification of Diseases and assures the continuity of the work which is being undertaken for the Tenth Revision version.

Cause of Death↗
PubMed2005

Investigation into sudden infant deaths and unascertained infant deaths in England and Wales, 1995-2003.

This article investigates whether the decline in the sudden infant death rates and the rise in unascertained death rates during the period 1995-2003 were linked. It concludes that changes in certification practices surrounding sudden infant deaths and unascertained deaths suggest that it is becoming more difficult to distinguish between these two causes of death. In addition, there is a huge overlap in the characteristics of babies whose deaths are certified as sudden infant death and those whose death is unascertained. These terms are to some extent used interchangeably. Based on this evidence it seems appropriate to include both groups in any analysis of unexplained infant deaths.

Death Certificates↗
PubMed2001

Apoptotic and necrotic cell death induced by death domain receptors.

Apoptosis and necrosis are two distinct forms of cell death. Caspases are indispensable as initiators and effectors of apoptotic cell death and are involved in many of the morphological and biochemical features of apoptosis. Major changes in mitochondrial membrane integrity and release of proapoptotic factors, such as cytochrome c from the mitochondrial intermembrane space, play an important sensor and amplifying role during apoptotic cell death. In vitro studies of cell death in cell lines have revealed that inhibition of the classical caspase-dependent apoptotic pathway leads in several cases to necrotic cell death. Thus, the same cell death stimulus can result either in apoptotic or necrotic cell death, depending on the availability of activated caspase. Therefore, death domain receptors may initiate an active caspase-independent necrotic signaling pathway. In this review, we describe what is known about the apoptotic and necrotic cell death pathways. Principal elements of necrosis include mitochondrial oxidative phosphorylation, reactive oxygen production, and non-caspase proteolytic cascades depending on serine proteases, calpains, or cathepsins.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Hypoxia-induced cell death of HepG2 cells involves a necrotic cell death mediated by calpain.

To elucidate mechanism of cell death in response to hypoxia, we attempted to compare hypoxia-induced cell death of HepG2 cells with cisplatin-induced cell death, which has been well characterized as a typical apoptosis. Cell death induced by hypoxia turned out to be different from cisplatin-mediated apoptosis in cell viability and cleavage patterns of caspases. Hypoxia-induced cell death was not associated with the activation of p53 while cisplatin-induced apoptosis is p53 dependent. In order to explain these differences, we tested involvement of micro-calpain and m-calpain in hypoxia-induced cell death. Calpains, especially micro-calpain, were initially cleaved by hypoxia, but not by cisplatin. Interestingly, the treatment of a calpain inhibitor restored PARP cleavage that was absent during hypoxia, indicating the recovery of activated caspase-3. The inhibition of calpains prevented proteolysis induced by hypoxia. In addition, hypoxia resulted in a necrosis-like morphology while cisplatin induced an apoptotic morphology. The calpain inhibitor prevented necrotic morphology induced by hypoxia and converted partially to apoptotic morphology with nuclear segmentation. Our result suggests that calpains are involved in hypoxia-induced cell death that is likely to be necrotic in nature and the inhibition of calpain switches hypoxia-induced cell death to apoptotic cell death without affecting cell viability.

Amino Acid Chloromethyl Ketones↗