Trend (1999–2009) in U.S. death rates from myelodysplastic syndromes: Utility of multiple causes of death in surveillance

BackgroundFor myelodysplastic syndromes (MDS) (formerly known as preleukemia), a diverse group of myeloid neoplasms usually involving anemia in elderly persons, trends in U.S. death rates apparently have not been reported.MethodsTrends in annual age-standardized rates per 100,000 from 1999 to 2009 were examined for MDS using multiple causes vs. underlying cause alone, coded on death certificates for U.S. residents.ResultsThe death rate (all ages combined) for MDS increased from 1999 to 2009, from 1.62 to 1.84 using underlying cause alone and from 2.89 to 3.27 using multiple causes. Rates using multiple causes were about 80% higher than those based on underlying cause alone. From 2001 to 2004 the rate for MDS using underlying cause alone (but not using multiple causes) declined, accompanied by an increase in the rate for deaths from leukemia as underlying cause with mention of MDS; this trend coincided with the advent of the 2001 World Health Organization's reclassification of certain MDS as leukemia. The MDS rate for age 65+ years increased after 2005, whereas the rate for age 25–64 years was low but declined from 2001 to 2003 and then stabilized. For deaths with MDS coded as other than underlying cause, rates did not decline for deaths from each of the two most common causes (i.e., cardiovascular diseases and leukemia).ConclusionsEvidence for decreases in MDS-related mortality rates was limited; the increase at age 65+ years is consistent with increases in incidence rates reported from cancer registries. Using multiple causes of death vs. only the underlying cause results in substantially higher MDS-related death rates, shows the impact of changes in the classification of myeloid neoplasms and emphasizes the importance of reducing cardiovascular disease mortality in MDS patients.     

Years of potential life lost caused by prostate cancer deaths in the United States—Projection from 2004 through 2050

BackgroundThe purpose of this study is to estimate and project the number of years of potential life lost (YPLL) among males who die of prostate cancer in the United States from 2004 through 2050 and compare the projections by race/ethnicity and age, accounting for demographic changes and population growth.MethodsWe applied the life expectancy method to estimate YPLL caused by deaths of prostate cancer and all cancers in men by using 1999–2004 national mortality data, 2008 census population demographic projections, and 2004 U.S. life tables. We performed sensitivity analyses by varying death rate and population projections, and examined increase in YPLL from population growth, changes in demographics, and death rates.ResultsThe number of YPLL caused by prostate cancer deaths was projected to increase by 226.1%, from 291,853 in 2004 to 951,753 in 2050. Hispanics were projected to have the fastest growth in YPLL (977.1% from 2004 to 2050) caused by prostate cancer, followed by non-Hispanic blacks (543.1%), and non-Hispanic others (269.7%). People aged 75 or older was projected to account for 62.0% of YPLL from prostate cancer in 2050 compared with 50.8% in 2004. Of the projected increase in YPLL caused by prostate cancer deaths by 2050, 9.8% were due to changes in demographic composition, 26.8% because of mortality change, and 63.4% because of population growth.ConclusionsYPLL due to prostate cancer deaths are projected to increase dramatically, and become a greater burden in the future. The projections highlight the importance of comprehensive cancer control and research on cancers including prostate cancer and racial/ethnic-specific estimates.     

Recent decline in the U.S. death rate from myeloproliferative neoplasms, 1999-2006

Background: Myeloproliferative neoplasms (MPNs) are classified as neoplasms of uncertain or unknown behavior in the International Classification of Diseases (ICD) Version 10 and can contribute to risk of death from complications (especially thrombosis). Methods: U.S age-standardized death rates using ICD-Version 10 codes relevant to classical MPN (i.e., polycythemia vera, essential thrombocythemia, and “chronic myeloproliferative disease”) were examined for 1999–2006. The underlying cause of death and also all causes (“multiple causes” or “mentions”) coded on death certificates were considered. Trends were assessed by using percentage change (PC) in rate between 1999 and 2006, and annual percentage change (APC) estimated from linear regression. Results: The decline in death rates was large for MPN, whether based only the underlying cause (PC = ?19.7%, APC = ?3.4%) or on the substantially higher rates based on any cause (PC = ?24.1%, APC = ?3.8%), and was consistent by gender and age group (<65 and 65+ years). For deaths with MPN coded as other than the underlying cause, cardiovascular diseases were the most common underlying cause and the ASR for these deaths declined substantially (PC = ?40.0%). Conclusions: Use of the underlying cause of death in surveillance will considerably underestimate MPN-related mortality rates in the population. Studies are needed on treatment in random samples of MPN patients from population-based cancer registries. Continued surveillance of MPN-related mortality rates in the population is needed in view of recent attempts (including the use of aspirin) to control cardiovascular complications of MPN.     

New label‐free automated survival assays reveal unexpected stress resistance patterns during C. elegans aging

Caenorhabditis elegans is an excellent model for high‐throughput experimental approaches but lacks an automated means to pinpoint time of death during survival assays over a short time frame, that is, easy to implement, highly scalable, robust, and versatile. Here, we describe an automated, label‐free, high‐throughput method using death‐associated fluorescence to monitor nematode population survival (dubbed LFASS for label‐free automated survival scoring), which we apply to severe stress and infection resistance assays. We demonstrate its use to define correlations between age, longevity, and severe stress resistance, and its applicability to parasitic nematodes. The use of LFASS to assess the effects of aging on susceptibility to severe stress revealed an unexpected increase in stress resistance with advancing age, which was largely autophagy‐dependent. Correlation analysis further revealed that while severe thermal stress resistance positively correlates with lifespan, severe oxidative stress resistance does not. This supports the view that temperature‐sensitive protein‐handling processes more than redox homeostasis underpin aging in C. elegans. That the ages of peak resistance to infection, severe oxidative stress, heat shock, and milder stressors differ markedly suggests that stress resistance and health span do not show a simple correspondence in C. elegans.     

黔中石漠化区衰老退化与正常生长顶坛花椒根区土壤质量特征

为了探讨顶坛花椒(Zanthoxylum planispimum var. dintanensis)衰老退化的原因,实现林分稳定与可持续性经营,该文以开黄花为典型标志的衰老退化植株和正常生长的植株为研究对象,采用土壤农业化学和环境矿物学的方法,分析不同植株根区土壤矿质元素含量,评价土壤综合质量。结果表明:(1)正常生长植株根区土壤的C、P、K、S、Se、Sr、Mo、氧化物等总体水平显著高于衰老退化植株,总氮、速效磷、速效氮、Cu、Pb、Zn、Cr无显著差异,其他元素的变化规律不明显。元素的有效态含量亦对植株生长产生影响。从植物营养需求角度看,大量、中量、微量元素均对土壤质量产生支配效应。(2)根区土壤质量指数表现为正常生长植株3最高、衰老退化植株1最低,说明土壤质量对顶坛花椒衰老退化具有影响。(3)顶坛花椒林分经营时,应培育良好的土壤结构,注重土壤养分的全面性和均衡性,关注矿质元素过低引起的亏缺效应。     

Mutations in the Escherichia coli23S rRNA Increase the Rate of Peptidyl-tRNA Dissociation from the Ribosome

We have studied in vivothe phenotypes of 23S rRNA mutations G2582A, G2582U, G2583C, and U2584C, which are located at the A site of Escherichia coli50S ribosomal subunit. All mutant rRNAs incorporated into 50S ribosomal subunits. Upon sucrose gradient fractionation of cell lysates, 23S rRNAs mutated at G2582 to A and G2583 to C accumulated in the 50S and 70S fractions and were underrepresented in the polysome fraction. Induction of 23S rRNAs mutated at G2582 and G2583 lead to a drastic reduction in cell growth. In addition, mutations G2582A and G2583C reduced to one-third the total protein synthesis but not the RNA synthesis. Finally, we show that 23S rRNA mutations G2582A, G2582U, and G2583C cause a significant increase in peptidyl-tRNA drop-off from ribosomes, thereby reducing translational processivity. The results clearly show that tRNA–23S rRNA interaction has an essential role in maintaining the processivity of translation.     

Mapping of Calf Death in Japanese Black Cattle

Weak calf syndrome (WCS) is a major cause of calf death in Japanese Black cattle. Among IARS disorders, the isoleucyl-tRNA synthetase c.235G>C mutation has been identified as one of the causes of WCS. However, calf deaths differing from those attributed to IARS disorder has been occurring. To identify other genes potentially responsible for these calf deaths, we constructed three populations of three bulls (Bull-1, -2 and -3) that did not carry the IARS mutation, and dead calves (18, 28, and 31 calves) and healthy cattle (18, 15, and 10 cattle) sired by these bulls. The populations were genotyped using the BovineSNP50 BeadChip, but homozygosity mapping did not detect any associated genomic regions with calf death. Linkage analysis performed using each population as a paternal half-sib family of Bull-1, Bull-2, and Bull-3 revealed that, in the Bull-1 population, calf death was mapped to the 8.94?Mb–14.53?Mb and 29.82?Mb–33.77?Mb regions of BTA29. The findings suggested that the incidence of calf death in calves sired by Bull-1 was a hereditary disease exhibiting a dominant, not recessive, inheritance pattern.     

Pathways of introduction of the invasive aquatic plant Cabomba caroliniana

The pathway and frequency of species' introductions can affect the extent, impact, and management of biological invasions. Here, we examine the pathway of introduction of the aquatic plant Cabomba caroliniana (fanwort) into Canada and the northern United States using plastid DNA sequence (intergenic spacers atpF‐atpH, trnH‐psbA, and trnL‐trnF) and DNA content analyses. We test the hypothesis that the spread of fanwort is a result of commercial trade by comparing a Canadian population (Kasshabog Lake, ON) to native populations from southern U.S., introduced populations in northern U.S., and plants from commercial retailers. Thirteen plastid haplotypes were identified throughout North America, including one dominant haplotype, which was present in all C. caroliniana populations. Several rare haplotypes were used to infer shared colonization history. In particular, the Canadian population shared two rare alleles with a population from Massachusetts, suggesting range expansion of C. caroliniana from the northern U.S. However, the possibility of a commercial introduction cannot be excluded, as common alleles were shared between the Canadian population and both commercial and southern U.S. sources. Variation in C. caroliniana genome size was bimodal and populations were classified into “high” and “low” categories. The Canadian population had DNA contents similar to several northern U.S. populations (low DNA content). This may provide additional support for range expansion from these introduced populations rather than from commercial sources or populations in the southern U.S., which had high DNA content.     

Evaluation of cause of deaths' validity using outcome measures from a prospective, population based cohort study in Tehran, Iran

Objective

The aim of this study was to evaluate the validity of cause of death stated in death certificates in Tehran using outcome measures of the Tehran Lipid and Glucose Study (TLGS), an ongoing prospective cohort study.

Methods

The cohort was established in 1999 in a population of 15005 people, 3 years old and over, living in Tehran; 3551 individuals were added to this population three years later. As part of cohort''s outcome measures, deaths occurring in the cohort are investigated by a panel of medical specialists (Cohort Outcome Panel-COP) and underlying cause of death is determined for each death. The cause of death assigned in a deceased''s original death certificate was evaluated against the cause of death determined by COP and sensitivity and positive predictive values (PPV) were determined. In addition, determinants of assigning accurate underlying cause of death were determined using logistic regression model.

Result

A total of 231 death certificates were evaluated. The original death certificates over reported deaths due to neoplasms and underreported death due to circulatory system and transport accidents. Neoplasms with sensitivity of 0.91 and PPV of 0.71 were the most valid category. The disease of circulatory system showed moderate degree of validity with sensitivity of 0.67 and PPV of 0.78. The result of logistic regression indicated if the death certificate is issued by a general practitioner, there is 2.3 (95% CI 1.1, 5.1) times chance of being misclassified compared with when it is issued by a specialist. If the deceased is more than 60 years, the chance of misclassification would be 2.5 times (95% CI of 1.1, 5.9) compared with when the deceased is less than 60 years.     

Physiological scenarios of programmed loss of mitochondrial DNA function and death of yeast

Recently it was convincingly shown that the yeast Saccharomyces cerevisiae does possess the basic modules of programmed cell death machinery. As programmed cell death is suicide for a unicellular organism, it is reasonable to assume that they trigger the program when the death is beneficial for the rest of the population. Not surprisingly, most of the scenarios of physiological death of S. cerevisiae, i.e. cell death in stationary culture, during meiosis, during mating, and driven by viruses are dependent on quorum sensing, meaning that they depend on the cell density. Here we also discuss possible mechanisms that govern fitness decline during replicative aging of S. cerevisiae cells. We argue that loss of mitochondrial DNA function that occurs during replicative aging is programmed and adaptive. Indeed, yeast cells with nonfunctional mitochondrial DNA are known to be extremely stress-resistant, and also the presence of a subpopulation of such cells might protect the culture from degeneration by preventing the fixation of opportunistic mutations.     

Host-specific aphid population responses to elevated CO2 and increased N availability

Sap-feeding insects such as aphids are the only insect herbivores that show positive responses to elevated CO₂. Recent models predict that increased nitrogen will increase aphid population size under elevated CO₂, but few experiments have tested this idea empirically. To determine whether soil nitrogen (N) availability modifies aphid responses to elevated CO₂, we tested the performance of Macrosiphum euphorbiae feeding on two host plants; a C₃ plant (Solanum dulcamara), and a C₄ plant (Amaranthus viridis). We expected aphid population size to increase on plants in elevated CO₂, with the degree of increase depending on the N availability. We found a significant CO₂× N interaction for the response of population size for M. euphorbiae feeding on S. dulcamara: aphids feeding on plants grown in ambient CO₂, low N conditions increased in response to either high N availability or elevated CO₂. No population size responses were observed for aphids infesting A. viridis. Elevated CO₂ increased plant biomass, specific leaf weight, and C : N ratios of the C₃ plant, S. dulcamara but did not affect the C₄ plant, A. viridis. Increased N fertilization significantly increased plant biomass, leaf area, and the weight : height ratio in both experiments. Elevated CO₂ decreased leaf N in S. dulcamara and had no effect on A. viridis, while higher N availability increased leaf N in A. viridis and had no effect in S. dulcamara. Aphid infestation only affected the weight : height ratio of S. dulcamara. We only observed an increase in aphid population size in response to elevated CO₂ or increased N availability for aphids feeding on S. dulcamara grown under low N conditions. There appears to be a maximum population growth rate that M. euphorbiae aphids can attain, and we suggest that this response is because of intrinsic limits on development time and fecundity.     

Lifespan extension by dietary intervention in a mouse model of Cockayne Syndrome uncouples early postnatal development from segmental progeria

Cockayne syndrome (CS) is a rare autosomal recessive segmental progeria characterized by growth failure, lipodystrophy, neurological abnormalities, and photosensitivity, but without skin cancer predisposition. Cockayne syndrome life expectancy ranges from 5 to 16 years for the two most severe forms (types II and I, respectively). Mouse models of CS have thus far been of limited value due to either very mild phenotypes, or premature death during postnatal development prior to weaning. The cause of death in severe CS models is unknown, but has been attributed to extremely rapid aging. Here, we found that providing mutant pups with soft food from as late as postnatal day 14 allowed survival past weaning with high penetrance independent of dietary macronutrient balance in a novel CS model (Csa^?/? | Xpa^?/?). Survival past weaning revealed a number of CS‐like symptoms including small size, progressive loss of adiposity, and neurological symptoms, with a maximum lifespan of 19 weeks. Our results caution against interpretation of death before weaning as premature aging, and at the same time provide a valuable new tool for understanding mechanisms of progressive CS‐related progeroid symptoms including lipodystrophy and neurodysfunction.     

Deaths from heat-stroke in Japan: 1968–1994

Global warming is increasingly recognized as a threat to the survival of human beings, because it could cause a serious increase in the occurrence of diseases due to environmental heat during intermittent hot weather. To assess the direct impact of extremely hot weather on human health, we investigated heat-related deaths in Japan from 1968 through 1994, analyzing the data to determine the distribution of the deaths by age and their correlation to the incidence of hot days in summer. Vital Statistics of Japan, published by the Ministry of Health and Welfare of Japan, was the source of the heat-related mortality data employed in this study. Meteorological data were obtained from the District Meteorological Observatories in Tokyo and Osaka, the two largest cities in Japan. Heat-related deaths were most prone to occur on days with a peak daily temperature above 38°C, and the incidence of these deaths showed an exponential dependence on the number of hot days. Thus, even a small rise in atmospheric temperature may lead to a considerable increase in heat-related mortality, indicating the importance of combating global warming. Furthermore, half (50.1%) of the above-noted deaths occurred in children (4 years and under) and the elderly (70 years and over) irrespective of gender, indicating the vulnerability of these specific age groups to heat. Since a warmer climate is predicted in the future, the incidence of heat waves will increase, and more comprehensive measures, both medical and social, should be adopted for children of 4 years and younger the elderly to prevent heat-related deaths in these age groups. Received: 20 January 1999 / Accepted: 15 June 1999     

Increasing Black:White disparities in breast cancer mortality in the 50 largest cities in the United States

Introduction: This paper presents race-specific breast cancer mortality rates and the corresponding rate ratios for the 50 largest U.S. cities for each of the 5-year intervals between 1990 and 2009. Methods: The 50 largest cities in the U.S. were the units of analysis. Numerator data were abstracted from national death files where the cause was malignant neoplasm of the breast (ICD-9 = 174 and ICD-10 = C50) for women. Population-based denominators were obtained from the U.S. Census Bureau for 1990, 2000, and 2010. To measure the racial disparity, we calculated non-Hispanic Black:non-Hispanic White rate ratios (RRs) and confidence intervals for each 5-year period. Results: At the final time point (2005–2009), two RRs were less than 1, but neither significantly so, while 39 RRs were >1, 23 of them significantly so. Of the 41 cities included in the analysis, 35 saw an increase in the Black:White RR between 1990–1994 and 2005–2009. In many of the cities, the increase in the disparity occurred because White rates improved substantially over the 20-year study period, while Black rates did not. There were 1710 excess Black deaths annually due to this disparity in breast cancer mortality, for an average of about 5 each day. Conclusion: This analysis revealed large and growing disparities in Black:White breast cancer mortality in the U.S. and many of its largest cities during the period 1990–2009. Much work remains to achieve equality in breast cancer mortality outcomes.     

Chemical genetic screen in fission yeast reveals roles for vacuolar acidification,mitochondrial fission,and cellular GMP levels in lifespan extension

The discovery that genetic mutations in several cellular pathways can increase lifespan has lent support to the notion that pharmacological inhibition of aging pathways can be used to extend lifespan and to slow the onset of age‐related diseases. However, so far, only few compounds with such activities have been described. Here, we have conducted a chemical genetic screen for compounds that cause the extension of chronological lifespan of Schizosaccharomyces pombe. We have characterized eight natural products with such activities, which has allowed us to uncover so far unknown anti‐aging pathways in S. pombe. The ionophores monensin and nigericin extended lifespan by affecting vacuolar acidification, and this effect depended on the presence of the vacuolar ATPase (V‐ATPase) subunits Vma1 and Vma3. Furthermore, prostaglandin J₂ displayed anti‐aging properties due to the inhibition of mitochondrial fission, and its effect on longevity required the mitochondrial fission protein Dnm1 as well as the G‐protein‐coupled glucose receptor Git3. Also, two compounds that inhibit guanosine monophosphate (GMP) synthesis, mycophenolic acid (MPA) and acivicin, caused lifespan extension, indicating that an imbalance in guanine nucleotide levels impinges upon longevity. We furthermore have identified diindolylmethane (DIM), tschimganine, and the compound mixture mangosteen as inhibiting aging. Taken together, these results reveal unanticipated anti‐aging activities for several phytochemicals and open up opportunities for the development of novel anti‐aging therapies.     

Waist circumference as compared with body-mass index in predicting mortality from specific causes

Background

Whether waist circumference provides clinically meaningful information not delivered by body-mass index regarding prediction of cause-specific death is uncertain.

Methods

We prospectively examined waist circumference (WC) and body-mass index (BMI) in relation to cause-specific death in 225,712 U.S. women and men. Cox regression was used to estimate relative risks and 95% confidence intervals (CI). Statistical analyses were conducted using SAS version 9.1.

Results

During follow-up from 1996 through 2005, we documented 20,977 deaths. Increased WC consistently predicted risk of death due to any cause as well as major causes of death, including deaths from cancer, cardiovascular disease, and non-cancer/non-cardiovascular diseases, independent of BMI, age, sex, race/ethnicity, smoking status, and alcohol intake. When WC and BMI were mutually adjusted in a model, WC was related to 1.37 fold increased risk of death from any cancer and 1.82 fold increase risk of death from cardiovascular disease, comparing the highest versus lowest WC categories. Importantly, WC, but not BMI showed statistically significant positive associations with deaths from lung cancer and chronic respiratory disease. Participants in the highest versus lowest WC category had a relative risk of death from lung cancer of 1.77 (95% CI, 1.41 to 2.23) and of death from chronic respiratory disease of 2.77 (95% CI, 1.95 to 3.95). In contrast, subjects in the highest versus lowest BMI category had a relative risk of death from lung cancer of 0.94 (95% CI, 0.75 to 1.17) and of death from chronic respiratory disease of 1.18 (95% CI, 0.89 to 1.56).

Conclusions

Increased abdominal fat measured by WC was related to a higher risk of deaths from major specific causes, including deaths from lung cancer and chronic respiratory disease, independent of BMI.     

Diet restriction‐induced healthy aging is mediated through the immune signaling component ZIP‐2 in Caenorhabditis elegans

Dietary restriction (DR) robustly delays the aging process in all animals tested so far. DR slows aging by negatively regulating the target of rapamycin (TOR) and S6 kinase (S6K) signaling pathway and thus inhibiting translation. Translation inhibition in C. elegans is known to activate the innate immune signal ZIP‐2. Here, we show that ZIP‐2 is activated in response to DR and in feeding‐defective eat‐2 mutants. Importantly, ZIP‐2 contributes to the improvements in longevity and healthy aging, including mitochondrial integrity and physical ability, mediated by DR in C. elegans. We further show that ZIP‐2 is activated upon inhibition of TOR/S6K signaling. However, DR‐mediated activation of ZIP‐2 does not require the TOR/S6K effector PHA‐4/FOXA. Furthermore, zip‐2 was not activated or required for longevity in daf‐2 mutants, which mimic a low nutrition status. Thus, DR appears to activate ZIP‐2 independently of PHA‐4/FOXA and DAF‐2. The link between DR, aging, and immune activation provides practical insight into the DR‐induced benefits on health span and longevity.     

Seasonality and Coronary Heart Disease Deaths in United States Firefighters

United States firefighters have a high on‐duty fatality rate, and coronary heart disease is the leading cause. Seasonality affects the incidence of cardiovascular events in the general population, but its effects on firefighters are unknown. This study statistically examined the seasonal and annual variation of all on‐duty coronary heart disease deaths among US firefighters between 1994 and 2004 using the chi‐square distribution and Poisson regression model of the monthly fatality counts. It also examined the effect of ambient temperature (apparent as well as wind chill temperature) on coronary heart disease fatalities during the study span using a time‐stratified, case‐crossover study design. When grouped by season, we observed the distribution of the 449 coronary heart disease fatalities to show a relative peak in winter (32%) and relative nadir in spring (21%). This pattern was significantly different (p=0.005) from the expected distribution under the null hypothesis of season having no effect. The pattern persisted in additional analyses, stratifying the deaths by the type of duty in which the firefighters were engaged at the time of their deaths. In the Poisson regression model of the monthly fatality counts, the overall goodness‐of‐fit between the actual and predicted case counts was excellent (χ₄²=16.63; p=0.002). Two distinct peaks were detected: one in January–February and the other in August–September. Overall temperature was not associated with increased risk of on‐duty death. After allowing for different effects of temperature in mild/hot versus cold periods, a 1°C increase was not protective in cold weather; nor did it increase the risk of death in warmer weather. The findings of this study reveal statistical evidence for excess coronary heart disease deaths among firefighters during winter; however, the temporal pattern of coronary heart disease deaths was not linked to temperature variation. The seasonal pattern was also found to be independent of duty‐related risks.     

Effect of mixed diets (cyanobacteria and green algae) on the population growth of the cladocerans <Emphasis Type="Italic">Ceriodaphnia dubia</Emphasis> and <Emphasis Type="Italic">Moina macrocopa</Emphasis>

Microcystis aeruginosa, a cosmopolitan form, is a colonial cyanobacterium, which is also common in many freshwater bodies in Mexico. In eutrophic water bodies cyanobacteria are often the main phytoplankton that co-exist with cladocerans. We evaluated the effect of mixed diets, comprising 0, 25, 50, 75, and 100% on dry weight basis of M. aeruginosa, and the rest of one of two green algal species (Chlorella vulgaris and Scenedesmus acutus), on the population growth of the cladocerans Ceriodaphnia dubia and Moina macrocopa. Regardless of the share of M. aeruginosa in the mixed diet, C. dubia fed Chlorella had a longer initial lag phase. However, in mixed diet with S. acutus, the lag phase of C. dubia increased with increasing proportion of M. aeruginosa. When raised on 100% M. aeruginosa, the population growth of C. dubia was lowered compared with 100% S. acutus or 100% C. vulgaris. Increased proportion of M. aeruginosa in the mixed diet also resulted in decreased abundance of M. macrocopa. Irrespective of diet type, M. macrocopa had a shorter lag phase than C. dubia. Depending on the diet type, the rate of population increase (r) of C. dubia varied from 0.07 to 0.26 d⁻¹ while that of M. macrocopa was higher (0.14–0.61 d⁻¹). For both cladoceran species, the lower r values were obtained when fed Microcystis. Our study showed that the strain of M. aeruginosa was not highly toxic to cause total elimination of either C. dubia or M. macrocopa. Addition of a green algal component to the diet improved the population growth rates of both cladoceran species.     

Forecasting the obesity epidemic in the aging U.S. population

Objective: The objective was to forecast BMI distribution in the U.S. population along with demographic changes based on past race‐, sex‐, and birth cohort‐specific secular trends. Research Methods and Procedures: We compiled data from 44,184 subjects from 4 National Health and Nutrition Examination Surveys (NHANES; 1971 to 2004). By race and sex, we fit regression models to create smoothed mean BMI curves by age for 1970 to 2010. Linking corresponding birth cohorts across age‐ and year‐specific mean BMI projections, we estimated the trajectory of relative BMI throughout each cohort's lifetime. These projections were validated using actual cohorts in the Nurses’ Health Study and Health Professionals Follow‐up Study. Combined with U.S. census, we predicted BMI distributions in 2010 and examined the joint impact of the obesity epidemic and population aging. Results: BMI secular trends in the past 3 decades differ significantly by birth cohort, sex, and race. If these trends continue, the prevalence of obesity is expected to reach 35%, 36%, 33%, and 55% in 2010 among white men, white women, black men, and black women, respectively, far from the Healthy People 2010 goal of 15%. Such forecasts translate into 9.3 million more obese adults 20 to 74 years of age than in 2000, 8.3 million of whom would be 50 years of age or older, and 8.5 million of whom would be white. The mean age among obese men and women is also expected to rise from 47 to 49 years among whites and from 43 to 44 years among blacks. Discussion: As the baby boom generation approaches retirement age, the continuing obesity epidemic signals a likely expansion in the population with obesity‐related comorbidities. A framework to combine BMI and demographic trends is essential in evaluating the burden and disparity associated with the epidemic in the aging U.S. population.