PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Causes Of Death--changes”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed2003

The tumor-selective viral protein apoptin effectively kills human biliary tract cancer cells.

Biliary tract cancer, or cholangiocarcinoma, has a poor prognosis. Resection is the only curative treatment, but only a minority of patients are eligible. Chemotherapy and gamma-irradiation are merely palliative, as they are unable to remove the malignancy completely. The chicken anemia virus-derived protein apoptin induces apoptosis in a wide range of human tumor cells and is not hindered by mutations inactivating p53 or by overexpression of Bcl-2, changes known to frustrate chemotherapy and radiation therapy. We examined whether apoptin kills human biliary tract cancer cells. Expression of apoptin by means of plasmids caused extensive cell death in three independent cholangiocarcinoma cell lines, CC-LP, CC-SW, and Mz-ChA-1, regardless of their oncogenic mutations, which included inactivated p16 and p53 and the disruption of the transforming growth factor beta signaling pathway. In vitro delivery of apoptin by an adenoviral vector completely eradicated cholangiocarcinoma cells. Moreover, coexpression of the broad-spectrum caspase inhibitor p35 with apoptin only delayed the induced cell death. Changes in nuclear morphology still occurred early after transfection, and nuclei eventually disintegrated, suggesting that apoptin-induced cell death in these cells is not blocked by mutations in either the initiation or execution phase of apoptosis. The efficient induction of cell death by apoptin in cholangiocarcinoma cell lines makes apoptin an attractive candidate for molecular therapy of biliary tract cancer.

Adenoviridae↗
PubMed2005

Fatal poisoning in childhood, England & Wales 1968-2000.

We analysed deaths certified as due to poisoning in England & Wales, 1968-2000, in children aged <10 years by age, sex, circumstances of death, intent, and agents involved. The number of deaths fell from 165 (20.6 per million children) in 1968 to 30 (4.6 per million) in 2000, a decrease of approximately 80%. The age-specific death rates were similar in boys and girls. The rate was initially much higher, and fell more, in those aged <5 years. Most deaths (n=1923) occurred in fires, and had been attributed to inhaling combustion products. A small number (n=104) occurred in fires resulting from motor vehicle and other transport accidents. From 1979 (use of ICD-9) the coding of some of these deaths changed from poisoning with carbon monoxide to poisoning with 'other gases, fumes or vapours'. These 'fire deaths' do not appear as poisonings in mortality statistics based on a single underlying cause of death, and cannot be tabulated as poisoning in many countries. Fire deaths and deaths coded to accidental, deliberate, or undetermined poisoning (n=702) decreased substantially with time, and by 2000 numbered 14 and 10, respectively. Accidental deaths declined from 151 in 1968 to 23 in 2000, but homicides and open verdicts varied from 5 to 20 per year, with no clear trend. Deaths attributed to carbon monoxide and to 'other gases, fumes or vapours' (mostly fire-related) totalled 2431 (84% of all poisoning deaths). Overall, 10% of these deaths were either certified as homicides or open verdicts. However, homicide or open verdict was recorded in half of the 47 fatal opiate poisonings. Opioids have now superseded antidepressants as the commonest agents encountered in fatal poisoning with drugs in children.

Accidents↗
PubMed2002

Patterns and trends in prostate cancer incidence, survival, prevalence and mortality. Part I: international comparisons.

The international patterns and trends in prostate cancer incidence, survival, prevalence and mortality were examined. Age-standardized incidence and death rates among men in a variety of countries worldwide were obtained from various sources, survival rates from European sources and elsewhere, and prevalence estimates from the EUROPREVAL study. Results from many published studies were summarized. The incidence of prostate cancer varies widely around the world, with by far the highest rates in the USA and Canada. There has been a gradual increase in the incidence of prostate cancer since the 1960s in many countries and in most continents; there were large increases in the late 1980s and early 1990s in the USA, but increases have also occurred in countries with comparatively low incidence, e.g. India. Survival from prostate cancer improved during the 1970s and 1980s; further increases in the 1990s may be largely a result of earlier diagnosis. There were wide differences in survival across Europe, with rates in the UK well below the average, but all European rates were far below those in the USA. There was wide variation in the prevalence of prostate cancer in Europe; in some countries with high incidence and high life-expectancy, prostate cancers formed approximately 15% of all prevalent cancers in men. Mortality from prostate cancer has also increased in many countries, but to a lesser extent than incidence; this is consistent with the observed trends in survival. Mortality decreased slightly in the mid to late 1990s in several countries, including the USA, Canada, England, France and Austria. Part of the apparent increases in the incidence of prostate cancer has been associated with diagnostic artefacts (particularly detecting preclinical tumours through the increased use of transurethral resection) which may also have had an effect on death certification through the incorrect attribution of prostate cancer as the underlying cause of death. However, the greatest effect on the registration of new cases of prostate cancer has been the increased availability of prostate specific antigen testing during the early- to mid-1990s. Possibly, in addition to the effect of attribution bias, the earlier diagnosis of prostate cancers has contributed to the recent slight decreases in mortality. However, this is unlikely to account for much of the reduction, given the slow development of the disease from onset to death. Changes in disease management are probably more important. There are many strong arguments against introducing population-based screening for prostate cancer.

Adult↗
PubMed1997

The effect of enteric bacterial toxins on the catecholamine levels of the rabbit.

The rabbit catecholamine responses to bacterial toxins commonly found in Sudden Infant Death Syndrome (SIDS) victims were studied as part of a proposed animal model for SIDS. Six bacterial toxins commonly isolated from SIDS baby feces and a comparison endotoxin were injected intravenously (i.v.) and intraluminarily (i.l.) to determine their effects on catecholamine levels. I.v. injected toxins clearly altered catecholamine levels causing sharp rises in adrenaline and noradrenaline levels and at critical toxin concentrations sudden death ensued. Clostridium perfringens enterotoxin and alpha-toxin, Clostridium difficile enterotoxin (A) and cytotoxin (B), Escherichia coli STa toxin and staphylococcal enterotoxin B caused rises in catecholamine levels similar to that caused by E. coli endotoxin. Control rabbits showed very little or no obvious change in catecholamine levels. Clostridium difficile enterotoxin (A) and cytotoxin (B) injected i.v. exhibited synergy. Toxins injected into the duodenum, jejunum, ileum, cecum and large intestine caused behavioural changes ranging from reduced appetite and diarrhea to, in rare cases, death. Changes in the catecholamine levels of these animals however were not significantly different from those of the control animals. The results are discussed in relation to the possible effect of certain conditions (physiological, viral infections and environmental) which increase toxin permeability and allow absorption of these toxins, possibly resulting in sudden infant death.

Animals↗
PubMed1990

Perinatal mortality in Matlab, Bangladesh: a community-based study.

Perinatal deaths, comprising stillbirths and deaths during the first week of life, were monitored over the eight-year period 1979 to 1986 in a rural Bangladeshi population of 196,000. The perinatal mortality rate was 75 per 1000 total births. The rate was 13% higher in males than females. Stillbirth and early neonatal mortality rates were 37 and 38 per 1000 total births, respectively. The major causes of perinatal deaths are presented, as well as some of the maternal determinants. During the period under study, perinatal mortality declined regularly and significantly over time in an area covered by an intensive Family Planning and Health Services programme, but not in the adjacent control area. This raises the issue of the impact of such a programme upon perinatal mortality, and the need to include a strong maternity care component into primary healthcare strategies if further reductions of perinatal mortality are to be achieved.

Bangladesh↗
PubMed1993

Changes of perinatal statistics in a semiurban setup between two time periods in Malaysia.

Hospital University Sains Malaysia (HUSM) functions as the state referral centre and the only hospital for the state of Kelantan that can offer neonatal intensive care service. The deliveries in HUSM with grand multiparity, late booking and problems of late referrals resembles a hospital serving a semiurban rather than an urban community. A comparison between the year 1989 and 1991 showed marked improvement of perinatal mortality rate from 41.32 to 24.88, which is significantly better than the improvement achieved from 1987 to 1989 (46.0 to 41.32). This was possible due to a marked fall in the early neonatal mortality rate from 10.02 in 1989 to 5.45 in 1991 and fall in the stillbirth rate from 31.61 to 19.53.

Female↗
PubMed1989

Perinatal mortality in rural Tanzania.

Prolonged labour was the most frequent cause of perinatal death in a rural hospital in the south western highlands of Tanzania. After the introduction of an obstetric policy aiming to prevent prolonged labour by making use of the guidelines of the partogram, perinatal mortality was reduced from 71 to 39 per 1000 births. Baird's clinico-pathological classification is still considered a useful instrument for the discovery of avoidable factors in perinatal deaths. The concept of the partogram should be an integral part of the training of medical auxiliaries in the field of maternal and child health (MCH).

Delivery, Obstetric↗
PubMed1989

Classification of perinatal death.

Three paediatric pathologists, one perinatal paediatrician, one obstetrician, and one epidemiologist separately used information collected on 239 babies in an attempt to validate the Wigglesworth classification of perinatal deaths. This was first done using clinical data only, then using the combination of clinical and gross necropsy findings and finally using clinical, gross necropsy, histological and any other information (for example, chromosome analyses, microbiological investigations). Only 14 (6%) of deaths changed groups within the Wigglesworth classification when gross necropsy findings were considered as well as clinical findings, and altogether only 21 (9%) changed classification when complete investigations were available. There was an unacceptable amount (15%) of disagreement between the classifiers, largely the result of failure to comply with the rules laid down for classification. We set out amendments to Wigglesworth's original definitions to clarify certain ambiguities.

Autopsy↗
PubMed1994

Intracellular calcium concentrations during metabolic inhibition in the motoneuron cell line NSC-19.

Changes in the concentrations of intracellular free calcium ([Ca2+]i) and adenine nucleotides were determined in response to metabolic inhibitors in the motoneuron cell line NSC-19. The NADH dehydrogenase inhibitor amobarbital (Amytal) and the mitochondrial uncoupler carbonylcyanide m-chlorophenylhydrazone (CCCP) were used to alter energy metabolism. Exposure of cells to 5 mM Amytal did not significantly change ATP concentrations but produced transient elevations of [Ca2+]i of approximately 80 nM, which were reduced by 32% when cells were studied in Ca(2+)-free solutions. CCCP (10 microM) caused a transient reduction in ATP concentration of 33%. CCCP also produced sustained elevations of [Ca2+]i of about 280 nM, which were reduced by 47% when in Ca(2+)-free solutions. In spite of the sustained elevation of [Ca2+]i induced by CCCP, NSC-19 showed no reduction in cell viability after 48 h compared with controls. Ruthenium red, a blocker of Ca2+ uptake by mitochondria, had little effect on the CCCP-induced [Ca2+]i increment. KCl or glutamate did not produce significant changes in [Ca2+]i, indicating that these cells do not possess significant numbers of voltage-dependent Ca2+ channels or excitatory amino acid receptor-gated channels. [Ca2+]i values in these cells were modified by changes in extracellular Ca2+ concentrations. In Ca(2+)-containing solutions, inhibition of Na+/Ca2+ exchange by amiloride and bepridil led to increased [Ca2+]i, as did blockade of Ca2+ ATPase by vanadate, suggesting that membrane transporters are important in Ca2+ efflux in NSC-19. The present studies indicate that exposure of NSC-19 cells to Amytal and CCCP produces Ca2+ increments by release from internal stores, as well as by transmembrane influx. These results demonstrate that small increments in [Ca2+]i can be produced by metabolic inhibitors or other compounds and that such changes are not associated with immediate cell death. Changes in [Ca2+]i could potentially result in abnormal cell function secondary to altered action of Ca(2+)-dependent enzymes.

Adenine Nucleotides↗
PubMed2000

Dynamic changes in apoptotic and necrotic cell death correlate with severity of ischemia-reperfusion injury in lung transplantation.

Ischemia-reperfusion (IR) injury is a major cause of organ dysfunction following lung transplantation. We have recently described increased apoptosis in transplanted human lungs after graft reperfusion. However, a direct correlation between ischemic time, cell death, and posttransplant lung function has not yet been demonstrated. We hypothesized that an increased ischemic period would lead to an increase in cell death, and that the degree and type of cell death would correlate with lung function. To investigate this, we preserved rat lungs at 4 degrees C for 20 min and 6, 12, 18, and 24 h, and then transplanted the lungs and reperfused them for 2 h. Cell viability was determined with a triple staining technique combining trypan blue, terminal deoxynucleotidyl transferase-uridine nucleotide end-labeling, and propidium iodide nuclear staining. Percentages of apoptotic and necrotic cells were calculated from total cell numbers. Following 20 min and 6 and 12 h of cold preservation, less than 2% of graft cells were dead, whereas after 18 and 24 h of cold preservation, 11% and 27% of cells were dead (p < 0.05), the majority of which were necrotic. After transplantation and reperfusion, the mode of cell death changed significantly. In the 6- and 12-h groups, approximately 30% of cells were apoptotic and < 2% were necrotic, whereas in the 18- and 24-h groups, 21% and 29% of cells, respectively, were necrotic and less than 1% were apoptotic. Lung function (Pa(O(2))) decreased significantly (p < 0.05) with increasing preservation time. The percentage of necrotic cells was inversely correlated with posttransplant graft function (p < 0.0001). The study demonstrates a significant association among cold preservation time, extent and mode of cell death, and posttransplant lung function, and suggests new potential strategies to prevent and treat IR injury.

Animals↗
PubMed1998

Pathophysiology of cerebral ischemia.

The purpose of this manuscript is to briefly review the pathophysiology of cerebral ischemia. Ischemic thresholds are well-defined in lower animals. The concept of the ischemic penumbra may include regions of brain around deeper regions of ischemia but has also been defined in terms of brain salvageable by reperfusion or by pharmacological therapies. The principal pathophysiological processes in cerebral ischemia are energy failure, loss of cell ion homeostasis, acidosis, increased intracellular calcium, excitotoxicity, and free radical-mediated toxicity. The underlying biochemical processes are similar regardless of the amount of brain that is made ischemic or the duration of ischemia. The relative contributions of each process are believed to vary significantly especially in relation to the level of cerebral blood flow. Neurons may die by necrosis or apoptosis. In the core of an infarct where blood flow is very low, the predominant process is energy failure and rapid necrotic cell death. Reperfusion of ischemic tissue produces an influx of inflammatory cells and of oxygen that can cause increases in oxygen-derived free radicals. Free radicals are also important in prolonged ischemia. There is interest in changes in gene expression after ischemia. Induction of heat shock proteins suggests that gene expression changes may protect neurons from death. Changes in gene expression also may initiate apoptosis or other detrimental processes. Although advances have been made, there are still no proven pharmacological therapies to rescue ischemic human neurons. Such therapies do appear to be on the horizon.

Animals↗
PubMed1985

Changing patterns of perinatal and infant mortality in Western Australia: implications for prevention.

Perinatal and infant mortality rates have fallen dramatically in the developed world this century. A review of perinatal and infant mortality in Western Australia from 1970 to 1981 was undertaken, to examine trends in birthweight-specific and cause-specific rates. The predominant causes of death are now congenital malformation, stillbirth of unknown cause, preterm birth and cot death. Perinatal and infant mortality rates are unlikely to be reduced substantially until the reasons for these four causes of death are elucidated.

Australia↗
PubMed2002

["Natural cause of death or not?" How do nursing home physicians act when in doubt of natural cause of death?].

The objective of the study was to explore if nursing home physicians act by law, when they doubt the natural cause of death. In May 1999, a questionnaire was sent to 153 nursing home physicians in the region of Utrecht and Nijmegen. They were asked if they consult the coroner when they have doubts about the natural cause of death. Eighty-six percent (104) returned the questionnaire. Thirty-two percent of the nursing home physicians always consult the coroner and 52% does so most of the time. Only 12% does not consult the coroner most of the time and 2% never does. The main reasons for not consulting the coroner were that nursing home physicians judge a death after a fall as an incident that fits in the descending lifeline of patients and that some nursing home physicians had bad experiences consulting the coroner. We conclude that this policy may lead to underregistration of unnatural deaths. Changing the definition or changing the law may reduce this problem. Education and information can also contribute to change in physician's attitudes.

Accidents↗
PubMed2001

Why Did Cancer Deaths Increase in Japan after the Introduction of the Tenth Version of the International Classification of Disease? : Assessment Based on a Population-Based Cancer Registry.

Considerable increase in cancer deaths has been observed since 1995, after when the tenth version of the international classification of disease (ICD) was introduced in Japan according with the revision of a death certificate form at the same time. We assessed the contributing factors for this unnatural fluctuation, using a population-based cancer registry data as a model. All deaths of the prefectural residents are collated with the cancer registry database in the registration process. For all Japanese deaths of Aichi Prefecture in 1994 (n=41,111) and in 1995 (n=42,944), the description of the death certificates were compared with the ICD classified as the cause of death. It was ascertained that 97-99% of cancer and 97-98% of non-cancer deaths classified by ICD were proper. Among those classified as cancer as the cause of death and stated as other than the direct cause of death (n=92 in 1994, n=428 in 1995), only 22% (1994) and 8% (1995) were considered to be classifiable to both cancer and non-cancer as the cause of death. Among those who were classified as non-cancer as the cause of death in spite of including cancer in the original statement (n=770 in 1994, n=638 in 1995), 24% (1994) 10% (1995) were considered to be non-cancer as the cause of death, and the rest were considered classifiable into both cancer and non-cancer. Even if all cancer deaths classifiable to non-cancer were classified as non-cancer deaths, change in the number of cancer deaths was inconsiderable in both years. Therefore, it is suggested that the increase of cancer deaths after introduction of the new ICD was caused not by the artifact such as change in selection rule of disease when classify the cause of death, but by the improvement of the description of death certificate by physicians as a result of revision of death certificate form.

Journal Article↗
PubMedDate not supplied

Experiences of patients and significant others with automatic implantable cardioverter defibrillators after discharge from the hospital.

Sudden cardiac death (SCD) is a leading cause of mortality in this country. The automatic implantable cardioverter defibrillator (AICD) is a technology which has proven successful in reducing the risk of SCD in patients who qualify for it. However, little is known about how individuals adjust to living with the device. This field study used a focus group technique to investigate the question "What are the experiences of patients and their significant others (S.O.) in the time since being discharged from the hospital with an AICD?" Fifteen AICD recipients and 14 S.O.s each attended one of three focus groups which were tape recorded. Data from the transcriptions were analyzed by a combination of content analysis and ethnographic summary. The major concerns of the patients were [Physiologic], the sensations of being shocked, medications, trouble sleeping, dizziness (accompanied by heat intolerance at times), physical awareness of the device; [Psychosocial], fear, including fear of death and preparation for death, changes in mental functioning, changes in lifestyle including clothing not fitting, loss of control, driving an automobile, and spousal overprotectiveness. The primary psychosocial concerns of the S.O.s were fears, including fear of death and preparation for death, family and role changes, being overprotective and driving an automobile. Mental changes and heat intolerance have not been addressed in the literature previously.

Adaptation, Psychological↗
PubMed2004

The association of 6-minute walk performance and outcomes in stable outpatients with heart failure.

BACKGROUND: We sought to evaluate the prognostic value of the 6-minute walk test in stable outpatients with heart failure. METHODS AND RESULTS: We examined the association of 6-minute walk test distance and outcomes among 541 patients enrolled in the Digitalis Investigation Group trial. Patients were grouped by total distance (< or =200 m, 201 m-300 m, 301 m-400 m, and >400 m) with median follow-up of 32 months. All-cause mortality for patients who walked < or =200 m was significantly higher than patients who walked >200 m (43.9% versus 23.3%, P<0.001), but mortality was comparable among patients who walked >200 m (201 m-300 m: 23.7%, 301 m-400 m: 25.2%, >400 m 19.8%, P for trend 0.45). Results were similar for death due to worsening heart failure (< or =200 m: 29.3%, 201 m-300 m: 7.6%, 301 m-400 m: 6.7%, >400 m: 6.1%, P for trend <0.001). In multivariable analysis, distance < or =200 m remained associated with increased mortality (< or =200 m: hazard ratio (HR) 1.47, 95% CI 0.96-2.27; >200 m: HR 1.00, Referent; P=0.07) and death due to worsening heart failure (< or =200 m: HR 2.89, 95% CI 1.54-5.41; >200 m: 1.00, Referent; P=0.001). CONCLUSIONS: The 6-minute walk test identifies patients who walk less than 200 m as being at markedly increased risk of death. Changing the 6-minute walk test to a time- and distance-based standard would improve the efficiency of the test while retaining the bulk of the prognostic information.

Aged↗
PubMed1991

Perinatal mortality statistics in Harare 1980-1989.

Perinatal and neonatal mortality rates, in the Greater Harare Maternity Unit, which showed a modest decline from 1980 to 1985, have rise dramatically since then. Half of the rise in neonatal mortality rate is due to increased numbers and an increased mortality rate in babies of birth weight less than 1001g. There is also an increase in the numbers of deaths of large babies. There is a strong case for a broad-based on-going enquiry into the reasons for such changes.

Birth Rate↗