Teaching cause-of-death certification : lessons from international experience

The accuracy of cause-of-death statistics substantially depends on the quality of cause-of-death information in death certificates, primarily completed by medical doctors. Deficiencies in cause-of-death certification have been observed across the world, and over time. Despite educational interventions targeting to improve the quality of death certification, their intended impacts are rarely evaluated. This review aims to provide empirical evidence that could guide the modification of existing educational programs, or the development of new interventions, which are necessary to improve the capacity of certifiers as well as the quality of cause-of-death certification, and thereby, the quality of mortality statistics.

Quality of cause-of-death reporting using ICD-10 drowning codes : a descriptive study of 69 countries

Background: The systematic collection of high-quality mortality data is a prerequisite in designing relevant drowning prevention programmes. This descriptive study aimed to assess the quality (i.e., level of specificity) of cause-of-death reporting using ICD-10 drowning codes across 69 countries.---------- Methods: World Health Organization (WHO) mortality data were extracted for analysis. The proportion of unintentional drowning deaths coded as unspecified at the 3-character level (ICD-10 code W74) and for which the place of occurrence was unspecified at the 4th character (.9) were calculated for each country as indicators of the quality of cause-of-death reporting.---------- Results: In 32 of the 69 countries studied, the percentage of cases of unintentional drowning coded as unspecified at the 3-character level exceeded 50%, and in 19 countries, this percentage exceeded 80%; in contrast, the percentage was lower than 10% in only 10 countries. In 21 of the 56 countries that report 4-character codes, the percentage of unintentional drowning deaths for which the place of occurrence was unspecified at the 4th character exceeded 50%, and in 15 countries, exceeded 90%; in only 14 countries was this percentage lower than 10%.---------- Conclusion: Despite the introduction of more specific subcategories for drowning in the ICD-10, many countries were found to be failing to report sufficiently specific codes in drowning mortality data submitted to the WHO.

The properties of the international classification of the external cause of injury when used as an instrument for injury prevention research

Objective: To demonstrate properties of the International Classification of the External Cause of Injury (ICECI) as a tool for use in injury prevention research. Methods: The Childhood Injury Prevention Study (CHIPS) is a prospective longitudinal follow up study of a cohort of 871 children 5–12 years of age, with a nested case crossover component. The ICECI is the latest tool in the International Classification of Diseases (ICD) family and has been designed to improve the precision of coding injury events. The details of all injury events recorded in the study, as well as all measured injury related exposures, were coded using the ICECI. This paper reports a substudy on the utility and practicability of using the ICECI in the CHIPS to record exposures. Interrater reliability was quantified for a sample of injured participants using the Kappa statistic to measure concordance between codes independently coded by two research staff. Results: There were 767 diaries collected at baseline and event details from 563 injuries and exposure details from injury crossover periods. There were no event, location, or activity details which could not be coded using the ICECI. Kappa statistics for concordance between raters within each of the dimensions ranged from 0.31 to 0.93 for the injury events and 0.94 and 0.97 for activity and location in the control periods. Discussion: This study represents the first detailed account of the properties of the ICECI revealed by its use in a primary analytic epidemiological study of injury prevention. The results of this study provide considerable support for the ICECI and its further use.

Cause of Death, Trend and Disease Burden in Shandong Province, China : the Third Retrospective Sampling Survey of Cause of Death Report

This book describes the mortality for all causes of death and the trend in major causes of death since 1970s in Shandong Province, China.

Suspected mechanisms in the cause of overuse running injuries : A clinical review

Context: Various epidemiological studies have estimated that up to 70% of runners sustain an overuse running injury each year. Although few overuse running injuries have an established cause, more than 80% of running-related injuries occur at or below the knee, which suggests that some common mechanisms may be at work. The question then becomes, are there common mechanisms related to overuse running injuries? Evidence Acquisition: Research studies were identified via the following electronic databases: MEDLINE, EMBASE PsycInfo, and CINAHL (1980–July 2008). Inclusion was based on evaluation of risk factors for overuse running injuries. Results: A majority of the risk factors that have been researched over the past few years can be generally categorized into 2 groups: atypical foot pronation mechanics and inadequate hip muscle stabilization. Conclusion: Based on the review of literature, there is no definitive link between atypical foot mechanics and running injury mechanisms. The lack of normative data and a definition of typical foot structure has hampered progress. In contrast, a large and growing body of literature suggests that weakness of hip-stabilizing muscles leads to atypical lower extremity mechanics and increased forces within the lower extremity while running.

Designing a continuum of quality external cause of injury information in Queensland : from ambulance to hospital

This study is the first to employ an epidemiological framework to evaluate the ‘fit-for-purpose’ of ICD-10-AM external cause of injury codes, ambulance and hospital clinical documentation for injury surveillance. Importantly, this thesis develops an evidence-based platform to guide future improvements in routine data collections used to inform the design of effective injury prevention strategies. Quantification of the impact of ambulance clinical records on the overall information quality of Queensland hospital morbidity data collections for injury causal information is a unique and notable contribution of this study.

A locus on the long arm of chromosome 1 as a possible cause of essential hypertension

None of the genes responsible for essential hypertension has been identified. Recent work in genetically hypertensive rats has shown linkage of blood pressure with alleles of the renin gene. Since the renin gene is a member of a conserved synteny group that in humans spans chromosome 1q21.3-32.3 and includes the gene for antithrombin III (AT3), we used linkage studies to examine the relationship between alleles of AT3 and hypertension in a family having 10 affected members. From the lod score obtained at a recombination fraction of zero the odds for linkage of AT3 and hypertension in this family were calculated as 6:1 in favour of linkage. This result provides grounds for further examination of the possible role of the 1q23 locus in the aetiology of essential hypertension.

Chronic immune activation and inflammation as the cause of malignancy

Several chronic infections known to be associated with malignancy have established oncogenic properties. However the existence of chronic inflammatory conditions that do not have an established infective cause and are associated with the development of tumours strongly suggests that the inflammatory process itself provides the prerequisite environment for the development of malignancy. This environment includes upregulation of mediators of the inflammatory response such as cyclo-oxygenase (COX)-2 leading to the production of inflammatory cytokines and prostaglandins which themselves may suppress cell mediated immune responses and promote angiogenesis. These factors may also impact on cell growth and survival signalling pathways resulting in induction of cell proliferation and inhibition of apoptosis. Furthermore, chronic inflammation may lead to the production of reactive oxygen species and metabolites such as malondialdehyde within the affected cells that may in turn induce DNA damage and mutations and, as a result, be carcinogenic. Here it is proposed that the conditions provided by a chronic inflammatory environment are so essential for the progression of the neoplastic process that therapeutic intervention aimed at inhibiting inflammation, reducing angiogenesis and stimulating cell mediated immune responses may have a major role in reducing the incidence of common cancers. © 2001 Cancer Research Campaign http://www.bjcancer.com.

Assessing the threshold temperatures among different age and cause-of-deaths

The relationship between temperature and mortality is non-linear and the effect estimates depend on the threshold temperatures selected. However, little is known about whether threshold temperatures differ with age or cause of deaths in the Southern Hemisphere. We conducted polynomial distributed lag non-linear models to assess the threshold temperatures for mortality from all ages (Dall), aged from 15 to 64 (D15-64), 65- 84(D65-84), ≥85 years (D85+), respiratory (RD) and cardiovascular diseases (CVD) in Brisbane, Australia, 1996–2004. We examined both hot and cold thresholds, and the lags of up to 15 days for cold effects and 3 days for hot effects. Results show that for the current day, the cold threshold was 20°C and the hot threshold was 28°C for the groups of Dall, D15-64 and D85+. The cold threshold was higher (23°C) for the group of D65-84 and lower (21°C) for the group of CVD. The hot threshold was higher (29°C) for the group of D65-84 and lower (27°C) for the group of RD. Compared to the current day, for the cold effects of up to 15-day lags, the threshold was lower for the group of D15-64, and the thresholds were higher for the groups of D65-84, D85+, RD and CVD; while for the hot effects of 3-day lags, the threshold was higher for the group of D15-64 and the thresholds were lower for the groups of D65-84 and RD. Temperature thresholds appeared to differ with age and death categories. The elderly and deaths from RD and CVD were more sensitive to temperature stress than the adult group. These findings may have implications in the assessment of temperature-related mortality and development of weather/health warning systems.

Discerning the timing and cause of historical mortality events in modern Porites from the Great Barrier Reef

The life history strategies of massive Porites corals make them a valuable resource not only as key providers of reef structure, but also as recorders of past environmental change. Yet recent documented evidence of an unprecedented increase in the frequency of mortality in Porites warrants investigation into the history of mortality and associated drivers. To achieve this, both an accurate chronology and an understanding of the life history strategies of Porites are necessary. Sixty-two individual Uranium–Thorium (U–Th) dates from 50 dead massive Porites colonies from the central inshore region of the Great Barrier Reef (GBR) revealed the timing of mortality to have occurred predominantly over two main periods from 1989.2 ± 4.1 to 2001.4 ± 4.1, and from 2006.4 ± 1.8 to 2008.4 ± 2.2 A.D., with a small number of colonies dating earlier. Overall, the peak ages of mortality are significantly correlated with maximum sea-surface temperature anomalies. Despite potential sampling bias, the frequency of mortality increased dramatically post-1980. These observations are similar to the results reported for the Southern South China Sea. High resolution measurements of Sr/Ca and Mg/Ca obtained from a well preserved sample that died in 1994.6 ± 2.3 revealed that the time of death occurred at the peak of sea surface temperatures (SST) during the austral summer. In contrast, Sr/Ca and Mg/Ca analysis in two colonies dated to 2006.9 ± 3.0 and 2008.3 ± 2.0, suggest that both died after the austral winter. An increase in Sr/Ca ratios and the presence of low Mg-calcite cements (as determined by SEM and elemental ratio analysis) in one of the colonies was attributed to stressful conditions that may have persisted for some time prior to mortality. For both colonies, however, the timing of mortality coincides with the 4th and 6th largest flood events reported for the Burdekin River in the past 60 years, implying that factors associated with terrestrial runoff may have been responsible for mortality. Our results show that a combination of U–Th and elemental ratio geochemistry can potentially be used to precisely and accurately determine the timing and season of mortality in modern massive Porites corals. For reefs where long-term monitoring data are absent, the ability to reconstruct historical events in coral communities may prove useful to reef managers by providing some baseline knowledge on disturbance history and associated drivers.

Introduction: Epitope mimicry as a component cause of autoimmune disease

The causes of autoimmune diseases have yet to be fully elucidated. Autoantibodies, autoreactive T cell responses, the presence of a predisposing major histocompatibility complex (MHC) haplotype and responsiveness to corticosteroids are features, and some are possibly contributory causes of autoimmune disease. The most challenging question is how autoimmune diseases are triggered. Molecular mimicry of host cell determinants by epitopes of infectious agents with ensuing cross-reactivity is one of the most popular yet still controversial theories for the initiation of autoimmune diseases [1]. Throughout the 1990s, hundreds of research articles focusing to various extents on epitope mimicry, as it is more accurately described in an immunological context, were published annually. Many of these articles presented data that were consistent with the hypothesis of mimicry but that did not actually prove the theory. Other equally convincing reports indicated that epitope mimicry was not the cause of the autoimmune disease despite sequence similarity between molecules of infectious agents and the host. Some 20 years ago, Rothman [2] proposed a model for disease causation and I have used this as a framework to examine the role of epitope mimicry in the development of autoimmune disease. The thesis of Rothman’s model is that an effect, in this instance autoimmune disease, arises as a result of a cause. In most cases, multiple-component causes contribute synergistically to yield the effect, and each of these components alone is insufficient as a cause. Logically, some component causes, such as the presence of a particular autoimmune response, are also necessary causes.