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PubMed2005

Pregnancy-associated death: a qualitative systematic review of homicide and suicide.

A systematic review of the literature on maternal homicide and suicide was performed to understand the causes of pregnancy-associated death. Forty-four studies examined homicide and/or suicide and pregnancy-associated death (defined as the death of a woman, from any cause, while she is pregnant or within 1 year of termination of pregnancy) (1). Of these studies, 747 homicides and 349 suicides were identified. All studies were included except duplicate datasets, case reports of less than 3 events, suicide attempts, unpublished manuscripts, review articles, or non-English studies. Homicide is a leading cause of pregnancy-associated death and suicide is also an important cause of death among pregnant and recently pregnant women. Healthcare providers should understand that homicide is a leading cause of pregnancy-associated death, most commonly as a result of partner violence. Therefore, screening for both partner violence and suicidal ideation are essential components of comprehensive medical care for women during and after pregnancy.

Adult↗
PubMed1995

Association between ease of suppression of ventricular arrhythmia and survival.

BACKGROUND: We tested the hypothesis that patients whose ventricular arrhythmias are easy to suppress have a lower rate of arrhythmic death, defined as arrhythmic death and nonfatal cardiac arrest, the primary end point in the Cardiac Arrhythmia Suppression Trials (CAST-I and CAST-II), than patients whose ventricular arrhythmias are hard to suppress. In addition, we evaluated the association between ease of suppression of ventricular arrhythmias and mortality of all causes. METHODS AND RESULTS: CAST-I investigated the effect on arrhythmic death of ventricular premature depolarization (VPD) suppression achieved by three drugs, encainide, flecainide, and moricizine, at two different dose levels; CAST-II investigated the same effect, using moricizine alone at three dose levels. If suppression was achieved, patients were randomized to the effective active drug or corresponding placebo. To examine the independence of easily suppressed ventricular arrhythmias as a predictor of arrhythmic death, we adjusted statistically for other variables that were related both to ease of suppression and arrhythmic death. Patients with ventricular arrhythmias (n = 1778) that were easy to suppress had fewer arrhythmic deaths during follow-up than those with ventricular arrhythmias that were hard to suppress (n = 1173) (relative risk, .59; P = .003). Patients whose VPDs were easily suppressed were older and had a lower frequency of prior history of heart failure and myocardial infarction. They also had a higher incidence of anterior myocardial infarction, VPD frequency, and average ejection fraction. After adjusting for these variables, we found that easily suppressed ventricular arrhythmias were still significant predictors of arrhythmic death (relative risk, .66; P = .013). CONCLUSIONS: This study shows that the ease of VPD suppression identifies a subgroup of postmyocardial infarction patients who have low risk of arrhythmic death.

Aged↗
PubMed1995

Sudden death, impaired glucose tolerance, and diabetes in Japanese American men.

BACKGROUND: Diabetes and glucose intolerance have been shown to increase the risk of cardiovascular mortality in a number of different populations. Most studies have been based on short follow-up periods, and few have had sufficient numbers to allow researchers to look at sudden death as an outcome. METHODS AND RESULTS: The relation of sudden death, defined as unexpected death occurring within either 1 or 24 hours of first symptoms, to glucose intolerance measured by a nonfasting 1-hour postload measurement made in 1965 or history of diabetes was examined by use of 23 years of follow-up on the 8006 participants enrolled in the Honolulu Heart Program. After adjustment for baseline body mass index, hypertension, cholesterol, triglycerides, smoking, alcohol consumption, and left ventricular hypertrophy or strain, the relative risks for sudden death within 24 hours in individuals with high-normal (151 to 224 mg/dL), asymptomatic high glucose values (> or = 225 mg/dL), and diabetes compared with those with lower glucose values (< 151 mg/dL) were 1.59, 2.22, and 2.76, respectively. All these relative risks were statistically significant (P < or = .05). Trends for sudden death in 1 hour were similar. Among men with sudden death < 1 hour after onset of symptoms, the strength of the association between diabetes and sudden death was stronger among those classified as having died of unknown causes who thus were more likely to have died of an arrhythmia than among those classified as having died of coronary heart disease. CONCLUSIONS: The relations seen in these analyses indicate that individuals with glucose intolerance or diagnosed diabetes are at increased risk for sudden death.

Aged↗
PubMed1990

Sudden death in ischemic heart disease.

Sudden death, defined as the death that occurs naturally, unexpectedly and instantaneously or within the first hour of the onset of premonitory symptoms, is one of the most important challenge of the modern cardiology. This is due to both, its elevated incidence (400,000 to 500,000 cases per year in United States alone) and its dramatic presentation (many of the victims are relatively young and have an acceptable quality of life). We have studied de Holter tapes of 233 patients who died suddenly and we can demonstrate that 80% of cases were due to ventricular tachyarrhythmias (ventricular fibrillation 60% and torsades de pointes 20%) and the rameinens 20% were due to bradyarrhythmias. It is well known that ischemic heart disease is the leading cause of sudden death, being responsible for more than 80% of cases. In the present article we will analyze the relationship between sudden death and the different types of ischemic heart disease: stable angina pectoris, unstable angina pectoris, acute myocardial infarction and postinfarction and silent myocardial ischemia.

Angina Pectoris↗
PubMed2026

A Multi-omics Regulated Cell Death Framework Defines Immune Phenotypes and Guides Precision Therapy in Colorectal Cancer.

Colorectal cancer (CRC) is molecularly and immunologically heterogeneous, contributing to variable treatment response. Because regulated cell death (RCD) intersects with tumor metabolism, immune regulation, and therapeutic susceptibility, we built an RCD-centered framework for CRC stratification. Multi-cohort transcriptomic data were used to infer RCD subtypes with non-negative matrix factorization (NMF) and non-negative least squares (NNLS). Genomic, bulk RNA-seq, single-cell RNA-seq, and spatial transcriptomic datasets were integrated to characterize subtype-associated biology. Machine-learning models were developed for immunotherapy response and survival-risk estimation. Candidate compounds were screened by GDSC2-based drug-sensitivity modeling and molecular docking, and FSTL3 was functionally assessed in vitro. The framework separated CRC samples into two RCD-related phenotypes resembling immune-hot and immune-cold states. RCD1 showed immune activation and higher mutational burden, whereas RCD2 showed immune-suppressed features, intratumoral heterogeneity, and aggressive biology. RCD-associated signatures showed potential for predicting immunotherapy response and survival risk. Dasatinib was prioritized for immune-cold, high-risk tumors, with preliminary evidence supporting its activity in CRC cells, while functional assays suggested a role for FSTL3 in growth, invasion, epithelial-mesenchymal transition, and apoptosis regulation. These findings suggest that RCD-based multi-omics analysis may refine CRC stratification and help generate therapeutic hypotheses.

Colorectal cancer↗
PubMed2003

Mortality rates and causes of death in a cohort of HIV-infected and uninfected women, 1993-1999.

HIV/AIDS-associated and non-HIV/AIDS-associated death rates and causes of death between 1993 and 1999 were examined in 885 HIV-infected women and 425 uninfected women of the HIV Epidemiology Research Study cohort. Causes of death were determined by review of death certificates and the National Death Index. Adjusted hazard ratios were calculated for mortality risk factors. In the 885 HIV-infected women and 425 uninfected women, 234 deaths and 8 deaths, respectively, occurred by December 31, 1999. All-cause death rates in the HIV-infected women were unchanged between the pre-HAART (1993-1996) and HAART eras (1997-1999)-5.1 versus 5.4 deaths per 100 person-years (py). AIDS as a cause of death decreased from 58% of all deaths in 1996 to 19% in 1999, while HAART use increased to 42% by the end of 1999. In spite of the modest proportion ever using HAART, HIV-related mortality rates did decline, particularly in women with CD4+ cell counts less than 200/mm(3). Drug-related factors were prominent: for the 129 non-AIDS-defining deaths, hepatitis C positivity (relative hazard [RH] 2.6, P <.001) and injection drug use (RH 1.7, P = 0.02) were strong predictors of mortality, but were not significant in the Cox model for 105 AIDS-defining deaths (RH 0.9, P >.30 and RH 0.7, P >.30, respectively. The regression analysis findings, along with the high percentage of non-AIDS deaths attributable to illicit drug use, suggest that high levels of drug use in this population offset improvements in mortality from declining numbers of deaths due to AIDS.

Adolescent↗
PubMed2006

Thorough validation of siRNA-induced cell death phenotypes defines new anti-apoptotic protein.

Loss-of-function by means of RNA interference in cultured human cells enables rapid pathway dissection on a genome-scale. Improved siRNA design and key validation protocols are required to eliminate falsely identified phenotypes resulting from potential off-target consequences. Here, we demonstrate a validation strategy involving several steps for verifying cell death phenotypes revealed during loss-of-function screening. First, from a set of 45 novel human genes we identified gene candidates that, when silenced, induce apoptosis in cultured HeLa cells. For those candidates, we performed more extensive validation with multiple effective siRNAs. In addition, we designed rescue experiments involving candidate genes delivered exogenously and containing silent mutations in the siRNA target regions. Rescue of the observed knockdown phenotype demonstrated an original and more stringent validation of the siRNA's selectivity and the phenotype specificity for the target gene. As a result, our data reveals an anti-apoptotic function for novel human breast adenocarcinoma marker BC-2, adding new depth to BC-2's description as a putative tumor marker involved in cancer related pathways.

Apoptosis↗
PubMed2005

The first organ transplant from a brain-dead donor.

In 1968, publication of the Harvard committee's report concerning "irreversible coma" established a paradigm for defining death by neurologic criteria (brain death [BD]). Five years earlier, Dr. Guy Alexandre, a Belgian surgeon, had not only adopted closely similar diagnostic criteria for BD but also applied those criteria in performing the first organ transplant from a brain-dead donor--a procedure many of his colleagues considered ethically unacceptable. To put those events into present-day perspective, the author reviewed the proceedings of a Ciba Symposium held in London in 1966 at which Alexandre introduced his pioneering view, obtaining information and documents from Alexandre and others who attended that meeting. Comparing Alexandre's approach with the Harvard report and later advances helps in understanding how both defining death by brain criteria and transplanting organs from a brain-dead donor have become morally tolerable today.

Brain↗
PubMed2005

Drotrecogin alfa (activated) for adults with severe sepsis and a low risk of death.

BACKGROUND: In November 2001, the Food and Drug Administration (FDA) approved drotrecogin alfa (activated) (DrotAA) for adults who had severe sepsis and a high risk of death. The FDA required a study to evaluate the efficacy of DrotAA for adults who had severe sepsis and a low risk of death. METHODS: We randomly assigned adult patients with severe sepsis and a low risk of death (defined by an Acute Physiology and Chronic Health Evaluation [APACHE II] score <25 or single-organ failure) to receive an intravenous infusion of placebo or DrotAA (24 microg per kilogram of body weight per hour) for 96 hours in a double-blind, placebo-controlled, multicenter trial. The prospectively defined primary end point was death from any cause and was assessed 28 days after the start of the infusion. In-hospital mortality within 90 days after the start of the infusion was measured, and safety information was collected. RESULTS: Enrollment in the trial was terminated early because of a low likelihood of meeting the prospectively defined objective of demonstrating a significant reduction in the 28-day mortality rate with the use of DrotAA. The study enrolled 2640 patients and collected data on 2613 (1297 in the placebo group and 1316 in the DrotAA group) at the 28-day follow-up. There were no statistically significant differences between the placebo group and the DrotAA group in 28-day mortality (17.0 percent in the placebo group vs. 18.5 percent in the DrotAA group; P=0.34; relative risk, 1.08; 95 percent confidence interval, 0.92 to 1.28) or in in-hospital mortality (20.5 percent vs. 20.6 percent; P=0.98; relative risk, 1.00; 95 percent confidence interval, 0.86 to 1.16). The rate of serious bleeding was greater in the DrotAA group than in the placebo group during both the infusion (2.4 percent vs. 1.2 percent, P=0.02) and the 28-day study period (3.9 percent vs. 2.2 percent, P=0.01). CONCLUSIONS: The absence of a beneficial treatment effect, coupled with an increased incidence of serious bleeding complications, indicates that DrotAA should not be used in patients with severe sepsis who are at low risk for death, such as those with single-organ failure or an APACHE II score less than 25.

APACHE↗
PubMed2006

Chemical genetic approaches to probing cell death.

Chemical genetics has arisen as a tool for the discovery of pathways and proteins in mammalian systems. This approach, comprising small-molecule screening combined with biochemical and genomic target identification methods, enables one to assess which proteins are involved in regulating a particular phenotype. Applied to cell death, this strategy can reveal novel targets and pathways regulating the demise of mammalian cells. Numerous diseases have been linked to the loss of regulation of cell death. Defining the mechanisms governing cell death in these diseases might lead to the discovery of therapeutic agents and targets and provide a richer understanding of the mortality of living systems. Recent advances include the discovery of novel small molecules regulating cell death pathways -- necrostatin and erastin -- as well as the elucidation of the mechanism of death induced in cancer cells by the cytotoxic agent Apratoxin A.

Animals↗
PubMed2000

Flow cytometry of apoptotic cell death.

The term apoptosis or programmed cell death defines a genetically encoded cell death program, which is morphologically and biochemically distinct from necrosis or accidental cell death. The characteristic morphological signs of apoptosis (cellular shrinkage, membrane blebbing, nuclear condensation and fragmentation) are the final results of a complex biochemical cascade of events which is an integral part of physiological homeostasis. Techniques designed to identify, quantitate and characterize apoptosis are numerous, but flow cytometry (FCM) remains the methodology of choice to study the apoptotic cascade in relation to cell type, trigger and time. This review outlines the main stages of the apoptotic cascade together with current FCM methods. All FCM apoptosis assays described have a solid experimental basis and have been used successfully in basic research on molecular and biochemical mechanisms of apoptosis. In various clinical settings the ability to follow the apoptotic process in patient samples may offer the rationale for optimal treatment schedules.

Apoptosis↗
PubMedDate not supplied

[Mortality in malignant brain tumors in Yugoslavia].

Malignant tumours of head and neck, as a common group of diseases, is mentioned in Yugoslavia for the first time in 1972, where as the american authors have been studying this group of diseases as a whole since 1954 (1969). The data about death persons of malignant brain tumours (codes 191), of all causes of death (codes 000-999), of defined death causes of all the neoplasms (codes 140-209) and neoplasms of head and necks (codes 140-149, 160-161, 190-193), according to the eighth and ninth Revision of the International Classification of Diseases, Lesions and Death Causes, are based on official data of the Institute of Statistics of Yugoslavia for the period 1969-1988 (1988). In the analysis of mortality were used the standardized death rates according to the method of direct standardization after the world population by Segi (1976), further specific death rates according to sex and age, proportions and linear trend (1983). The results of these researches have shown that in the period from 1969 to 1988 there were recorded in Yugoslavia 13687 dead of malignant brain tumours in all. The average standardized mortality rate was 2.94 per 100,000 inhabitants; it is higher in men (3.59), than in women (2.40). On the basis of the results of linear trend it is shown that the average standardized rates of total mortality are increasing (y = 2.94 + 0.16x); it is in the males y = 3.59 + 0.23x, in females y = 2.40 + 0.12x. Age specific mortality rates are the highest in the group 55-64 years (10.37%). In this group the risk of dying is much greater in the males (13.63%), than in the females (7.85%).

Brain Neoplasms↗
PubMedDate not supplied

Risk of perinatal death associated with labor after previous cesarean delivery in uncomplicated term pregnancies.

CONTEXT: Trial of labor after previous cesarean delivery is associated with increased risk of uterine rupture. However, no reliable data exist on the effect of a trial of labor on the risk of perinatal death in otherwise uncomplicated term pregnancies. OBJECTIVE: To determine the risk of intrapartum stillbirth or neonatal death not related to congenital abnormality among women with uncomplicated term pregnancies who had a trial of labor after previous cesarean delivery, compared with women having a planned repeat cesarean delivery, and multiparous and nulliparous women at term not delivered by planned cesarean method. DESIGN AND SETTING: Population-based, retrospective cohort study of data from the linked Scottish Morbidity Record and Stillbirth and Neonatal Death Enquiry encompassing births in Scotland between January 1, 1992, and December 31, 1997. POPULATION: A total of 313 238 singleton births between 37 and 43 weeks' gestational age in which the fetus was in a cephalic presentation. MAIN OUTCOME MEASURE: Delivery-related perinatal death, defined as intrapartum stillbirth or neonatal death unrelated to congenital anomaly, compared among the 4 groups. RESULTS: Among women who had a trial of labor following previous cesarean delivery (n = 15 515), the overall rate of delivery-related perinatal death was 12.9 (95% confidence interval [CI], 7.9-19.9) per 10 000 women. This was approximately 11 times greater (odds ratio [OR], 11.6; 95% CI, 1.6-86.7) than the risk associated with planned repeat cesarean delivery (n = 9014), more than twice (OR, 2.2; 95% CI, 1.3-3.5) the risk associated with other multiparous women in labor (n = 151 549), and similar to the risk among nulliparous women in labor (n = 137 160; OR, 1.3; 95% CI, 0.8-2.1). The associations were not explained by differences in maternal height, smoking status, socioeconomic status, age, fetal growth, or week of gestation at delivery. Among women having a trial of labor, the rate of death due to mechanical causes, including uterine rupture, was 4.5 (95% CI, 1.8-9.3) per 10 000 women. This was more than 8 times greater than other multiparous women (OR, 8.5; 95% CI, 3.2-22.3) and nulliparous women (OR, 8.8; 95% CI, 3.2-24.2). CONCLUSIONS: The absolute risk of perinatal death associated with trial of labor following previous cesarean delivery is low. However, in our study, the risk was significantly higher than that associated with planned repeat cesarean delivery, and there was a marked excess of deaths due to uterine rupture compared with other women in labor.

Adult↗