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PubMed1997

Comparison of the APACHE III, APACHE II and Glasgow Coma Scale in acute head injury for prediction of mortality and functional outcome.

OBJECTIVES: This study examines the efficacy of the predicting power for hospital mortality and functional outcome of three different scoring systems for head injury in a neurosurgical intensive care unit (NICU). DESIGN: On the day of admission, data were collected from each patient to compute the Acute Physiology, Age, and Chronic Health Evaluation (APACHE) II and III, and Glasgow Coma Scale (GCS) scores. Hospital mortality was defined as the deaths of patients before discharge from hospital. Early mortality was defined as death before the 14th day after admission. Late mortality was defined as death after the 15th day from admission. Functional outcome was evaluated by Index of Independence in Activities of Daily Living (Index of ADL). SETTING: An 8-bed NICU in a 1270-bed medical center in Taichung Veterans General Hospital. PATIENTS AND PARTICIPANTS: Two hundred non-selected patients with acute head injury were included in our study in a consecutive period of 2 years. Patients less than 14 years old were not included. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Sensitivity, specificity and correct prediction outcome were measured by the chi-square method in three scoring systems. The Youden index was also obtained. The best cut-off point in each scoring system was determined by the Youden index. The difference in Youden index was calculated by Z score. A difference was also considered if the probability value was less than 0.05. The area under Receiver Operating Characteristic (ROC) curve was computed. Then the area under ROC of each scoring system was compared by Z score. There was statistical significance if p was less than 0.05. For prediction of hospital mortality, the best cut-off points are 55 for APACHE III, 17 for APACHE II and 5 for GCS. The correct prediction outcome is 82.4% in APACHE III, 78.4% in APACHE II and 81.9% in the GCS. The Youden index has best cut-off points at 0.68 for APACHE III 0.59 for APACHE II, and 0.56 for GCS. The area under Receiver Operating Characteristic (ROC) curve is 0.90 in the APACHE III, 0.84 in the APACHE II and 0.86 in the GVS. There are no statistical differences among APACHE III and II, and GCS in terms of correct prediction outcome, Youden Index and the area under the ROC curve. Other physiological variables excluding GCS in APACHE III and II (AP III-GCS, AP II-GCS) have less statistical value in the determination of mortality for acute head injury. For the prediction of late mortality, APACHE III and II yield significantly better results in the area under the ROC curve, correct prediction and Youden index than those of GCS. Other physiological variables (AP III-GCS and AP II-GCS) play an important role in the prediction of late mortality in APACHE scores. For prediction of the functional outcome of surviving patients with acute head injury, the APACHE III yields the best results of correct prediction outcome, Youden index and the area under the ROC curve. CONCLUSION: The APACHE III and II may not replace the role of GCS in cases of acute head injury for hospital or early mortality assessment. But for prediction of the late mortality, the APACHE III and II have better accuracy than GCS. Other physiological variables excluding GCS in the APACHE system play a crucial contribution for late mortality. GCS is simple, less time-consuming and economical for patients with acute head injury for the prediction of hospital and early mortality. The APACHE III provides better prediction for severe morbidity than GCS and APACHE II. Therefore, the APACHE III provides a good assessment not only for hospital and late mortality, but also for functional outcome.

APACHE↗
PubMed2004

Apoptosis-modulating agents in combination with radiotherapy-current status and outlook.

PURPOSE: To increase the therapeutic efficacy of ionizing radiation or to reduce radiation-mediated side effects, diverse research centers for translational radiation oncology have headed for a specific modulation of defined cellular death pathways. In this regard, several signaling systems have proved to be of high potential value. RESULTS: It has previously been shown that apoptotic pathways induced by ionizing radiation are distinct from death pathways triggered by death ligands such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). The combination of both radiation and TRAIL was highly efficient in vitro and in preclinical mouse models. However, several aspects of normal tissue toxicity have not been solved, and no Phase I data are available yet. A second approach tested in a Phase I trial is based on the observation that synthetic phospholipid derivatives (alkyllysophospholipids and alkylphosphocholines) strongly enhance apoptotic effects by modulating the balance among the mitogenic, anti-apoptotic MAPK, phosphatidylinositol 3'-kinase (PI3K)/Akt, and the pro-apoptotic SAPK/JNK signaling pathways. Furthermore, others have provided evidence that inhibition of anti-apoptotic signals generated by mitogenic stimuli may increase radiation responses. In this context, controversial data are available regarding the influence of a pharmacologic abrogation of MEK1, Erk1/2 signaling on apoptotic sensitivity but no Phase I trials of MEK inhibitors either alone or in combination with radiation have yet been published. However, inhibition of the PI3K/Akt survival pathway using compounds such as the protein kinase C (PKC) inhibitor PKC412 has been shown to induce apoptosis or to increase the apoptotic sensitivity of tumor cells. Therefore, these drugs may be used alone or in combination with radiation to increase tumor control; however, Phase I data are lacking. Several other drugs, including cyclooxygenase-2 inhibitors, betulinic acid, and proteasome inhibitors, have been shown to interact with apoptotic signal transduction. Again, most of the drugs have not been tested in combination with radiation in vivo or-in the case of cyclooxygenase-2 inhibitors-exert pleiotropic effects. CONCLUSION: Although the examples do not reflect all available strategies, it is clear that several promising approaches targeting defined cell death pathways have been developed and entered into clinical trials. The use of synthetic phospholipid derivatives in a Phase I trial is an important example, proving that basic research in radiation biology finally guides the development of new treatment strategies. This, and other approaches, will hopefully increase tumor control rates and reduce side effects in the future.

Apoptosis↗
PubMed2003

Defining the sudden infant death syndrome.

Sudden infant death syndrome (SIDS) is a term that was first proposed in 1969 for a distinctive subgroup of unexpected infant deaths that occur during the postneonatal period with relatively consistent clinical, epidemiological, and pathological features. This term played an important role by focusing attention on a major category of postneonatal infant death, providing support to grieving families, and diminishing the guilt and blame characteristic of these deaths. Unfortunately, the application of this term has become increasingly controversial. Some have applied it too liberally, and others not at all. According to the definition proposed in 1969, despite slight changes suggested in 1989, SIDS remains a diagnosis of exclusion. Although this syndrome has several distinctive features, including age distribution and apparent occurrence during sleep, there has been reluctance to include these features in the definition. The problems created by the lack of an adequate definition are discussed. A 2-tiered approach is suggested, with a more general definition intended primarily for case management and death administration, and a more restrictive one intended primarily for research purposes, which distinguishes those deaths closely fitting the classic SIDS profile from those with one or more less typical features.

Humans↗
PubMed2004

Fundamental principals of tumor necrosis factor-alpha gene therapy approach and implications for patients with lung carcinoma.

Apoptosis, known as programmed cell death, is defined as a cell's preferred form of death under hectic conditions through genetically conserved and complex pathways. There is a decisive balance between stimulatory and inhibitory signaling pathways to maintain homeostasis in cells. In order to shift the balance towards apoptosis, the modulation of both apoptotic and anti-apoptotic pathways represents an attractive target for cancer therapeutics. Currently, chemotherapy and radiotherapy are among the most commonly used treatment modalities against lung cancer. Tumor suppressor gene, p53, is required in order for both of these treatment methods to work as anti-tumor agents. As a result, tumors lacking p53 display resistance to both chemotherapy and radiotherapy. However, death ligands induce apoptosis regardless of p53 status of cells. Thus, these methods constitute a complementary therapeutic approach to currently employed conventional treatment modalities. At present, death ligands are being evaluated as potential cancer therapeutic agents. Since resistance to tumor necrosis factor (TNF)-alpha-mediated apoptosis represented an obstacle for the treatment of patients with lung carcinoma in the earlier attempts, an extensive research was recently initiated to understand molecular mechanism of TNF-alpha signaling. NF-kappaB transcription factors have been demonstrated to modulate the apoptotic program, mostly as blockers of apoptosis in different cell types. In this review, we concentrate on the current progress in the understanding of TNF-alpha-mediated apoptosis for lung carcinoma. Representative models of NF-kappaB-inhibiting gene therapy strategies from various labs including ours are also provided as examples of up-to-date approaches to defeat TNF resistance. In order to give the reader better understanding and appreciation of such approaches, previously unpublished in vivo assays are also incorporated into this review. Current progress in clinical trials using adenovirus-mediated delivery of TNF-alpha is also discussed.

Antineoplastic Agents↗
PubMed2002

Trends in fatal coronary heart disease among people aged 25-74 years in Oita City, Japan, from 1987-1998.

Serum cholesterol has been increasing in recent years in Japan. There is concern that risk of coronary heart disease (CHD) may be increasing too, but there is little information on validated fatal CHD trends in the Japanese population. We identified 1,056 deaths from heart disease and other deaths possibly hiding CHD from death certificates of residents aged 25-74 years in Oita City, Japan in 1987-1988, 1992-1993, and 1997-1998 (mean population, 273,000 in 1997-1998). We validated 994 of them by medical record review and physician interviews, classifying them into definite fatal acute myocardial infarction (AMI) and possible fatal AMI or CHD death based on Monitoring Trends and Determinants in Cardiovascular Disease project's criteria. Sudden death was defined to estimate the number of CHD sudden deaths. In men, age-adjusted mortality rates due to validated fatal CHD remained quite stable over 10 years (25.3 per 100,000 [95% CI, 15.0-35.5] in 1987-1988 to 24.2 per 100,000 [95% CI, 16.1-32.3] in 1997-1998). When 50% or all sudden deaths were included as fatal CHD, the rates for men tended to decline. This was due to decreasing out-of-hospital deaths in connection with a declining CHD death rate among men aged 65-74 years, whereas in-hospital CHD deaths were level. In women, the rate of validated fatal CHD was highest in 1992-1993, but the 1997-1998 rate was similar to the 1987-1988 rate. We did not find that fatal CHD rates increased in Oita men and women from 1987-1998. Rather, out-of-hospital fatal CHD tended to decline in Oita men.

Adult↗
PubMed2005

Mammographic screening before age 50 years in the UK: comparison of the radiation risks with the mortality benefits.

Mammographic screening before age 50 years is less effective than at older ages and the associated radiation risks are higher. We estimated how many breast cancer deaths could be caused and how many could be prevented by a decade of annual two-view mammographic screening starting at ages 20, 30 and 40 years, respectively, in the UK; for all women, and for women with first-degree relatives affected with breast cancer. We extrapolated from a radiation risk model to estimate the number of radiation-induced breast cancer deaths, and used results from randomised trials, which suggest a reduction in breast cancer mortality of 10-20% in women invited to screening before age 50 years, to estimate the number of deaths that could be prevented. The net change in breast cancer deaths was defined as the number of radiation-induced deaths minus the number of prevented deaths. For all women, assuming a reduction in mortality from screening of 20%, a decade of annual screening was estimated to induce more deaths than it prevents if started at age 20 years and at age 30 years (net increase = 0.86 and 0.37 breast cancer deaths, respectively, per 1000 women screened). The corresponding estimate for screening starting at age 40 years was a net decrease of 0.46 deaths/1000 women screened and a zero net change assuming a 10% mortality reduction. Results for women with first-degree relatives with breast cancer were generally in the same direction but, because their background incidence rates are higher, the net increases or decreases were greater. In conclusion, our estimates suggest that a decade of annual two-view mammographic screening before age 40 years would result in a net increase in breast cancer deaths, and that starting at age 40 years could result in a material net decrease only if breast cancer mortality is reduced by about 20% or more in women screened. Although these calculations were based on a number of uncertain parameters, in general, the conclusions were not altered when these parameters were varied within a feasible range.

Adult↗
PubMed1998

Risk of death or incapacitation after heart transplantation, with particular reference to pilots.

Pilots who have received a heart transplant may subsequently want to resume flying. This study was undertaken to determine whether a group of heart transplant recipients who had a particularly low risk of sudden unexpected death could be identified from clinical data. An event, "rapid-onset death," was defined incorporating a number of possible causes of death that could result in a heart transplant recipient-pilot losing control of an airplane. The survival of 3676 patients undergoing a first heart transplantation was 85% and 73% at 1 and 5 years, respectively, the hazard function having a high early phase of risk. When time zero was moved to the beginning of the second year after transplantation, the freedom from "rapid-onset death" at posttransplantation year 2 and posttransplantation year 5 was 96.8% and 88%, respectively. For patients who had both a "normal" coronary angiogram and no episodes of acute heart rejection during the first year transplantation, the probability of "rapid onset death" during the second posttransplantation year was 1.4%, and given the same circumstances, during the third posttransplantation year the risk of "rapid-onset death" was 1.6%. This information is potentially useful to the Federal Aviation Administration for policy decisions regarding this issue.

Adolescent↗
PubMed2005

Impact of definition on the study of avoidable mortality: geographical trends in British deaths 1981-1998 using Charlton and Holland's definitions.

Avoidable mortality is defined as deaths that should not occur given current medical knowledge and technology. Numerous different lists of causes of death and the ages at which they should be considered avoidable have been used to measure avoidable mortality. In this analysis of the importance of definition we compare the two most commonly used approaches using a data set including all 11.8 million deaths that occurred in Britain in 1981-1998. These mortality data, disaggregated by age and sex, are analysed within a multilevel statistical framework, which allows analysis at a number of geographical scales simultaneously. A substantial difference in both the average trends and spatial patterns of the two definitions of avoidable mortality is found, indicating that the causes of death chosen have a considerable impact on the results found. Indeed, one particular cause of death was found to be largely responsible for the differences between the definitions. In addition, the spatial pattern of the two types of avoidable mortality is very different at the larger geographical scale while the pattern at the smaller scale is very similar. The findings illustrate the importance of considering the goals of any study before deciding on the definition of avoidable mortality to use.

Adolescent↗
PubMed1997

Sudden cardiac death--preventable--reversible.

SCD is defined as unexpected death due to cardiac causes that occurs within 1 hour of acute symptoms. SCD can be reversed with the use of an ICD. These devices now can be implanted by catheter techniques, obviating thoracotomy. SCD is preventable. The incidence of SCD can be significantly reduced by addressing the fundamental pathophysiology of SCD, which primarily is CAD. Our combined and aggressive implementation of preventive regimens to reduce the risk of cardiac events will save lives. These measures include diet, weight reduction, smoking cessation, regular exercise, and therapeutic drugs. Amiodarone, although effective in preventing lethal ventricular arrhythmias, has not matched the long-term results of the ICD in the successful management of SCD.

Death, Sudden, Cardiac↗
PubMed1996

Aortic root complications in Marfan's syndrome: identification of a lower risk group.

OBJECTIVES: The purpose of this study was to examine clinical and echocardiographic predictors of outcome in a cohort of patients with Marfan's syndrome. BACKGROUND: Serial echocardiographic measurements of aortic root dimensions are an important clinical method for monitoring patients with Marfan's syndrome. However, there are few data on the prognostic importance of echocardiographic variables for risk stratification and timing of aortic root replacement. METHODS: In 89 consecutive patients with Marfan's syndrome (age range 1-54 years) clinical and serial echocardiographic data (n = 62) were evaluated as potential predictors of outcome (mean (range) follow up 4 (< 1-16) years). Aortic sinus diameter and an aortic ratio normalised for age and body surface area were examined using Kaplan-Meier life table and Cox regression analysis, with the end point defined as death or surgery for ascending aortic dissection and events defined as an end point or surgery for ascending aortic aneurysm. RESULTS: Overall actuarial survival at two and five years was 96% and 92% and event free survival was 85% and 76%, respectively. There were five deaths due to aortic dissection, four patients survived surgery for ascending dissection, and nine underwent root replacement with a composite graft for ascending aneurysm. Those with aortic events were older (35 (12) v 25 (13) years, P = 0.007) and had greater initial aortic root dimensions (47 (14) v 33 (8) mm, P < 0.0001) and ratios (1.6 (0.5) v 1.3 (0.2), P < 0.0001). In the 62 patients with serial echocardiographic follow up, the rate of aortic root dilatation was more rapid in those with events (15 (17) v 0 (3)%/year, P < 0.0001). Utilising a Cox proportional hazards model, the groups with an initial aortic ratio > or = 1.3 or an annual change in aortic ratio > or = 5% had a relative risk of an aortic complication of 2.7 and 4.1, respectively (95% confidence limits 1.5 to 4.8 and 1.8 to 9.3). Only one of 31 patients with an initial aortic ratio of < 1.3 and a rate of change of < 5% had an event (five year event free survival 97%). CONCLUSIONS: A low risk subgroup of patients with Marfan's syndrome can be identified as those with an aortic ratio < 1.3 and an annual change in aortic ratio of < 5%. These findings are helpful in optimising echocardiographic monitoring and risk stratification of patients with Marfan's syndrome.

Adolescent↗
PubMed1990

Symptoms, signs, and ill-defined conditions: a leading cause of death among minorities.

The Manual of the International Classification of Diseases, Injuries, and Causes of Death includes the category, "symptoms, signs, and ill-defined conditions" for nonspecific causes of death. To determine whether this categorization of cause of death is commonly applied to New Mexico's minority populations, the authors examined state vital records data for 1958-1982. Age-specific and age-adjusted death rates were calculated by 5-year intervals for Hispanics, American Indians, and non-Hispanic whites. Death rates attributed to symptoms, signs, and ill-defined conditions in all three major ethnic groups in New Mexico far exceeded the national rate for whites. For males in the period 1978-1982, American Indians had the highest rates (115.6 per 100,000 males), followed by Hispanics (58.3 per 100,000 males), and non-Hispanic whites (49.2 per 100,000 males); the national rates were 41.3 and 13.1 per 100,000 males for blacks and whites, respectively. Comparable differences were observed among females. The authors suggest that the death rate for deaths attributed to symptoms, signs, and ill-defined conditions may be a potential indicator of access to and use of health services and that the categorization may strongly affect cause-specific death rates in minority populations.

Adult↗
PubMed2000

[Death and dying - definition and determination.].

For the first half of this century there was no major dispute over the criteria for death. This was to change dramatically with major technological breakthroughs in modern medicine starting with the advent of the respirators. The consequences of their use raised serious questions about the traditional ways of diagnosing death. Today there are two different philosophical positions about what it means to be dead in terms of brain functions: One, which is not currently law in any jurisdiction, would pronounce a person dead when there is an irreversible loss of higher brain functions. This has been called cognitive death. The patient is not in a coma, because arousal mechanisms are present, the brain stem functions being relatively intact. The other philosophical position considers a person dead if there is an irreversible loss of the functions of the brain stem or the entire brain. The neurologic syndrome of brain death has been accepted by the medical profession as a distinct clinical entity that experienced physicians can diagnose with an extremely high degree of certainty, and can usually easily be distinguished from other neurologic syndromes. However, we must not lose sight of the fact that this is less a conclusion than a beginning. It is the task of philosophy to offer analyses of personhood and of personal identity that might support practical formulations for the determination of death and theology has reflected upon the meaning of death, if not its definition, from time immemorial. To define the death of a human being we must recognize the characteristics that are essential to humaneness. It is quite inadequate to limit the discussion to the death of the heart or the brain.

English Abstract↗
PubMed2004

Mitochondrial function in apoptotic neuronal cell death.

Apoptosis can be defined as the regulated death of a cell and is conducted by conserved pathways. Apoptosis of neurons after injury or disease differs from programed cell death, in the sense that neurons in an adult brain are not "meant" to die and results in a loss of function. Thus apoptosis is an honorable process by a neuron, a cell with limited potential to replace itself, choosing instead to commit suicide to save neighboring cells from release of cellular components that cause injury directly or trigger secondary injury resulting from inflammatory reactions. The excess of apoptosis of neuronal cells underlies the progressive loss of neuronal populations in neurodegenerative disorders and thus is harmful. Mitochondria are the primary source for energy in neurons but are also poised, through the "mitochondrial apoptosis pathway," to signal the demise of cells. This duplicity of mitochondria is discussed, with particular attention given to the specialized case of pathological neuronal cell death.

Animals↗
PubMed2006

[Probable cause of death after reclassification of ill-defined causes on hospital admissions forms in the Unified National Health System, Rio de Janeiro, Brazil].

This article describes the clinical and socio-demographic characteristics of deaths from ill-defined causes in the State of Rio de Janeiro, Brazil, in 1998, and reclassifies the groups of probable causes based on data from death certificates in the Mortality Information System and the Hospital Information System of the Unified National Health System (SIH-SUS) for 1997-98. Reclassification required a random sample of defined causes from the SIH-SUS. The technique used was probabilistic relationship of records. As compared to deaths with defined causes, in those with ill-defined causes the individuals were predominantly non-white, had less schooling, had died in Greater Metropolitan Rio de Janeiro, were less likely to have been hospitalized in the SUS, and were more likely to have died at home and without medical care. It was possible to reclassify 20% of deaths with ill-defined causes. Reclassification had a minor impact on proportional mortality, due to the size of this group (10% of the deaths). However, if the results could be applied to all deaths with ill-defined causes, the impact might be greater on proportional mortality.

Adolescent↗
PubMed2004

Interplay among platelet-activating factor, oxidative stress, and group I metabotropic glutamate receptors modulates neuronal survival.

Platelet-activating factor (PAF) is a potent phospholipid messenger in the nervous system that participates in synaptic plasticity and in pathologic processes, including neurodegeneration. Oxidative stress plays important roles in neuronal cell death. To define the interaction between PAF and oxidative radicals in neuronal death, we studied the effects of PAF in the presence of oxidative radicals in primary neurons in culture. Exogenous PAF (50 microM) caused PAF receptor-independent injury to neurons. A nonneurotoxic PAF concentration (500 nM) potentiated neuronal death caused by hydrogen peroxide as determined by lactate dehydrogenase (LDH) assay, Hoechst staining, and TUNEL analysis, but it did not potentiate neuronal death caused by menadione, a superoxide donor, or by the nitric oxide donors 3-morpholino-sydnonimine (SIN-1) and sodium nitroprusside (SNP). This potentiation of the hydrogen peroxide effect was selectively blocked by a PAF membrane-receptor antagonist, BN52021 (5 microM). The neurotoxic effect of PAF and hydrogen peroxide was also completely blocked by ebselen and partially decreased by pretreatment with (S)-3,5-dihydroxyphenylglycine (DHPG), a group I metabotropic glutamate receptor (mGluR) agonist. This study suggests that PAF-receptor antagonists may be useful for neuroprotection. A similar effect might also be obtained with group I mGluR agonists, probably by way of a different underlying mechanism.

Animals↗