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Evolution drives, and is driven by, demography. A genotype moulds its phenotype's age patterns of mortality and fertility in an environment; these two patterns in turn determine the genotype's fitness [...]

Objective: Death rates in Australia are higher in rural than urban areas. Our objective is to examine causes of death of urban and rural women to gain insight into potential explanations for differences in mortality. Methods: Participants were a community-based random sample of women (n=12,400) aged 70-75 years when recruited in 1996 to the Australian Longitudinal Study on Women's Health. The main variables used were: area of residence classified according to the Australian Standard Geographic Classification (ASGC), survival to 31 October 2006, cause of death, selected risk factors. Results: The total number of deaths at 31 October 2006 was 2,803 and total number of women still alive was 9,597. Mortality was higher for women in rural areas overall (hazard ratio (HR)=1.09; 95% confidence interval (CI): 1.01-1.18) and for most major causes of death compared to urban women. In particular, death rates were substantially higher for lung cancer (HR=1.52; 95% CI: 1.03-2.25) and chronic obstructive pulmonary disease (COPD) (HR=1.83; 95% CI: 1.25-2.69). Nevertheless there were almost no differences among the groups for current smoking or smoking history. Prevalence of overweight and obesity was slightly higher and levels of physical activity lower among women in remote areas. Conclusion: There is little evidence that differences in mortality are due to the risk factors considered. Alternative explanations such as inequities in health services and environmental hazards should be considered. Implications: People in rural areas may suffer from a double disadvantage of poorer health services and exposure to health hazards that are less common in urban areas. Key words: Women's health, rural health, mortality. doi: 10.1111/j.1753-6405.2010.00623.x

Objectives. We examined mortality patterns across the lifespan of Native Hawaiians and compared mortality disparities across races. Methods. We determined the age-specific and age-adjusted mortality rates of Native Hawaiians from 1990 to 2000 by using national census and vital registration data. Results. Among Native Hawaiians aged younger than 1 year, expected deaths were 15% lower than for Blacks and 50% higher than for Whites. Among older adults, Native Hawaiians had higher rates of mortality compared with the general population, particularly in 1990 and 1995. Crude death rates for Native Hawaiians were similar to those for Blacks in 1990 and 1995 but were 20% lower than those for Blacks by 2000. Crude death rates for Native Hawaiians were 30% higher than for Whites in 1990 and 1995 and more than 40% higher than for Whites in 2000. Conclusions. Compared with Whites, Native Hawaiians and Blacks face similar challenges regarding infant and early-life mortality and increasing risks of mortality in mid-life and early old age. Our analyses document a need for renewed efforts to identify the determinants of ill health and commitment to address them. (Am J Public Health. 2010;100:2304-2310. doi:10.2105/AJPH.2009. 183541)

Objectives. We explored whether the introduction of 3 lifesaving innovations introduced between 1989 and 1996 increased, decreased, or had no effect on disparities in Black-White mortality in the United States through 2006. Methods. Centers for Disease Control and Prevention data were used to assess disease-, age-, gender-, and race-specific changes in mortality after the introduction of highly active anti-retroviral therapy (HAART) for treatment of HIV, surfactants for neonatal respiratory distress syndrome, and Medicare reimbursement of mammography screening for breast cancer. Results. Disparities in Black-White mortality from HIV significantly increased after the introduction of HAART, surfactant therapy, and reimbursement for screening mammography. Between 1989 and 2006, these circumstances may have accounted for an estimated 22441 potentially avoidable deaths among Blacks. Conclusions. These descriptive data contribute to the formulation of the hypothesis that federal laws promote increased disparities in Black-White mortality by inadvertently favoring Whites with respect to access to lifesaving innovations. Failure of legislation to address known social factors is a plausible explanation, at least in part, for the observed findings. Further research is necessary to test this hypothesis, including analytic epidemiological studies designed a priori to do so. (Am J Public Health. 2010;100:2176-2184. doi: 10.2105/ AJPH.2009.170795)

Objectives. We examined whether racial disparities in stage-specific colorectal cancer survival changed between 1960 and 2005. Methods. We used US Mortality Multiple-Cause-of-Death Data Files and intercensal estimates to calculate standardized mortality rates by gender and race from 1960 to 2005. We used Surveillance, Epidemiology, and End Results (SEER) data to estimate stage-specific colorectal cancer survival. To account for SEER sampling uncertainty, we used a bootstrap resampling procedure and fit a Cox proportional hazards model. Results. Between 1960-2005, patterns of decline in mortality rate as a result of colorectal cancer differed greatly by gender and race: 54% reduction for White women, 14% reduction for Black women, 39% reduction for White men, and 28% increase for Black men. Blacks consistently experienced worse rates of stage- specific survival and life expectancy than did Whites for both genders, across all age groups, and for localized, regional, and distant stages of the disease. Conclusions. The rates of stage-specific colorectal cancer survival differed among Blacks when compared with Whites during the 4-decade study period. Differences in stage-specific life expectancy were the result of differences in access to care or quality of care. More attention should be given to racial disparities in colorectal cancer management. (Am J Public Health. 2010;100: 1912-1916. doi: 10.2105/AJPH.2009.184192)

Objectives. Although research on health limitations has investigated gender differences in health and mortality, gender differentials in individual-level trajectories have been studied less frequently. Moreover, there are no studies on the relationship between course types and subsequent mortality. We investigate course types, explore confounding by socioeconomic and demographic correlates, and pose the question of whether the gender gap in morbidity results from differences in the onset of, and/or survival with, health limitations. Methods. Using the German Socioeconomic Panel, we identify individual trajectories of health limitations and use multinomial logistic regressions to explore confounding and the relationship with mortality. Results. The frequency of stable trajectories without limitations is lower among women because they tend to experience courses that involve extended periods of limitations and deteriorating health. Women also experience more frequently improvement after deterioration. The female mortality advantage is particularly large after health deterioration. Discussion. Health limitations do not make men and women more equal in the face of death. Our results are consistent with earlier studies showing that mortality selection and differences in chronic conditions may explain the gender gap in health and mortality. We extend previous research showing that the female health disadvantage is largely the result of their mortality advantage. Key Words: Gender--Germany Health limitations--Mortality--Trajectories. doi: 10.1093/geronb/gbp051.

A current focus of ecology is the investigation of spatial effects on population and community dynamics; however, spatiotemporal theory remains largely untested by empirical observations or experimental studies. For example, the segregation hypothesis predicts that intraspecific aggregation should increase the importance of intraspecific competition relative to interspecific competition, thereby enhancing local coexistence in plant communities. We applied recent methods of point pattern analysis to analyze a unique long-term data set on fully mapped seedling emergence and subsequent survival in a Mediterranean gorse shrubland after experimental fires and simulated torrential rainfall events. Our overall aim was to test if the observed spatial patterns were consistent with the segregation hypothesis during the entire community dynamics from early seedling emergence to the establishment of a mature community, i.e., we explored if the observed initial segregation did indeed prevent interspecific competition from becoming dominant. We used random labeling as the null model and specific test statistics to evaluate different biological effects of the spatial interactions that determine mortality. We found that mortality was clearly not random. Comparison of the probability of mortality in dependence on the distance to conspecific and to heterospecific plants showed that mortality was controlled almost entirely by intraspecific interactions, which is consistent with the segregation hypothesis. Dead plants were aggregated and segregated from surviving plants, indicating two-sided scramble competition. Spatial interactions were density dependent and changed their sign over the course of time from positive to negative when plants grew to maturity. The simulated torrential rainfall events and subsequent erosion caused nonspecific mortality of seedlings but did not reduce the prevalence of intraspecific competition. Our results provide support for the hypothesis that the spatial distribution of plants may profoundly affect competition and can be an important determinant in the coexistence of species and biodiversity. Key words: facilitation; fire; Mediterranean shrubland; pair correlation function; random mortality hypothesis; scramble and contest competition; spatial point pattern analysis.

Whether different sources of mortality are additive, compensatory, or depensatory is a key question in population biology. A way to test for additivity is to calculate the correlation between cause-specific mortality rates obtained from marked animals. However, existing methods to estimate this correlation raise several methodological issues. One difficulty is the existence of an intrinsic bias in the correlation parameter. Although this bias can be formally expressed, it requires knowledge about natural survival without any competing mortality source, which is difficult to assess in most cases. Another difficulty lies in estimating the true process correlation while properly accounting for sampling variation. Using a Bayesian approach, we developed a state-space model to assess the correlation between two competing sources of mortality. By distinguishing the mortality process from its observation through dead recoveries and live recaptures, we estimated the process correlation. To correct for the intrinsic bias, we incorporated experts' opinions on natural survival. We illustrated our approach using data on a hunted population of wild boars. Mortalities were not additive and natural mortality increased with hunting mortality likely as a consequence of non-controlled mortality by crippling loss. Our method opens perspectives for wildlife management and for the conservation of endangered species. Key words: Bayesian inference; cause-specific mortalities; compensatory mortality; depensatory mortality; mark--recapture; mixture of information; multistate models; ring-recoveries; wild boar.

We hypothesized that a small molecule CXCR4 antagonist, AMD3100 (AMD), could augment the mobilization of bone marrow (BM)-derived endothelial progenitor cells (EPCs), thereby enhancing neovascularization and functional recovery after myocardial infarction. Single-dose AMD injection administered after the onset of myocardial infarction increased circulating EPC counts and myocardial vascularity, reduced fibrosis, and improved cardiac function and survival. In mice transplanted with traceable BM cells, AMD increased BM-derived cell incorporation in the ischemic border zone. In contrast, continuous infusion of AMD, although increasing EPCs in the circulation, worsened outcome by blocking EPC incorporation. In addition to its effects as a CXCR4 antagonist, AMD also up-regulated VEGF and matrix metalloproteinase 9 (MMP-9) expression, and the benefits of AMD were not observed in the absence of MMP-9 expression in the BM. These findings suggest that AMD3100 preserves cardiac function after myocardial infarction by enhancing BM-EPC-mediated neovascularization, and that these benefits require MMP-9 expression in the BM, but not in the ischemic region. Our results indicate that AMD3100 could be a potentially useful therapy for the treatment of myocardial infarction. angiogenesis | stem cell | vasculogenesis doi/ 10.1073/pnas.0914248107

The effect of the presence of sulfide on the survival of benthic organisms under hypoxia was tested using a meta-analysis of published experimental results evaluating the effects of the presence of hydrogen sulfide on the median survival time of benthic macrofauna under hypoxia. The meta-analysis confirmed that survival times under hypoxia are reduced by an average of 30% in marine benthic communities exposed to hydrogen sulfide. The effect of sulfide on survival was higher for egg forms than for juvenile or adult stages. The aggravation of the negative effects of spreading hypoxia in the presence of sulfide suggests that the threats derived from hypoxia to marine biodiversity are greater than anticipated on the basis of the direct effects of low oxygen concentration alone. doi: 10.4319/lo.2010.55.3.1075

Objective: Maori women in New Zealand have higher incidence of and mortality from cervical cancer than non-Maori women, however limited research has examined differences in treatment and survival between these groups. This study aims to determine if ethnic disparities in treatment and survival exist among a cohort of Maori and non-Maori women with cervical cancer. Methods: A retrospective cohort study of 1911 women (344 Maori and 1567 non-Maori) identified from the New Zealand Cancer Register with cervical cancer (adenocarcinoma, adenosquamous or squamous cell carcinoma) between 1 January 1996 and 31 December 2006. Results: Maori women with cervical cancer had a higher receipt of total hysterectomies, and similar receipt of radical hysterectomies and brachytherapy as primary treatment, compared to non-Maori women (age and stage adjusted). Over the cohort period, Maori women had poorer cancer specific survival than non-Maori women (mortality hazard ratio (HR) 2.07, 95% confidence interval (CI): 1.63-2.62). From 1996 to 2005, the survival for Maori improved significantly relative to non-Maori. Conclusion: Maori continue to have higher incidence and mortality than non-Maori from cervical cancer although disparities are improving. Survival disparities are also improving. Treatment (as measured) by ethnicity is similar. Implications: Primary prevention and early detection remain key interventions for addressing Maori needs and reducing inequalities in cervical cancer in New Zealand. Key words: Cervix neoplasms, cervical cancer, survival, survival analyses, ethnicity, treatment. Aust NZ J Public Health. 2010; 34:193-99 doi: 10.1111/j.1753-6405.2010.00506.x

Objective: To estimate occupational light vehicle (OLV) fatality numbers using vehicle registration and crash data and compare these with previous estimates based on workers' compensation data. Method: New South Wales (NSW) Roads and Traffic Authority (RTA) vehicle registration and crash data were obtained for 2004. NSW is the only Australian jurisdiction with mandatory work-use registration, which was used as a proxy for work-relatedness. OLV fatality rates based on registration data as the denominator were calculated and comparisons made with published 2003/04 fatalities based on workers' compensation data. Results: Thirty-four NSW RTA OLV-user fatalities were identified, a rate of 4.5 deaths per 100,000 organisationally registered OLV, whereas the Australian Safety and Compensation Council (ASCC), reported 28 OLV deaths Australia-wide. Conclusions: More OLV user fatalities were identified from vehicle registration-based data than those based on workers' compensation estimates and the data are likely to provide an improved estimate of fatalities specific to OLV use. Implications: OLV-use is an important cause of traumatic fatalities that would be better identified through the use of vehicle-registration data, which provides a stronger evidence base from which to develop policy responses. Key words: light vehicles, occupational driving, work fatalities, non-traditional work arrangements. Aust NZ J Public Health. 2010; 34:142-5 doi: 10.1111/j.1753-6405.2010.00498.x

Objectives. We tested the data artifact hypothesis regarding the Hispanic mortality advantage by investigating whether and to what degree this advantage is explained by Hispanic origin misclassification on US death certificates. Methods. We used the National Longitudinal Mortality Study, which links Current Population Survey records to death certificates for 1979 through 1998, to estimate the sensitivity, specificity, and net ascertainment of Hispanic ethnicity on death certificates compared with survey classifications. Using national vital statistics mortality data, we estimated Hispanic age-specific and age-adjusted death rates, which were uncorrected and corrected for death certificate misclassification, and produced death rate ratios comparing the Hispanic with the non-Hispanic White population. Results. Hispanic origin reporting on death certificates in the United States is reasonably good. The net ascertainment of Hispanic origin is just 5% higher on survey records than on death certificates. Corrected age-adjusted death rates for Hispanics are lower than those for the non-Hispanic White population by close to 20%. Conclusions. The Hispanic mortality paradox is not explained by an incongruence between ethnic classification in vital registration and population data systems. (Am J Public Health. 2010;100:S171-S177. doi: 10.2105/AJPH.2008. 135863)

Background. The mortality after hip fracture has remained high and stable the past 50 years despite improved surgical treatment. The aim of this study was to identify medications and medical factors associated with mortality after hip fracture. Methods. This is a prospective observational study with median observation time of 21 months. Three hundred and sixty-four patients, mean age 83.4 years and 75.8% women, were enrolled. Information on comorbidity, medications, surgery, and clinical findings were collected at the time of fracture. Information on cause and time of death was obtained from the Norwegian Cause of Death Register. Results. Six risk factors and one protective factor were identified by Cox proportional hazards model adjusted for propensity score: the use of diuretics (adjusted hazard ratio [HR] = 4.03, 95% confidence interval [CI] = 2.13-7.64), history of coronary heart disease (CHD) (HR = 2.61, CI = 1.37-4.98), male sex (HR = 2.32, CI = 1.27-4.24), Barthel Index [less than or equal to] 18/20 (HR = 2.48, CI = 1.23-5.01), heart rate > 100 on admission (HR = 2.47, CI = 1.18-5.14), body mass index [less than or equal to] 20 (HR = 1.94, CI = 1.13-3.34), and the use of statins (HR = 0.23, CI = 0.08-0.68). Patients using diuretics had increased risk of death from all causes, including death from CHD, chronic obstructive pulmonary disease, and falls or other accidents. Conclusions. The use of diuretics is the strongest predictor of mortality, followed by CHD at the time of fracture, whereas the use of statins is associated with improved survival. Future research is needed to evaluate whether improved diagnosis and management of CHD and congestive heart failure among hip fracture patients would improve survival. Key Words: Mortality--Hip fracture--Diuretics--Coronary heart disease. doi: 10.1093/gerona/glp199

Background. We examined whether older adults who had continuity of care with a primary care physician (PCP) had lower mortality. Methods. Secondary analyses were conducted using baseline interview data (1993-1994) from the nationally representative Survey on Assets and Health Dynamics among the Oldest Old (AHEAD). The analytic sample included 5,457 self-respondents 70 years old or more who were not enrolled in managed care plans. AHEAD data were linked to Medicare claims for 1991-2005, providing up to 12 years of follow-up. Two time-dependent measures of continuity addressed whether there was more than an 8-month interval between any two visits to the same PCP during the prior 2-year period. The 'present exposure' measure calculated this criterion on a daily basis and could switch 'on' or 'off' daily, whereas the 'cumulative exposure' measure reflected the percentage of follow-up days, also on a daily basis allowing it to switch on or off daily, for which the criterion was met. Results. Two thousand nine hundred and fifty-four (54%) participants died during the follow-up period. Using the cumulative exposure measure, 27% never had continuity of care, whereas 31%, 20%, 14%, and 8%, respectively, had continuity for 1%-33%, 34%-67%, 68%-99%, and 100% of their follow-up days. Adjusted for demographics, socioeconomic status, social support, health lifestyle, and morbidity, both measures of continuity were associated (p < .001) with lower mortality (adjusted hazard ratios of 0.84 for the present exposure measure and 0.31, 0.39, 0.46, and 0.62, respectively, for the 1%-33%, 34%-67%, 68%-99%, and 100% categories of the cumulative exposure measure). Conclusion. Continuity of care with a PCP, as assessed by two distinct measures, was associated with substantial reductions in long-term mortality. Key Words: Continuity--Primary care--Mortality--Medical home. doi: 10.1093/gerona/glp188

Human senescence has been delayed by a decade. This finding, documented in 1994 and bolstered since, is a fundamental discovery about the biology of human ageing, and one with profound [...]

Background. Reduced insulin and insulin-like growth factor-1 (IGF-1) signaling extends the life span of invertebrate and mammals. Recently, reduced insulin receptor substrate-2 (IRS2) signaling was found associated with increased longevity in mice. The aim of our study was to evaluate whether a common polymorphism (Gly1057Asp) in human IRS2 gene is associated with human longevity. Methods. Six hundred seventy-seven participants (289 males and 388 females) between 16 and 104 years of age, categorized as long lived (LL; >85 years old) or controls (C; Results. In the whole population, homozygous [IRS2.sup.Asp/Asp] participants were more represented among LL versus C participants (16.7% vs 12.0%; p = .04). The association between IRS2 gene polymorphism with longevity (being LL) was independent of anthropometric and metabolic covariates (odds ratio: 2.07, 95% confidence interval [CI] = 1.38-3.12; p = .001). Categorizing participants into percentiles by age, [IRS2.sp.Asp/Asp] participants were more likely to reach extreme old age ([greater than or equal to] 90 percentile, 96-104 years; odds ratio: 2.03, 95% CI = 1.39-2.99; p = .0003). Conclusions. These results support the hypothesis that the IRS2 branch of the insulin and IGF signaling is associated with human longevity. Further studies will be necessary for replicating our finding in an independent larger population group with sufficient power before the association between IRS2 gene polymorphism and longevity can be regarded as proven. Furthermore, studies of genetic and/or environmental background interactions may be useful after basic replication is complete. Key Words: IRS2 gene polymorphism--Longevity--Insulin signaling. doi: 10.1093/gerona/glp154

Background. Red cell distribution width (RDW) is a quantitative measure of variability in the size of circulating erythrocytes with higher values reflecting greater heterogeneity in cell sizes. Recent studies have shown that higher RDW is associated with increased mortality risk in patients with clinically significant cardiovascular disease (CVD). Whether RDW is prognostic in more representative community-based populations is unclear. Methods. Seven relevant community-based studies of older adults with RDW measurement and mortality ascertainment were identified. Cox proportional hazards regression and meta-analysis on individual participant data were performed. Results. Median RDW values varied across studies from 13.2% to 14.6%. During 68,822 person-years of follow-up of 11,827 older adults with RDW measured, there was a graded increased risk of death associated with higher RDW values (p < .001). For every 1% increment in RDW, total mortality risk increased by 14% (adjusted hazard ratio [HR]: 1.14; 95% confidence interval [CI]: 1.11-1.17). In addition, RDW was strongly associated with deaths from CVD (adjusted HR: 1.15; 95% Cl: 1.12-1.25), cancer (adjusted HR: 1. l 3; 95% CI: 1.07-1.20), and other causes (adjusted HR: 1.13; 95% CI: 1.07-1.18). Furthermore, the RDW-mortality association occurred in all major demographic, disease, and nutritional risk factor subgroups examined. Among the subset of 1,603 older adults without major age-associated diseases, RDW remained strongly associated with total mortality (adjusted HR: 1.32; 95% CI: 1.21-1.44). Conclusions. RDW is a routinely reported test that is a powerful predictor of mortality in community-dwelling older adults with and without age-associated diseases. The biologic mechanisms underlying this association merit investigation. Key Words: Aging--Erythrocyte Indices--Mortality--Risk Factors. doi: 10.1093/gerona/glp 163

OBJECTIVE: To evaluate the influence of cardiorespiratory fitness (fitness) on the obesity paradox in middle-aged men with known or suspected coronary artery disease. PATIENTS AND METHODS: This study consists of [...]

Objectives. A 1993 study found a 25% higher risk of death among uninsured compared with privately insured adults. We analyzed the relationship between uninsurance and death with more recent data. Methods. We conducted a survival analysis with data from the Third National Health and Nutrition Examination Survey. We analyzed participants aged 17 to 64 years to determine whether uninsurance at the time of interview predicted death. Results. Among all participants, 3.1% (95% confidence interval [CI]=2.5%, 3.7%) died. The hazard ratio for mortality among the uninsured compared with the insured, with adjustment for age and gender only, was 1.80 (95% CI=1.44, 2.26). After additional adjustment for race/ethnicity, income, education, self- and physician-rated health status, body mass index, leisure exercise, smoking, and regular alcohol use, the uninsured were more likely to die (hazard ratio=1.40; 95% CI=1.06, 1.84) than those with insurance. Conclusions. Uninsurance is associated with mortality. The strength of that association appears similar to that from a study that evaluated data from the mid-1980s, despite changes in medical therapeutics and the demography of the uninsured since that time. (Am J Public Health. 2009;99:2289-2295. doi: 10.2105/AJPH.2008.157685)