Specific Causes Of Mortality Research Articles

Competing risks analysis of lamb mortality in a terminal sire composite population.

Mortality records from birth to weaning of 8,301 lambs from a composite population at the U.S. Meat Animal Research Center were analyzed using a competing risks model. The advantage of the competing risks model over traditional survival analyses is that different hazards of mortality can be assigned to different causes, such as disease, dystocia, and starvation. In this study, specific causes of mortality were grouped into dam-related (DAMR; e.g., dystocia and starvation), pneumonia (PNEU), disease (DIS; excluding pneumonia), and other (OTHER) categories. The hazard of mortality was analyzed using a competing risk approach, where each mortality category was assumed to be independent. Continuous- and discrete-time survival analyses were implemented using sire, animal, and maternal effects mixed models. The continuous-time survival analysis used the Weibull model to describe the hazard of mortality for each category of mortality. Under the discrete-time survival analysis, a complementary log-log link function was used to analyze animal-time data sets using weekly intervals for each category of mortality. Explanatory variables were sex, type of birth, contemporary group, and age of dam. The significant influences of type of birth and age of dam effects were consistent across category of mortality, and the sex effect was significant for all categories except the OTHER category. Estimates of variance components indicated strong maternal effects for all categories except for PNEU. Estimates of additive genetic heritabilities from the discrete maternal effects models were 0.08+/-0.04, 0.09+/-0.18, 0.16+/-0.12, 0.19+/-0.09, and 0.14+/-0.10 for OVERALL (all causes combined), DIS, DAMR, PNEU, and OTHER categories, respectively. Ignoring the cause of the defining event in mortality and longevity studies may hide important genetic differences. Therefore, the effectiveness of breeding programs relying on models that ignore multiple causes of an event in time-to-event data, such as mortality and longevity, could be affected.

ASSESSING THE RELATIVE IMPORTANCE OF DIFFERENT SOURCES OF MORTALITY FROM RECOVERIES OF MARKED ANIMALS

Overall mortality rates often are based upon a variety of mortality sources such as predation, disease, and accidents, and each of these sources may influence population dynamics differently. To better understand population dynamics or to derive effective conservation plans, it is thus crucial to know the frequency of specific mortality causes as well as their variation over time. However, although the mortality cause of retrieved marked animals is often known, this information cannot be used directly to estimate the frequency of a mortality cause. By calculating the ratio of the number of animals reported dead from a specific cause to the total number of retrieved animals, one does not consider the fact that the probability of finding a dead individual depends on the cause of its death. Although frequently used, such ad hoc estimates can be heavily biased. Here we present a new way of estimating the frequency of a mortality cause from ring-recovery (band-recovery) data without bias. We consider the states “alive,” “dead because of mortality cause A,” and “dead due to all other causes” and estimate within a multistate capture–recapture framework the transition probabilities as well as the state-specific resighting probabilities. Among the transition probabilities are the overall survival probability and the proportion of animals dying because of A. From these, the probability that an animal dies during a year due to the specific cause of interest (cause A kill rate) can easily be calculated. We illustrate this model using data from White Storks Ciconia ciconia ringed in Switzerland to estimate the proportion of storks that died due to power line collision. Average unbiased estimates of this proportion were 0.37 ± 0.08 (mean ± 1 se) for juveniles, about 25% lower than ad hoc estimates, and 0.35 ± 0.09 for adults. The annual survival rate of juveniles was 0.33 ± 0.05 and of adults, 0.83 ± 0.02. Power line mortality is thus important for White Storks, with about one in four juveniles and one in 17 adults dying each year because of power line collision. We discuss advantages and disadvantages of the new model and how the results could be used to explore the link between a specific mortality cause and population dynamics.

Commentary: Why the educational effect is so strong in differentials of mortality in Korea?

This paper presents educational mortality differentials in Korea. In particular this study stresses that amongst young people the poorly educated have a higher mortality than the well-educated group. This study agrees with findings from previous studies: there is a strong inverse relationship between education and all cause as well as specific causes of mortality in Korea and education contributes to the wider inequalities in health in Korea. (excerpt)

Effects of Dementia on Mortality in the Radiation Effects Research Foundation Adult Health Study

Background: Although dementia is rarely listed on death certificates, it does contribute to mortality. The predominant immediate causes of death coincident with dementia are pneumonia and cardiovascular diseases. Objective: To estimate the impact of dementia on specific mortality risks. Methods: We applied DSM-III/R criteria for Alzheimer’s disease (AD) and vascular dementia (VaD) to 2,172 subjects of the Adult Health Study of the Radiation Effects Research Foundation who were 60 or more years old when examined from 1992 to 1996. The underlying causes of death were compiled from death certificates. We performed a Poisson regression analysis to evaluate specific causes of mortality for which AD or VaD was a significant risk factor. Results: The relative risk of mortality was 2.2 for AD and 2.4 for VaD. Mortality from pneumonia and stroke was elevated for both types of dementia, independent of other medical conditions. AD was also associated with death from trauma. Conclusion: Dementia was a predictor of death due to pneumonia, stroke, and trauma among the Japanese elderly. The prevention and early detection of those conditions are important in the medical care and treatment of dementia cases.

Obesity in Teens Predicts Adult Mortality

Epidemiology| August 01 2003 Obesity in Teens Predicts Adult Mortality AAP Grand Rounds (2003) 10 (2): 16. https://doi.org/10.1542/gr.10-2-16 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Obesity in Teens Predicts Adult Mortality. AAP Grand Rounds August 2003; 10 (2): 16. https://doi.org/10.1542/gr.10-2-16 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search nav search search input Search input auto suggest search filter All PublicationsAll JournalsAAP Grand RoundsPediatricsHospital PediatricsPediatrics In ReviewNeoReviewsAAP NewsAll AAP Sites Search Advanced Search Topics: obesity Source: Engeland A, Bjørge T, Søgaard AJ, et al. Body mass index in adolescence in relation to total mortality: 32-year follow-up of 227,000 Norwegian boys and girls. Am J Epidemiol. 2003; 157:517–523. The relation between adult body mass index (BMI) and mortality has been extensively studied, but the relation between adolescent BMI and later mortality has not been previously established in a large population. These investigators from the Norwegian Institute of Public Health and the Norwegian Radium Hospital, Oslo, Norway, followed a cohort of 227,003 14- to 19-year-old Norwegian youth whose heights and weights were measured during tuberculosis screening in 1963–1975. They were followed for an average of 31.5 years, approximately 7.2 million person-years. A total of 7,516 deaths were recorded, with an increasing risk of death in adolescents whose BMI levels were greater than the 75th percentile. Mortality in males with baseline BMI between 85th-95th percentiles and above the 95th percentile (using US norms) was higher (RR 1.29; 95% CI, 1.14–1.47; and RR 1.82; 95% CI, 1.48–2.25, respectively) compared with those with baseline BMI between 25th-75th percentiles. The corresponding risk ratios among females were 1.31 (95% CI, 1.14–1.52) and 2.03 (95% CI, 1.51–2.72), respectively. Males with baseline BMI of 30 or greater had 125% higher mortality (95% CI, 79–185%) compared with BMI less than 25. Females with baseline BMI of 30 or greater had 114% higher mortality (95% CI, 61–182%). The specific causes of mortality were not determined in these data. The excess mortality among adolescents with high BMI was not detectable before they reached the age of 30 years. This study adds more weight to the evidence of the adverse impact of childhood obesity on adult mortality. Similar long-term risk of mortality related to adolescent obesity was found in a Dutch study.1 The authors of the current study recognize that the lack of information on many potential confounders—including smoking, social class, and physical activity—as well as the lack of cause-specific mortality information, adds some uncertainty to the interpretation of their results. Nonetheless, the data from this study are of concern and should strengthen our resolve to find effective ways to prevent and treat obesity in children. Prevention seems of paramount importance since obesity is notoriously difficult to reverse in children and adolescents.2 The oldest person in this study was 58, so longer follow-up may reveal even more about the long-term impact of adolescent obesity. This study adds to the list of potentially preventable adult diseases that have their origins in the pediatric age period including, among others, lung cancer, skin cancer, coronary heart disease, and osteoporosis. You do not currently have access to this content.

Recessions lower (some) mortality rates:: evidence from Germany

In his article with the provocative title “Are Recessions Good for Your Health?”, Ruhm (J. Health Econ. 21(4) (2000) 659) has found robust and consistent evidence that the total mortality rate, age-specific mortality rates as well as most specific mortality causes are pro-cyclical. His finding that high unemployment rates are associated with lower mortality and vice versa stands in stark contrast to Brenner's earlier work, who found the opposite effect, possibly after a time lag. Ruhm controls for state-specific effects in a panel of US states over the period 1972–1991, whereas Brenner's work is based on time-series analysis. Extending and improving upon Ruhm's original analysis, we analyse the effect of state unemployment and economic growth rates on mortality in the states of Germany over the period 1980–2000, both in a static and a dynamic econometric model. Controlling for state-specific effects, we find evidence that aggregate mortality rates for all age groups taken together as well as most specific age groups are lower in recessions. The same is true for mortality from cardiovascular diseases, pneumonia and influenza, motor vehicle accidents and suicides, but not for necessarily for other specific mortality causes. In particular, there is never a statistically significant effect on homicides, other external effects and malignant neoplasms. There are also few differences apparent between the effect on male and female mortality. If we do not control for state-specific effects, then we often arrive at the opposite result with higher unemployment being associated with higher mortality. This suggests that a failure to control for time-invariant state-specific effects leads to omitted variable bias, which would erroneously suggest that mortality rates move counter-cyclically. Overall, we can confirm Ruhm's main finding for another country: recessions lower some, but not all, mortality rates in the case of Germany.

Reliability of causes of death in persons with Type I diabetes

To compare causes of death assessed by a clinical review committee, the information given on death certificates, and ICD-codes provided by the State Documentation Office in deceased persons with Type 1 (insulin-dependent) diabetes mellitus. A cohort of 3674 patients were monitored for 10+/-3 (mean +/- SD) years. Vital status and end-stage diabetic complications were documented for 97%; 251 patients had died. Causes of death were assessed by a clinical review committee and compared to the information provided by death certificates and ICD-9 codes. The review committee defined a leading cause of death in 94% of cases, whereas death certificates were available for 73% and ICD-codes for 79% of patients; 10% of death certificates could not be evaluated due to insufficient information. Diabetes was mentioned on 71% of death certificates, and renal disease in 75% of cases with renal replacement therapy. There was acceptable agreement between the committee, death certificates and ICD-codes only for deaths due to neoplasma, and between the committee and death certificates for deaths due to acute myocardial infarction, cerebrovascular events and accidents. In only one out of four deaths due to hypoglycaemia and in four of seven deaths due to ketoacidosis was this diagnosis mentioned on the death certificate. No death due to hypoglycaemia or ketoacidosis and 41% due to suicide were identifiable by ICD-codes. Reliance on death certificates or ICD-codes as the only sources of information on the cause of specific mortality does not provide data of sufficient reliability for evaluation of clinical outcome in Type I diabetes.

Mortality in a Chinese Rubber Factory: A Prospective Cohort Study

Mortality in a Chinese Rubber Factory: A Prospective Cohort Study: Li Ke, et al. Preventive Branch, Shantou University Medical College—To determine the specific causes of mortality in the rubber industry with emphasis on the associations between cancer sites, ischemic heart, and cerebrovascular disorders and work places, A cohort of 1598 rubber workers (934 men, 664 women) were followed up for mortality from 1 January 1973 to 31 December 1997. Work histories of cohort members at the relevant work place were coded and computed by the factory personnel concerned and the record incorporated all job changes with relevant years. Standardized mortality ratios (SMRs) and 95% confidence intervals (95% CIs), controlling for age and calendar year and stratified by work area (employment in respective work areas for at least one year) were calculated from the reference rate. Significant increases in mortality were found for lung cancer among male workers in the curing department (16 deaths, 6.7 expected, SMR 2.39), liver cancer among male workers in the rubber overshoes department (2 deaths, 0.2 expected, SMR 10.00), cerebrovascular disorders among male workers in the rubber overshoes department (4 deaths, 1.0 expected, SMR 4.00), and cerebrovascular disorders among female workers in the mixing and milling department (7 deaths, 2.0 expected, SMR 3.50). Mortality from the remaining cancers was not substantially increased in any of the work departments. Mortality from several diseases was associated with specific work departments. Some of these associations have been reported previously and they may be causally related to occupational exposure in this industry, for example, lung cancer and the curing department. The study also found new risks, such as a possible increase in cerebrovascular disorders.

中華人民共和国のゴム工場における死亡状況 : 前向きコホート研究

Mortality in a Chinese Rubber Factory: A Prospective Cohort Study: Li KE, et al. Preventive Branch, Shantou University Medical College—To determine the specific causes of mortality in the rubber industry with emphasis on the associations between cancer sites, ischemic heart, and cerebrovascular disorders and work places, A cohort of 1598 rubber workers (934 men, 664 women) were followed up for mortality from 1 January 1973 to 31 December 1997. Work histories of cohort members at the relevant work place were coded and computed by the factory personnel concerned and the record incorporated all job changes with relevant years. Standardized mortality ratios (SMRs) and 95% confidence intervals (95% CIs), controlling for age and calendar year and stratified by work area (employment in respective work areas for at least one year) were calculated from the reference rate. Significant increases in mortality were found for lung cancer among male workers in the curing department (16 deaths, 6.7 expected, SMR 2.39), liver cancer among male workers in the rubber overshoes department (2 deaths, 0.2 expected, SMR 10.00), cerebrovascular disorders among male workers in the rubber overshoes department (4 deaths, 1.0 expected, SMR 4.00), and cerebrovascular disorders among female workers in the mixing and milling department (7 deaths, 2.0 expected, SMR 3.50). Mortality from the remaining cancers was not substantially increased in any of the work departments. Mortality from several diseases was associated with specific work departments. Some of these associations have been reported previously and they may be causally related to occupational exposure in this industry, for example, lung cancer and the curing department. The study also found new risks, such as a possible increase in cerebrovascular disorders. (J Occup Health 2002; 44: 76–82)

Physical activity and all-cause mortality: what is the dose-response relation?

The purpose of this review is to assess the dose-response relation between physical activity and all-cause mortality. We examined these parameters of physical activity dose: volume, intensity, duration, and frequency. We used a computer-assisted literature search to identify papers on this topic. After excluding papers examining only two levels of physical activity or fitness, papers investigating specific causes of mortality, reviews, and those not written in English, 44 papers satisfying all criteria were included in this review. There is clear evidence of an inverse linear dose-response relation between volume of physical activity and all-cause mortality rates in men and women, and in younger and older (> or = 60 yr) persons. Minimal adherence to current physical activity guidelines, which yield an energy expenditure of about 1000 kcal x wk(-1) (4200 kJ x wk(-1)), is associated with a significant 20--30% reduction in risk of all-cause mortality. Further reductions in risk are observed at higher volumes of energy expenditure. It is unclear whether a volume of <1000 kcal x wk(-1) also may be associated with lower risk; there are some data supporting this. Due to limited data, it is also unclear whether vigorous-intensity activity confers additional benefit beyond its contribution to volume of physical activity when compared with moderate-intensity activity. No data are available on duration and frequency of physical activity in relation to all-cause mortality rates after controlling for volume of physical activity. All studies in this review are observational studies, so conclusions are based on Evidence Category C. There is an inverse linear dose-response relation between volume of physical activity and all-cause mortality. Further research is needed to clarify the contributions of its components--intensity, duration, and frequency--to decreased all-cause mortality rates.

Sickle hemoglobin (HbS) allele and sickle cell disease: a HuGE review.

Sickle cell disease is caused by a variant of the beta-globin gene called sickle hemoglobin (Hb S). Inherited autosomal recessively, either two copies of Hb S or one copy of Hb S plus another beta-globin variant (such as Hb C) are required for disease expression. Hb S carriers are protected from malaria infection, and this protection probably led to the high frequency of Hb S in individuals of African and Mediterranean ancestry. Despite this advantage, individuals with sickle cell disease exhibit significant morbidity and mortality. Symptoms include chronic anemia, acute chest syndrome, stroke, splenic and renal dysfunction, pain crises, and susceptibility to bacterial infections. Pediatric mortality is primarily due to bacterial infection and stroke. In adults, specific causes of mortality are more varied, but individuals with more symptomatic disease may exhibit early mortality. Disease expression is variable and is modified by several factors, the most influential being genotype. Other factors include beta-globin cluster haplotypes, alpha-globin gene number, and fetal hemoglobin expression. In recent years, newborn screening, better medical care, parent education, and penicillin prophylaxis have successfully reduced morbidity and mortality due to Hb S.

Mortality and causes of death in a total national sample of patients with affective disorders admitted for the first time between 1973 and 1993.

The high mortality from suicide in patients admitted to hospital with an affective disorder is well documented, although specific causes of mortality and changes in mortality are less well studied. To describe the pattern of mortality in patients with affective disorder and to study changes in suicide risk during the study period. All patients (n = 54,103) admitted for the first time to a psychiatric hospital in Denmark during the period 1973-1993 because of affective disorder were included in this study. The mortality rate was compared with that of the general population. Mortality from natural and unnatural causes was elevated in all subgroups of affective disorder. The risk of suicide among patients ill for one year or less after first admission increased during the period 1973-1993. More attention should be paid to the risk of suicide and to physical illness in patients with affective disorders.

A further analysis of race differences in the National Longitudinal Mortality Study.

The purpose of this study was to investigate associations between race and specific causes of mortality among adults 25 years and older in the National Longitudinal Mortality Study. Mortality hazard ratios between races during 9 years of follow-up were estimated with Cox proportional hazards models, with control for multiple indicators of socioeconomic status (SES) and SES-relevant variables. Black persons younger than 65 years were at higher risk than others for all-cause and cardiovascular mortality; the strongest effects were observed among persons aged 25 through 44 years. Race, independent of SES, is related to mortality in American society, but these effects vary by age and disease categories.

Can Antiarrhythmic Drugs Survive Survival Trials?

Sudden cardiac death due to arrhythmic events is the major cause of mortality among early post-myocardial infarction (MI) patients, accounting for >250,000 deaths annually in the United States alone. Antiarrhythmic drugs can be used in such patients as well as in those who have not had a recent MI but are at high risk for sudden cardiac death (e.g., those with ventricular tachycardia/fibrillation, or who have survived cardiac arrest). Most antiarrhythmic drugs available, however, have limitations arising from their toxic and proarrhythmic potential. Thus, research and development of new agents and treatment modalities are desirable. This article seeks to enumerate the lessons of past clinical trials with these agents and to provide guidelines for future trials. That a variety of antiarrhythmic drugs have been associated with an increased mortality has been a disturbing observation. It is therefore imperative that candidates for antiarrhythmic therapy be selected appropriately. We recommend that future clinical trials use stringent criteria for the identification of patients at “high risk” for arrhythmia or sudden cardiac death, and limit recruitment to such patients. Traditional markers, such as the increased frequency and complexity of ventricular premature beats, and low left ventricular ejection fraction, have not been successful in identifying these high-risk patients. However, decreased heart rate variability and cardiac late potentials recorded on a signal-averaged electrocardiogram appear to be more specific markers of post-MI arrhythmia or sudden cardiac death and may, in conjunction with the traditional markers, be used to improve selection of trial populations. Since the risk of sudden cardiac death diminishes with time after MI, it is also recommended that the temporal window of treatment with antiarrhythmic agents be limited to 1 year post-MI. It is also important to define clearly the endpoints of efficacy evaluations. A short-term reduction on markers like ventricular ectopic beats, for example, does not translate into a long-term decrease in arrhythmia-related mortality. Therefore, a reduction in overall mortality is the only meaningful endpoint to define the true risk–benefit ratio. To limit exposure to the potentially adverse effects of these agents, target populations for prophylactic antiarrhythmic drugs should be limited to recent post-MI patients at high risk for sudden cardiac death due to arrhythmia. Avoiding exposure of low-risk patients to antiarrhythmic drugs is equally imperative. “Low risk” of all-cause mortality includes the group of post-MI patients with a left ventricular ejection fraction >36%. Risk must be continuously evaluated in the setting of other pharmacologic (angiotensin-converting enzyme [ACE] inhibitors, aspirin, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors [“statins”], and others) and/or nonpharmacologic interventions (coronary artery bypass graft, angioplasty, implantable cardioverter/defibrillator). There is also a need to improve noninvasive techniques for identifying patients in the high-risk category—at present, the presence of ventricular premature beats and a left ventricular ejection fraction <36% is considered somewhat predictive of sudden cardiac death. Thus, patients with a recent MI and moderately low left ventricular ejection fraction (≤36% but not <20%) may be considered for antiarrhythmic therapy. A subset analysis of patients with low heart rate variability can provide valuable additional information. It is important to note that although all-cause mortality is a valid endpoint for such trials, stratification by specific cause of mortality is desirable.

Causes of Losses Including a Borna Disease Paralytic Syndrome Affecting Young Ostriches of One Breeding Organization over a Five-Year Period (1989-1993)

Necropsy records and causes of mortality of ostriches up to 3 months old over a 5-year period (1989-1993) are presented. The data relate to one ostrich enterprise that comprises 10 breeding flocks, five rearing farms, and one hatchery. Causes of mortality are classified into nine major categories. The annual mortality percentages of all hatched ostriches over the 5-year period were 61%, 58%, 30%, 29%, and 16.6%, and the most significant cause of death was a paresis syndrome that accounted for 20%, 11%, 16%, 10.1%, and 2% mortality, respectively. Limb deformities and gastroenteritis were the other principal specific causes of mortality. The paresis syndrome was caused by an agent serologically related to Borna disease virus. Brain extracts from paralyzed ostriches, when given orally or intramuscularly to 5-week-old birds, reproduced the clinical signs and microscopic lesions. The mean time to death was less than 3 weeks for the intramuscularly infected group and was almost twice as long for the orally infected group.

Chronic lymphocytic leukemia: a retrospective study of 122 cases.

During the period 1978-1982 in the three northernmost countries of Sweden all 143 patients with a registered diagnosis of chronic lymphocytic leukemia (CLL) were retrospectively analyzed. After re-evaluation, 122 cases remained in the study. The mean age was 71 years and the male/female ratio was 2.2:1. Sixty-one patients were Binet stage A, 29 stage B and 32 stage C. The diagnosis CLL was made after routine check-up for other diseases in most of the patients and they had no symptoms from the CLL. The median survival was 51 months and there were no differences in crude survival according to stage or other prognostic factors such as hemoglobin, lymphocytes or thrombocytes in peripheral blood. Analysis of CLL as a cause of specific mortality showed the stage of CLL to have a slight prognostic significance. This could be due to the fact that many of the patients suffered from other serious diseases, allowing the detection of early stage or advanced CLL with no symptoms.

Postmarketing surveillance of the safety of cimetidine: 10 year mortality report.

A total of 9928 cimetidine users were identified from prescriptions in four centres and followed for 10 years. The 'all-cause' mortality ratio fell from 1.9 in year 1 to 1.0 in years 8 to 10. Most of the early excess in mortality was attributable to cimetidine being given in the late stages of many diseases, often to counter adverse gastric effects of other drugs. Specific causes of mortality during years 5-10 of the study, were generally unremarkable. Significant increases in mortality ratios were apparent, however, for oesophageal cancer (years 5-7, 2.3; years 8-10, 1.9); lung cancer (years 5-7, 1.1; years 8-10, 1.7); diseases of the oesophagus, stomach, and duodenum (years 5-7, 3.3; years 8-10, 2.3); and chronic liver disease (years 5-7, 2.4; years 8-10, 3.3). None of these increases in mortality seems to be attributable to an adverse effect of cimetidine use. Data are also presented for mortality from diseases of the nervous system. Eight deaths (of which one was miscoded) were certified as being from motor neurone disease, representing a mortality ratio of 2.6 for years 2-10 of the study which is of borderline statistical significance. This study confirms that cimetidine is safe. Mortality from some diseases increased over the study period, but selection rather than any adverse effect of the drug is likely to be the explanation.

Isolation of infectious pancreatic necrosis virus (serotype Ab) from diverse species of estuarine fish

Two significant fish kills occurred in the Pamlico River estuary (North Carolina, USA), one in December 1981 and January 1982, and the other in June 1982. The first involved only the southern flounder(Paralichthys lethostigma). Histopathologic examination of morbid and moribund flounder revealed extensive sloughing and necrosis of the mucosa of the pyloric caeca and intestine, and inflammation of the submucosa of the pyloric caeca. Brain and internal organ homogenates from morbid and moribund flounder were assayed on CHSE-214 cells, and a virus was isolated. Virus titers ranged from≤8.4 · 102 to 6.3 · 107 TCID50 per gram of tissue. Cross-plaque neutralization assays indicated that the southern flounder virus was infectious pancreatic necrosis virus serotype Ab. Immersion challenge showed the isolate is only slightly virulent for fry of brook trout(Salvelinus fontinalis). The second fish kill involved the southern flounder and six other species: hogchoker(Trinectes maculatus), Atlantic silverside(Menidia menidia), spot(Leiostomus xanthurus), Atlantic croaker(Micropogon undulatus), silver perch(Bairdiella chrysura), and striped mullet(Mugil cephalus). Virus was isolated from southern founder, hogchoker, Atlantic silverside, and spot. Neutralization assays indicated that the four isolates were nearly identical; however, the diversity of species affected suggests that the virus might not have been the specific cause of mortality.

Medication use and mortality

A logistic regression analysis of the association among specific causes of mortality and indices of psychotropic medication use was carried out among 722 psychiatric inpatient deaths and age, sex, diagnosis, and length of stay matched controls. Overall findings revealed remarkably few significant associations between death and drug use. Of the significant findings, an increased proportion of dead patients in three categories were using piperidine phenothiazines at death while young male patients dying of heart disease tended to be receiving significantly higher average daily doses of medications with strong anticholinergic effects than controls, often in combination. On the positive side, elderly living patients tended to be receiving tricyclic antidepressants for longer durations than controls for several death categories, suggesting a possible beneficial effect of medication use.

Variations in cancer mortality among local authority areas in England and Wales: relations with environmental factors and search for causes.

Geographical variations in specific causes of mortality among the 1366 local authority areas of England and Wales as defined at 1971 were studied by examining extracts from death certificates held on computer tape. Five items of information on each death--year of death, age at death, sex, local authority area of residence, and the underlying cause of death, during the 11 years 1968-78--permitted a more detailed investigation than had been possible before. Analysis of some early results of the study--including maps of mortality for pleural mesothelioma, nasal cancer and bladder cancer--suggested that, despite the known limitations of death certification, systematic study of the mortality of small areas may give clues to aetiological factors in the environment. Analyses relating mortality to the distribution of environmental factors and examining disease profiles of each area may also provide clues. These will be followed up by other methods of study, such as case-control techniques.