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PubMed1992

Risk perception and the value of safety.

This paper examines the relationship between perceived risk and willingness-to-pay (WTP) for increased safety from technological hazards in both conceptual and empirical terms. A conceptual model is developed in which a given household's WTP for risk reductions is a function of traditional socioeconomic variables (i.e., income and base level of risk) and perceived characteristics of the hazards (i.e., dread, knowledge, and exposure). Data to estimate the model are obtained through a combined contingent valuation and risk perception survey that considers 10 technological hazards, five of which are well-defined (e.g., death rates are known and the risks are relatively common) and five are less well-defined. Econometric results, using TOBIT estimation procedures, support the importance of both types of variables in explaining WTP across all 10 hazards. When the risks are split into two groups, the results show that WTP for well-defined hazards is most influenced by perceived personal exposure, while WTP for less well-defined risks is most influenced by levels of dread and severity.

Data Collection↗
PubMed1988

[Hypothalamic pituitary function in brain death patients--from blood pituitary hormones and hypothalamic hormones].

According to the report of the Health and Welfare Ministry's research committee on brain death (1985), "brain death is defined as an irreversible cessation of the total brain function including brain stem." However, in brain death patients, whether the hypothalamic function which belongs to the brain stem function has completely ceased or not is unknown. In order to evaluate the hypothalamic function in brain death patients, the blood levels of the pituitary hormones and hypothalamic hormones were measured, and anterior pituitary stimulation test with triple bolus injection (TRH 500 micrograms, LH-RH 100 micrograms, regular insulin 0.3-0.7 unit/kg) was performed. The subjects were 13 brain death patients whose clinical states fully satisfied the criteria proposed by the committee. 1) The average blood levels of anterior pituitary hormones in these brain death patients were within normal range, and that of growth hormone was more than the twice of the normal level. 2) The blood anterior pituitary hormones were detectable in almost all cases even several days after the diagnosis of the brain death. 3) LH reserve was maintained in three cases. FSH reserve was maintained in three cases. Prolactin reserve was maintained in two cases. TSH reserve was maintained in one case. 4) Blood ADH (antidiuretic hormones) were detectable in 7 cases out of 9 cases. The blood ADH level of one case, in particular, was rather high (above 10 pg/ml). 5) Histopathologically anterior pituitaries were examined in three autopsy cases. The central necrotic areas were observed in all cases, but normal pituitary tissues existed peripherally. And all anterior pituitary hormones could be recognized immunohistochemically. 6) The blood levels of the hypothalamic hormones (GRF, CRF, LH-RH) were measured in four cases. The hypothalamic hormones were detectable in all cases. In one case, the levels of GRF were within normal range even 9 or 15 days after the diagnosis of brain death.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Heterogeneous cellular environments modulate one-hit neuronal death kinetics.

We recently demonstrated that cell loss kinetics in diverse forms of neurodegeneration (ND) suggests a universal death switch mechanism in which each cell is at a constant risk to initiate apoptosis. We proposed that mutant and injured neurons exist in a viable state typified by an increased risk of initiating death processes [Clarke, Collins, Leavitt, Andrews, Hayden, Lumsden, McInnes, A one-hit model of cell death in inherited neuronal degenerations, Nature 406 (2000) 195-199]. To date, however, measurements of cell death risk have been available only as averages across the affected cell population. Here we develop and apply a method of death kinetic analysis in which the risk factors vary across the neuronal population, as for example due to regional heterogeneities in the cellular microenvironment. We find that most cases of ND for which cell loss data has been obtained are better explained by death risks that vary from cell to cell, compared to death risk that is constant across the neuronal population. Strikingly, a common form of the frequency distribution defining the death risk heterogeneity is shared across most of these cases. This first characterization of the kinetic heterogeneity in one-hit neuronal death, therefore, suggests that the wide variety of ND now known may share mechanisms through which regional differences in the cellular microenvironment modulate the kinetics of cell loss.

Animals↗
PubMed2001

Outcome after lung cancer surgery. Factors predicting early mortality and major morbidity.

OBJECTIVE: This study was undertaken to assess mortality, complications and major morbidity during the first 30 days after lung cancer surgery and to estimate the significance of presurgical risk factors. METHODS: The study was based on all patients referred for surgery for primary lung cancer from 1 January 1987 to 1 September 1999. There were in total 616 patients with primary lung cancer. Three-hundred and ninety-four were men and 222 women. Postoperative events studied were divided into major and minor complications or death during the first 30 days after surgery. The significance of risk factors for an adverse outcome (defined as death or major complication in the first 30 days postoperatively) was assessed by uni- and multivariate logistic regression analyses. RESULTS: During the study period an increasing number of women and of patients older than 70 years underwent surgery. Overall 30-day mortality was 2.9, 0.6% after single lobectomy and 5.7% after pneumonectomy. Major complications occurred in 54 patients (8.8%). Fifty-eight patients (9.5%) had an adverse outcome during the first 30 days. Male gender, smoker, FEV(1)< or =70% of expected value, squamous cell carcinoma and pneumonectomy were risk factors predicting adverse outcome in the univariate model. Pneumonectomy and FEV(1)< or =70%, were the only independently significant factors for adverse outcome. Only pneumonectomy was independently associated with an increased risk for early death. CONCLUSION: Our results show low mortality and morbidity after lung cancer surgery. However, patients with reduced lung capacity and those undergoing pneumonectomy should be treated with great care, as they run a considerable risk of major complications or death during the first 30 days postoperatively. Older age (>70 years) does not appear to be a contraindication to lung cancer surgery, but patients in this group should undergo careful preoperative evaluation.

Adult↗
PubMed2002

Prognostic value of continuous ST-segment monitoring in patients with non-ST-segment elevation acute coronary syndromes.

BACKGROUND: Patients with non-ST-segment elevation acute coronary syndromes constitute a heterogeneous group concerning prognosis. The 12-lead ECG at rest is recommended for early risk stratification but is unable to reflect the dynamic nature of myocardial ischemia and coronary thrombosis. This study investigated whether continuous ST-segment monitoring provides early prognostic information in such patients. METHODS: We prospectively studied 183 patients admitted due to chest pain at rest suggestive of an acute coronary syndrome. ST-segment monitoring was performed continuously for 24 hours from admission. Cardiac-specific troponin I levels were determined on admission and every 6 hours for the first 24 hours. The endpoint was defined as death or nonfatal myocardial infarction, whichever occurred first by 30 days follow-up. RESULTS: ST episodes, defined as transient ST deviations of at least 0.1 mV, were detected in 50 patients (27.3%) and associated with worse 30-day outcome: 22.0% endpoint rate compared to 6.8% for patients without ST episodes (P = 0.003). In a multivariate analysis, the presence of ST episodes (hazard ratio, 3.07; 95% CI, 1.26 to 7.46; P = 0.014) and peak troponin I levels > 0.2 microg/L (hazard ratio, 2.65; 95% CI, 1.01 to 6.95; P = 0.048) were independent predictors of prognosis. The combination of ST-segment monitoring and peak troponin I identified patients at low (2.5%, n = 79), intermediate (14.5%, n = 76), and high (25.0%, n = 28) risk for the 30-day endpoint. CONCLUSIONS: In patients with non-ST-segment elevation acute coronary syndromes, continuous ST-segment monitoring provides on-line early prognostic information, in addition to troponin I levels.

Aged↗
PubMed2006

Diabetes/obesity-related inflammation, cardiac cell death and cardiomyopathy.

Pathogenesis of diabetic cardiomyopathy (DCM) is a complicate and chronic process that is secondary to acute cardiac responses to diabetes. One of the acute responses is cardiac cell death that plays a critical role in the initiation and development of DCM. Besides hyperglycemia, inflammatory response in the diabetic heart is also a major cause for cardiac cell death. Diabetes or obesity often causes systemic and cardiac increases in tumor necrosis factor-alpha, interleukin-18 and plasminogen activator inhibitor-1. However, how these cytokines cause cardiac cell death remains unclear. It has been considered to relate to oxidative and/or nitrosative stress. We have demonstrated that metallothionein as a potent antioxidant or stress protein significantly protected the heart from oxidative damage and cell death caused by these cytokines, leading to effective prevention of DCM. The direct link of the inhibition of oxidative stress and damage to the prevention of cardiac cell death was defined by addition of superoxide or peroxynitrite specific inhibitor to completely prevent cytokine-induced cardiac cell death. Cardiac cell death is induced by the inflammatory cytokines that is increased in response to diabetes. Inflammatory cytokine-induced cardiac cell death is mediated by oxidative stress and is also the major initiator for DCM development.

Animals↗
PubMed1991

[Criteria of death and time of death--do Norwegian physicians follow laws and regulations?].

In Norway, death is defined as total and irreversible damage of the whole central nervous system. This means that the time of death is some minutes after circulatory arrest. The time lapse may vary from about five minutes up to 45 minutes, depending on the temperature in the brain when the circulation ceased. Five cases of spontaneous circulation after cessation of resuscitation are described. All the patients had asystoly, diagnosed on ECG by anaesthesiologists. The resuscitation had lasted for 30 minutes when the crew of the ambulance, which included a doctor, gave up. Two of the patients left the hospital alive, three died after some hours. One of the patients had no cerebral sequelae, the other developed dementia. Circulation may also start spontaneously after the doctor has diagnosed circulatory arrest in patients suffering from suffocation and exsanguination.

Aged↗
PubMed1985

Brain death and bioelectrical brain activity.

The effect of mechanical vibration and light stimulation on the ongoing and evoked bioelectrical activity was studied in two cases with clinically defined brain death and two other patients with severe head injury, one of them with an isoelectric EEG. The importance of such stimulation sequences for the definition of brain death is discussed, with particular emphasis on mechanical vibration.

Adult↗
PubMed1992

Apoptosis and DNA fragmentation precede TNF-induced cytolysis in U937 cells.

The hypothesis that activation of apoptosis and DNA fragmentation is involved in TNF-mediated cytolysis of U937 tumor cells was investigated. Morphological, biochemical, and kinetic criteria established that TNF activates apoptosis as opposed to necrosis. Within 2-3 h of exposure to TNF, U937 underwent the morphological alterations characteristic of apoptosis. This was accompanied by cleavage of DNA into multiples of nucleosome size fragments. Both of these events occurred 1-2 h prior to cell death as defined by trypan blue exclusion or 51Cr release. DNA fragmentation was not a non-specific result of cell death since U937 cells lysed under hypotonic conditions did not release DNA fragments. The percentage of cells undergoing apoptosis depended on the concentration of TNF and was augmented by the addition of cycloheximide. A TNF-resistant variant derived from U937 did not undergo apoptosis in response to TNF, even in the presence of cycloheximide. Furthermore, TNF could still activate NFkB in this variant, suggesting that this pathway is not involved in TNF-mediated cytotoxicity. Two agents known to inhibit TNF-mediated cytotoxicity, ZnSO4 and 3-aminobenzamide, were shown to inhibit TNF-induced apoptosis. Taken altogether, these data support the hypothesis that activation of apoptosis is at least one essential step in the TNF lytic pathway in the U937 model system.

Benzamides↗
PubMed2003

Pancreatitis in HIV infection: predictors of severity.

OBJECTIVES: Acute pancreatitis occurs at greater frequency in HIV-infected patients than in the general population. We set out to determine the frequency of severe acute pancreatitis in HIV-positive patients and to study the accuracy of The Acute Physiology and Chronic Health Evaluation (APACHE II), Ranson, and Glasgow scales for prediction of clinical disease severity. METHODS: A total of 73 HIV-infected patients with acute pancreatitis were identified retrospectively. Demographic and clinical parameters as well as clinical outcomes were established. Sensitivities and specificities of the three scales mentioned above were calculated and compared. RESULTS: Of the patients, 63 (83.6%) had AIDS. The majority of cases were medication-induced (46%) or idiopathic (26%). The incidence seemed to be declining in the late 1990s. Eleven patients (15%) had a severe course as defined by death, admission to the intensive care unit, or local complications requiring surgery. Eighteen case (24.6%) were considered severe as defined by the criteria established at the International Symposium on Acute Pancreatitis in Atlanta in 1992. APACHE II criteria best predicted outcome with an overall accuracy of 75% (Glasgow 69%, Ranson 48%). Maximal accuracy was achieved with cut-offs of 14 for APACHE II and 4 for the Glasgow and Ranson criteria. CONCLUSIONS: HIV-infected patients have a clinical outcome similar to that of the general population. Clinical predictive scales are applicable and useful in this population.

APACHE↗
PubMed2000

Validation of death certificate diagnosis of out-of-hospital coronary heart disease deaths in Olmsted County, Minnesota.

OBJECTIVE: To evaluate the validity of death certificate diagnosis of out-of-hospital (OOH) coronary heart disease (CHD) and sudden cardiac death (SCD) in Olmsted County, Minnesota, between 1981 and 1994. METHODS: In this review of the medical records, autopsy reports, and coroner's files, OOH deaths with heart disease as the underlying cause of death on the death certificate were classified into CHD (International Classification of Diseases, 9th Revision, Clinical Modification [ICD-9-CM] codes 410-414) and non-CHD (other ICD-9-CM heart disease codes) deaths. A 10% random sample (n = 174) of these death certificates was reviewed by physicians, and published validation criteria were applied to classify these deaths into validated CHD or non-CHD categories. Sudden cardiac death was defined as validated CHD that occurred at an OOH location with less than 24 hours between symptom onset and death. RESULTS: The death certificate definition of OOH CHD death (ICD-9-CM codes 410-414) had high sensitivity and positive predictive value of 91% and 96%, respectively. The specificity and the negative predictive value were slightly lower at 86% and 72%, respectively. The sensitivity of death certificate diagnosis of CHD for validated SCD was 89%, and the positive predictive value was 77%. Using a more restrictive definition of SCD, that is, less than 1 hour between the onset of symptoms and death, the positive predictive value of CHD codes for SCD was lower at 52%. CONCLUSIONS: In Olmsted County, the positive predictive values of death certificate diagnosis for OOH CHD and SCD are high. Relying on death certificate diagnoses results in about 5% underestimation of the true CHD rates, whereas their use as a surrogate for SCD yields a 16% overestimation of the true SCD rates.

Autopsy↗
PubMed2007

Mechanisms of mitotic cell death induced by chemotherapy-mediated G2 checkpoint abrogation.

The novel concept of anticancer treatment termed "G(2) checkpoint abrogation" aims to target p53-deficient tumor cells and is currently explored in clinical trials. The anticancer drug UCN-01 is used to abrogate a DNA damage-induced G(2) cell cycle arrest leading to mitotic entry and subsequent cell death, which is poorly defined as "mitotic cell death" or "mitotic catastrophe." We show here that UCN-01 treatment results in a mitotic arrest that requires an active mitotic spindle checkpoint, involving the function of Mad2, Bub1, BubR1, Mps1, Aurora B, and survivin. During the mitotic arrest, hallmark parameters of the mitochondria-associated apoptosis pathway become activated. Interestingly, this apoptotic response requires the spindle checkpoint protein Mad2, suggesting a proapoptotic function for Mad2. However, although survivin and Aurora B are also required for the mitotic arrest, both proteins are part of an antiapoptotic pathway that restrains the UCN-01-induced apoptosis by promoting hyperphosphorylation of Bcl-2 and by inhibiting the activation of Bax. Consequently, inhibition of the antiapoptotic pathway by genetic ablation of survivin or by pharmacologic inhibitors of Aurora B or cyclin-dependent kinase 1 lead to a significant enhancement of apoptosis and therefore act synergistically with UCN-01. Thus, by defining the mechanism of cell death on G(2) checkpoint abrogation we show a highly improved strategy for an anticancer treatment by the combined use of UCN-01 with abrogators of the survivin/Aurora B-dependent antiapoptotic pathway that retains the selectivity for p53-defective cancer cells.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

The person from Porlock. Ethical issues in terminal care: the Dutch perspective.

In the Netherlands medical decisions concerning end of life (MDEL) play a role in 38% of all deaths. Euthanasia, defined as an intentional termination of life by somebody else at an individual's request, is done in 1.8% of deaths. Only 4% of Dutch physicians would never perform or refer for euthanasia, and over 50% have performed euthanasia. Around 25,000 Dutch patients per year bring up euthanasia as a possibility in case suffering becomes unbearable; around 10% will finally have euthanasia performed. On the basis of these opinions and data the Dutch legislation has recently been reformed. Euthanasia remains a crime and each case will be reviewed by the district attorney. Court decisions, however, have confirmed the view that in some cases of euthanasia the physician may be confronted with conflicting obligations and therefore will not be punished. As a consequence, cases fulfilling a number of requirements will not be prosecuted. In conclusion, MDEL including euthanasia are considered ethically justifiable and legally permissible if they are part of an open, honest and careful approach to patients with unbearable suffering, in particular in the case of cancer.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Operative obstetric mortality at Harare Central Hospital 1992-1994: an anaesthetic view.

A prospective review of anaesthetic-associated deaths (AAD) was undertaken at the maternity unit of Harare Central Hospital, Zimbabwe, for the triennium 1992-1994. AAD was defined as death within 24 h of anaesthesia or failure to regain consciousness. Three groups of avoidable factors (obstetric, anaesthetic and administrative) were considered, and a scoring system used to allocate one avoidability point for each death with avoidable factors. Out of 9833 operative procedures (91% under general anaesthesia) there were 22 AADs. Avoidable factors were identified in 17 deaths (77%). Seven deaths were directly attributable to anaesthesia. Haemorrhage was the commonest cause of death, accounting for 10 cases. Common factors, identified in all instances of substandard anaesthetic and obstetric care, were emergency cases and lack of senior involvement. The problems are discussed and also viewed in the context of overall maternal mortality (outcome period 42 days). The mortality data are compared with those from the UK and some hospitals in South Africa. It is concluded that improvements in resources, education, guidelines and monitoring are necessary if the mortality rate is to be reduced.

Journal Article↗
PubMed2006

Cell death induced by serum deprivation in luteal cells involves the intrinsic pathway of apoptosis.

The corpus luteum is a transient endocrine gland specializing in the production of progesterone. The regression of the corpus luteum involves an abrupt decline in its capacity for producing progesterone followed by its structural involution, which is associated with apoptosis of the luteal cells. An in vitro experimental approach is needed to study the molecular mechanisms underlying hormonal regulation of luteal cell death under defined experimental conditions. In this study, we investigated simian virus-40-transformed luteal cells to determine whether they can be driven to apoptosis and, if so, to define the intracellular pathway involved. Luteal cells were cultured in the presence or absence of fetal bovine serum for 24 or 48 h. Under serum starvation conditions, the luteal cells underwent growth arrest accompanied by cell death as evaluated by dye exclusion, and confirmed by two-color fluorescence cell viability/cytotoxicity assay. We next studied whether serum starvation-induced death of luteal cells occurred by apoptosis. Morphologic features of apoptosis were observed in cells stained with hematoxylin after being subjected to serum starvation for 48 h. The apoptotic nature was further confirmed by in situ 3'-end labeling and fragmentation of genomic DNA. Apoptosis of serum-deprived luteal cells was dependent upon caspase activation. Serum starvation induced cleavage of poly (ADP-ribose) polymerase (PARP), suggesting that caspase-3 had been activated under the stress of withdrawal of growth factors. This was confirmed by cleavage of full-length procaspase-3. Finally, the fact that serum starvation promoted the cleavage of full-length procaspase-9 and the decrease in the expression of endogenous Bid, a BH-3-only proapoptotic protein of the Bcl-2 family, indicates that the intrinsic (i.e., mitochondrial) pathway of apoptosis was activated. In summary, we have characterized an in vitro experimental model of luteal cell death that can be utilized to evaluate the role of hormones in apoptosis of luteal cells under defined culture conditions, and to study the mechanism of luteal regression.

Animals↗
PubMed2003

Intravenous epinephrine in life-threatening asthma.

STUDY OBJECTIVE: Intravenous epinephrine is a potentially vital therapy for patients with life-threatening asthma but is often avoided because of concerns about its safety. We evaluated the safety of intravenous epinephrine in a series of adults with life-threatening asthma. METHODS: We performed an explicit retrospective chart review on a case series of 27 emergency department patients aged 19 to 58 years (mean 25 years) who were treated with intravenous epinephrine for a life-threatening exacerbation of asthma between 1989 and 1997. Explicit criteria for adverse effects, including cardiac arrhythmia or ischemia, hypotension or hypertension, neurologic injury, and death, were defined before chart review. RESULTS: No patient had an arrhythmia other than sinus tachycardia, and there were no cases of cardiac ischemia, hypotension, neurologic deficit, or death. CONCLUSION: Intravenous epinephrine was safe in this small series of younger adults with acute life-threatening asthma. A prospective trial of its use to better define an efficacy and risk-benefit relationship is justified.

Adult↗
PubMed1987

Auditing perioperative mortality.

An audit of mortality following operation was performed over ten years classifying deaths into those that were 'expected' and 'unexpected'. 'Unexpected' deaths were defined as those in which, after careful consideration of the prevailing clinical circumstances at the time of operation, the probability of death following operation was felt to be low. This definition is a more helpful assessment of surgical performance than overall perioperative mortality as it highlights cases where improvements in surgical management might be achieved. In audits involving surgical mortality, the classification of deaths into 'expected' and 'unexpected' is recommended.

Hospitalization↗