849 resultados para causes of death
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Objective To estimate the magnitude and characteristics of the injury burden in South Africa within a global context. Methods The Actuarial Society of South Africa demographic and AIDS model (ASSA 2002) – calibrated to survey, census and adjusted vital registration data – was used to calculate the total number of deaths in 2000. Causes of death were determined from the National Injury Mortality Surveillance System profile. Injury death rates and years of life lost (YLL) were estimated using the Global Burden of Disease methodology. National years lived with disability (YLDs) were calculated by applying a ratio between YLLs and YLDs found in a local injury data source, the Cape Metropole Study. Mortality and disability-adjusted life years’ (DALYs) rates were compared with African and global estimates. Findings Interpersonal violence dominated the South African injury profile with age-standardized mortality rates at seven times the global rate. Injuries were the second-leading cause of loss of healthy life, accounting for 14.3% of all DALYs in South Africa in 2000. Road traffic injuries (RTIs) are the leading cause of injury in most regions of the world but South Africa has exceedingly high numbers – double the global rate. Conclusion Injuries are an important public health issue in South Africa. Social and economic determinants of violence, many a legacy of apartheid policies, must be addressed to reduce inequalities in society and build community cohesion. Multisectoral interventions to reduce traffic injuries are also needed. We highlight this heavy burden to stress the need for effective prevention programmes.
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Although the effect of adverse environments on the well-being of children is an important global health issue, it remains underrecognized in health care and underconsidered in terms of both research and public policy. Children have developmentally distinct patterns of environmental exposure and susceptibilities that increase their risk of disease. Young children, especially those who are impoverished, have disproportionately heavier exposures to environmental threats in a given environment. They also have decreased metabolic capacity to detoxify and eliminate contaminants. Furthermore, rapid growth and development before and after birth and the continuing growth and postnatal maturation of the respiratory, immune, and neurological systems, in particular, make them increasingly vulnerable to environmental threats...
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An updated analysis of the previous analysis available here: http://eprints.qut.edu.au/76230/
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People humanize their ingroup to address existential concerns about their mortality, but the reasons why they do so remain ambiguous. One explanation is that people humanize their ingroup to bolster their social identity in the face of their mortality. Alternatively, people might be motivated to see their ingroup as more uniquely human (UH) to distance themselves from their corporeal “animal” nature. These explanations were tested in Australia, where social identity is tied less to UH and more to human nature (HN) which does not distinguish humans from animals. Australians attributed more HN traits to the ingroup when mortality was salient, while the attribution of UH traits remained unchanged. This indicates that the mortality-buffering function of ingroup humanization lies in reinforcing the humanness of our social identity, rather than just distancing ourselves from our animal nature. Implications for (de)humanization in intergroup relations are discussed.
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Chlamydial infections of fish are emerging as an important cause of disease in new and established aquaculture industries. To date, epitheliocystis, a skin and gill disease associated with infection by these obligate intracellular pathogens, has been described in over 90 fish species, including hosts from marine and fresh water environments. Aided by advances in molecular detection and typing, recent years have seen an explosion in the description of these epitheliocystis-related chlamydial pathogens of fish, significantly broadening our knowledge of the genetic diversity of the order Chlamydiales. Remarkably, in most cases, it seems that each new piscine host studied has revealed the presence of a phylogenetically unique and novel chlamydial pathogen, providing researchers with a fascinating opportunity to understand the origin, evolution and adaptation of their traditional terrestrial chlamydial relatives. Despite the advances in this area, much still needs to be learnt about the epidemiology of chlamydial infections in fish if these pathogens are to be controlled in farmed environments. The lack of in vitro methods for culturing of chlamydial pathogens of fish is a major hindrance to this field. This review provides an update on our current knowledge of the taxonomy and diversity of chlamydial pathogens of fish, discusses the impact of these infections on the health, and highlights further areas of research required to understand the biology and epidemiology of this important emerging group of fish pathogens of aquaculture species.
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Cardiovascular disease is the leading causes of death in the developed world. Wall shear stress (WSS) is associated with the initiation and progression of atherogenesis. This study combined the recent advances in MR imaging and computational fluid dynamics (CFD) and evaluated the patient-specific carotid bifurcation. The patient was followed up for 3 years. The geometry changes (tortuosity, curvature, ICA/CCA area ratios, central to the cross-sectional curvature, maximum stenosis) and the CFD factors (Velocity distribute, Wall Shear Stress (WSS) and Oscillatory Shear Index (OSI)) were compared at different time points.The carotid stenosis was a slight increase in the central to the cross-sectional curvature, and it was minor and variable curvature changes for carotid centerline. The OSI distribution presents ahigh-values in the same region where carotid stenosis and normal border, indicating complex flow and recirculation.The significant geometric changes observed during the follow-up may also cause significant changes in bifurcation hemodynamics.
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Stroke is one of the leading causes of death in the world, resulting mostly from the sudden ruptures of atherosclerosis carotid plaques. Until now, the exact plaque rupture mechanism has not been fully understood, and also the plaque rupture risk stratification. The advanced multi-spectral magnetic resonance imaging (MRI) has allowed the plaque components to be visualized in-vivo and reconstructed by computational modeling. In the study, plaque stress analysis using fully coupled fluid structure interaction was applied to 20 patients (12 symptomatic and 8 asymptomatic) reconstructed from in-vivo MRI, followed by a detailed biomechanics analysis, and morphological feature study. The locally extreme stress conditions can be found in the fibrous cap region, 85% at the plaque shoulder based on the present study cases. Local maximum stress values predicted in the plaque region were found to be significantly higher in symptomatic patients than that in asymptomatic patients (200±43. kPa vs. 127±37. kPa, p=0.001). Plaque stress level, defined by excluding 5% highest stress nodes in the fibrous cap region based on the accumulative histogram of stress experienced on the computational nodes in the fibrous cap, was also significantly higher in symptomatic patients than that in asymptomatic patients (154±32. kPa vs. 111±23. kPa, p<0.05). Although there was no significant difference in lipid core size between the two patient groups, symptomatic group normally had a larger lipid core and a significantly thinner fibrous cap based on the reconstructed plaques using 3D interpolation from stacks of 2D contours. Plaques with a higher stenosis were more likely to have extreme stress conditions upstream of plaque throat. The combined analyses of plaque MR image and plaque stress will advance our understanding of plaque rupture, and provide a useful tool on assessing plaque rupture risk.
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Individual and/or co-offenders fraudulent activities can have a devastating effect on a company’s reputation and credibility. Enron, Xerox, WorldCom, HIH Insurance and One.Tel are examples where stakeholders incurred substantial financial losses as a result of fraud and led to a loss of confidence in corporate dealings by the public in general. There are numerous theoretical approaches that attempt to explain how and why fraudulent acts occur, drawing on the fields of sociology, organisational, management and economic literature, but there is limited empirical evidence published in accounting literature. This qualitative inductive study analyses perceptions and experiences of forensic accountants to gain insights into individual fraud and co-offending in order to determine whether the conceptual framework developed from literature accurately depicts the causes of fraud committed by individuals and groups in the twenty-first century. Findings from the study both support and extend the conceptual framework, demonstrating that strain and anomie can result in fraud, that deviant sub-groups recruit and coerce members by providing relief from strain, and that inadequate corporate governance mechanisms both contribute to fraud occurring, and provide the opportunity for fraudulent activities to be executed and often remain undetected. Additional factors emerging from this study (the ‘technoconomy’, addiction and IT measures) were also identified as contributors to fraud, particularly relevant to the twenty-first century, and consequently, a refined conceptual framework is presented in the discussion and conclusion to the paper.
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To evaluate the underreporting rate of death -cause data in Shandong province during 2012 to 2013 by capture -mark -recapture method and to provide the base for health strategy. Methods All counties were divided into 5 stratifications according the death rates of 2012, and 14 counties were selected, then 3 towns or streets were selected in each country, 10 villages or neighborhood committees were selected in each town (street). The death data collected from security bureau and civil affairs bureau were compared with the reporting death data from the National Cause of Death Surveillance, and the underreporting rate was calculated. Results In present study, 6 929 death cases were collected, it was found that 1 556 cases were underreported. The death cases estimated by CMR method were 6 227 cases (95%CI: 7 593-7 651), and the average underreporting rate was 23.15%. There were significantly differences between different stratifications (P<0.01). The underreporting rate in 0-4 years old group was 56.93%, the male underreporting rate was 22.31% and the female underreporting rate was 24.09%. There was no significant difference between male and female groups (P>0.05). Conclusion There is an obvious underreport in the cause of death surveillance of Shandong province, and the underreporting rates are different among the 5 stratifications. The underreporting rate is higher in 0-4 years old group, and the investigation of the death cause surveillance for young residents is not perfect in some countries. The investigation quality of the death cause surveillance should be improved, increasing the integrity of the report data and adjusting the mortalities in different stratifications for obtaining a accurate mortality in Shandong province.
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Regardless of the existence of antibiotics, infectious diseases are the leading causes of death in the world. Staphylococci cause many infections of varying severity, although they can also exist peacefully in many parts of the human body. Most often Staphylococcus aureus colonises the nose, and that colonisation is considered to be a risk factor for spread of this bacterium. S. aureus is considered to be the most important Staphylococcus species. It poses a challenge to the field of medicine, and one of the most problematic aspects is the drastic increase of the methicillin-resistant S. aureus (MRSA) strains in hospitals and community world-wide, including Finland. In addition, most of the clinical coagulase-negative staphylococcus (CNS) isolates express resistance to methicillin. Methicillin-resistance in S. aureus is caused by the mecA gene that encodes an extra penicillin-binding protein (PBP) 2a. The mecA gene is found in a mobile genomic island called staphylococcal chromosome cassette mec (SCCmec). The SCCmec consists of the mec gene and cassette chromosome recombinase (ccr)gene complexes. The areas of the SCCmec element outside the ccr and mec complex are known as the junkyard J regions. So far, eight types of SCCmec(SCCmec I- SCCmec VIII) and a number of variants have been described. The SCCmec island is an acquired element in S. aureus. Lately, it appears that CNS might be the storage place of the SCCmec that aid the S. aureus by providing it with the resistant elements. The SCCmec is known to exist only in the staphylococci. The aim of the present study was to investigate the horizontal transfer of SCCmec between the S. aureus and CNS. One specific aim was to study whether or not some methicillin-sensitive S. aureus (MSSA) strains are more inclined to receive the SCCmec than others. This was done by comparing the genetic background of clinical MSSA isolates in the health care facilities of the Helsinki and Uusimaa Hospital District in 2001 to the representatives of the epidemic MRSA (EMRSA) genotypes, which have been encountered in Finland during 1992-2004. Majority of the clinical MSSA strains were related to the EMRSA strains. This finding suggests that horizontal transfer of SCCmec from unknown donor(s) to several MSSA background genotypes has occurred in Finland. The molecular characteristics of representative clinical methicillin-resistant S. epidermidis (MRSE) isolates recovered in Finnish hospitals between 1990 and 1998 were also studied, examining their genetic relation to each other and to the internationally recognised MRSE clones as well, so as to ascertain the common traits between the SCCmec elements in MRSE and MRSA. The clinical MRSE strains were genetically related to each other; eleven PFGE types were associated with sequence type ST2 that has been identified world-wide. A single MRSE strain may possess two SCCmec types III and IV, which were recognised among the MRSA strains. Moreover, six months after the onset of an outbreak of MRSA possessing a SCCmec type V in a long-term care facility in Northern Finland (LTCF) in 2003, the SCCmec element of nasally carried methicillin-resistant staphylococci was studied. Among the residents of a LTCF, nasal carriage of MR-CNS was common with extreme diversity of SCCmec types. MRSE was the most prevalent CNS species. Horizontal transfer of SCCmec elements is speculated to be based on the sharing of SCCmec type V between MRSA and MRSE in the same person. Additionally, the SCCmec element of the clinical human S. sciuri isolates was studied. Some of the SCCmec regions were present in S. sciuri and the pls gene was common in it. This finding supports the hypothesis of genetic exchange happening between staphylococcal species. Evaluation of the epidemiology of methicillin-resistant staphylococcal colonisation is necessary in order to understand the apparent emergence of these strains and to develop appropriate control strategies. SCCmec typing is essential for understanding the emergence of MRSA strains from CNS, considering that the MR-CNS may represent the gene pool for the continuous creation of new SCCmec types from which MRSA might originate.
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Within coronial investigations, pathologists are called upon to given evidence as to cause of death. This evidence is given great weight by the coroners; after all, scientific ‘truth’ is widely deemed to be far more reliable than legal ‘opinion’. The purpose of this paper is to examine the ontological and epistemological status of that evidence, from the perspectives of both the pathologists and the coroners. As part of an Australian Research Council Linkage Grant, interviews were conducted with seven pathologists and 10 coroners from within the Queensland coronial system. Contrary to expectations, and the work of philosophers of science, such as Feyerabend (1975), pathologists did not present their findings in terms of unequivocal facts or objective truths relating to causes of death. Rather, their evidence was largely presented as ‘educated opinion’ based upon ‘the weight of evidence’. It was actually the coroners who translated that opinion into ‘medical fact’ within the proceedings of their death investigations, arguably as a consequence of the administrative necessity to reach a clear-cut finding as to cause of death, and on the basis of their own understanding of the ontology of medical knowledge. These findings support Latour’s (2010) claim that law requires a fundamentally different epistemology to science, and that science is not entirely to blame for the extravagant truth-claims made on its behalf
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Regular electrical activation waves in cardiac tissue lead to the rhythmic contraction and expansion of the heart that ensures blood supply to the whole body. Irregularities in the propagation of these activation waves can result in cardiac arrhythmias, like ventricular tachycardia (VT) and ventricular fibrillation (VF), which are major causes of death in the industrialised world. Indeed there is growing consensus that spiral or scroll waves of electrical activation in cardiac tissue are associated with VT, whereas, when these waves break to yield spiral- or scroll-wave turbulence, VT develops into life-threatening VF: in the absence of medical intervention, this makes the heart incapable of pumping blood and a patient dies in roughly two-and-a-half minutes after the initiation of VF. Thus studies of spiral- and scroll-wave dynamics in cardiac tissue pose important challenges for in vivo and in vitro experimental studies and for in silico numerical studies of mathematical models for cardiac tissue. A major goal here is to develop low-amplitude defibrillation schemes for the elimination of VT and VF, especially in the presence of inhomogeneities that occur commonly in cardiac tissue. We present a detailed and systematic study of spiral- and scroll-wave turbulence and spatiotemporal chaos in four mathematical models for cardiac tissue, namely, the Panfilov, Luo-Rudy phase 1 (LRI), reduced Priebe-Beuckelmann (RPB) models, and the model of ten Tusscher, Noble, Noble, and Panfilov (TNNP). In particular, we use extensive numerical simulations to elucidate the interaction of spiral and scroll waves in these models with conduction and ionic inhomogeneities; we also examine the suppression of spiral- and scroll-wave turbulence by low-amplitude control pulses. Our central qualitative result is that, in all these models, the dynamics of such spiral waves depends very sensitively on such inhomogeneities. We also study two types of control chemes that have been suggested for the control of spiral turbulence, via low amplitude current pulses, in such mathematical models for cardiac tissue; our investigations here are designed to examine the efficacy of such control schemes in the presence of inhomogeneities. We find that a local pulsing scheme does not suppress spiral turbulence in the presence of inhomogeneities; but a scheme that uses control pulses on a spatially extended mesh is more successful in the elimination of spiral turbulence. We discuss the theoretical and experimental implications of our study that have a direct bearing on defibrillation, the control of life-threatening cardiac arrhythmias such as ventricular fibrillation.