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BACKGROUND: The most common methods for measuring mobility in older adulthood include performance-based tests, such as the Timed-Up-and-Go and gait speed. While these measures have strong predictive validity for adverse outcomes, they are limited to assessing what older adults do in standardized settings, rather than what they do in their daily life. Life-space mobility, which is the ability to move within environments that expand from one's home to the greater community, has been proposed as a more comprehensive measure of mobility. The aim of this study was to determine the association between modifiable factors and life-space mobility in older adults enrolled in the Canadian Longitudinal Study on Aging (CLSA). METHODS: Life-space mobility was measured using the Life Space Index (LSI). Explanatory factors included physical, psychosocial and cognitive determinants, as well as pain, fatigue, driving status, nutrition, body mass index, smoking status, and vision. To estimate the association between the LSI and explanatory variables, univariate and multivariable ordinary least squares regression analyses were performed. RESULTS: All adults 65 years and older (n = 12,646) were included in the analysis. Fifty percent were women and the mean age was 73.0 (SD5.7). The mean LSI score was 80.5, indicating that, on average, the sample was able to move outside of their neighborhood independently. All explanatory variables were significantly associated with the LSI except for balance and memory. The top 3 variables that explained the most variation in the LSI were driving, social support and walking speed. CONCLUSION: To our knowledge, this was the first study to examine the association between life-space mobility and a comprehensive set of modifiable factors that were selected based on a theoretical framework and existing research evidence. This study had two important messages. First, driving, social support and walking speed emerged as the most significant correlates of life-space mobility in older adults. Second, life-space mobility is multifactorial and interventions that are pragmatic in their design and testing are needed that consider the complexity involved. A multi-disciplinary approach to examining life-space mobility in older adults is needed to optimize opportunities for healthy aging and develop strategies that support mobility in older adulthood.
Assuntos
Atividades Cotidianas , Envelhecimento/fisiologia , Avaliação Geriátrica/métodos , Vida Independente , Adulto , Idoso , Canadá/epidemiologia , Feminino , Humanos , Estudos Longitudinais , Limitação da MobilidadeRESUMO
Genetic predisposition to obesity presents a paradox: how do genetic variants with a detrimental impact on human health persist through evolutionary time? Numerous hypotheses, such as the thrifty genotype hypothesis, attempt to explain this phenomenon yet fail to provide a justification for the modern obesity epidemic. In this critical review, we appraise existing theories explaining the evolutionary origins of obesity and explore novel biological and sociocultural agents of evolutionary change to help explain the modern-day distribution of obesity-predisposing variants. Genetic drift, acting as a form of 'blind justice,' may randomly affect allele frequencies across generations while gene pleiotropy and adaptations to diverse environments may explain the rise and subsequent selection of obesity risk alleles. As an adaptive response, epigenetic regulation of gene expression may impact the manifestation of genetic predisposition to obesity. Finally, exposure to malnutrition and disease epidemics in the wake of oppressive social systems, culturally mediated notions of attractiveness and desirability, and diverse mating systems may play a role in shaping the human genome. As an important first step towards the identification of important drivers of obesity gene evolution, this review may inform empirical research focused on testing evolutionary theories by way of population genetics and mathematical modelling.
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Obesidade/etiologia , Obesidade/genética , Adaptação Fisiológica , Adiposidade/genética , Adiposidade/fisiologia , Metabolismo Energético/genética , Metabolismo Energético/fisiologia , Epigênese Genética , Interação Gene-Ambiente , Deriva Genética , Predisposição Genética para Doença , Variação Genética , Humanos , Modelos Teóricos , Obesidade/fisiopatologiaRESUMO
WHAT IS KNOWN AND OBJECTIVE: With resource constraints in Thailand, directly observed therapy (DOT) for treating tuberculosis (TB) may not be feasible to implement. To improve patients' adherence, hospitals either modify DOT or adopt different approaches: pharmaceutical care or home visit. Our objective was to assess pulmonary TB treatment success rate of pharmaceutical care compared to home visit and modified DOT in Thailand. METHODS: We conducted a retrospective cohort study using data collected in adult pulmonary TB patients starting treatment between October 2010 and September 2013 in three hospitals in Thailand. This study was approved by the Research Ethics Board at each of the participating hospitals. We built a propensity score matching to account for differences in patient baseline characteristics. RESULTS: Analysis included 1398 patients. Before matching, the treatment success rate for patients receiving pharmaceutical care was 94.9%, home visit 93.6% and modified DOT 90.1%. The propensity score-matched cohorts indicated that differences in the treatment success rate were not statistically significant when comparing pharmaceutical care with either home visit (success rate: 92.76% vs 94.74%, risk difference: 1.97%, 95% CI -3.64 to 7.59) or modified DOT (success rate 93.37% for both, risk difference: 0%, 95% CI -5.30 to 5.30). WHAT IS NEW AND CONCLUSION: Pharmaceutical care, home visit and modified DOT are all associated with high success rate for pulmonary TB treatment and exceeded the WHO target, in this retrospective analysis.
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Antituberculosos/uso terapêutico , Terapia Diretamente Observada/métodos , Adesão à Medicação , Assistência Farmacêutica/organização & administração , Tuberculose Pulmonar/tratamento farmacológico , Adolescente , Adulto , Estudos de Coortes , Feminino , Hospitais , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Autoadministração , Tailândia , Resultado do Tratamento , Adulto JovemRESUMO
Despite the availability of inexpensive antimicrobial treatment, syphilis remains prevalent worldwide, affecting millions of individuals. Furthermore, syphilis infection is suspected of increasing both susceptibility to, and tendency to transmit, HIV. Development of a syphilis vaccine would be a potentially promising step towards control, but the value of dedicating resources to vaccine development should be evaluated in the context of the anticipated benefits. Here, we use a detailed mathematical model to explore the potential impact of rolling out a hypothetical syphilis vaccine on morbidity from both syphilis and HIV and compare it to the impact of expanded 'screen and treat' programmes using existing treatments. Our results suggest that an efficacious vaccine has the potential to sharply reduce syphilis prevalence under a wide range of scenarios, while expanded treatment interventions are likely to be substantially less effective. Our modelled interventions in our simulated study populations are expected to have little effect on HIV, and in some scenarios lead to small increases in HIV incidence, suggesting that interventions against syphilis should be accompanied with interventions against other sexually transmitted infections to prevent the possibility that lower morbidity or lower perceived risk from syphilis could lead to increases in other sexually transmitted diseases.
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Vacinas Bacterianas/administração & dosagem , Transmissão Vertical de Doenças Infecciosas/prevenção & controle , Modelos Teóricos , Sífilis/prevenção & controle , Treponema pallidum/imunologia , Vacinação , Adolescente , Adulto , Idoso , Simulação por Computador , Feminino , Infecções por HIV/epidemiologia , Infecções por HIV/transmissão , Infecções por HIV/virologia , Heterossexualidade , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Prevalência , Sífilis/epidemiologia , Sífilis/microbiologia , Sífilis/transmissão , Adulto JovemRESUMO
Malaria is an important cause of global morbidity and mortality. The fact that some people are bitten more often than others has a large effect on the relationship between risk factors and prevalence of vector-borne diseases. Here we develop a mathematical framework that allows us to estimate the heterogeneity of infection rates from the relationship between rates of infectious bites and community prevalence. We apply this framework to a large, published data set that combines malaria measurements from more than 90 communities. We find strong evidence that heterogeneous biting or heterogeneous susceptibility to infection are important and pervasive factors determining the prevalence of infection: 20% of people receive 80% of all infections. We also find that individual infections last about six months on average, per infectious bite, and children who clear infections are not immune to new infections. The results have important implications for public health interventions: the success of malaria control will depend heavily on whether efforts are targeted at those who are most at risk of infection.
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Malária Falciparum/epidemiologia , Malária Falciparum/transmissão , Modelos Biológicos , Plasmodium falciparum/fisiologia , Adolescente , África/epidemiologia , Distribuição por Idade , Animais , Mordeduras e Picadas/epidemiologia , Mordeduras e Picadas/parasitologia , Criança , Culicidae/parasitologia , Culicidae/fisiologia , Suscetibilidade a Doenças , Humanos , Insetos Vetores/parasitologia , Insetos Vetores/fisiologia , Malária Falciparum/imunologia , Malária Falciparum/parasitologia , Plasmodium falciparum/imunologia , Prevalência , Sensibilidade e EspecificidadeRESUMO
Biodiversity plays a vital role for ecosystem functioning in a changing environment. Yet theoretical approaches that incorporate diversity into classical ecosystem theory do not provide a general dynamic theory based on mechanistic principles. In this paper, we suggest that approaches developed for quantitative genetics can be extended to ecosystem functioning by modeling the means and variances of phenotypes within a group of species. We present a framework that suggests that phenotypic variance within functional groups is linearly related to their ability to respond to environmental changes. As a result, the long-term productivity for a group of species with high phenotypic variance may be higher than for the best single species, even though high phenotypic variance decreases productivity in the short term, because suboptimal species are present. In addition, we find that in the case of accelerating environmental change, species succession in a changing environment may become discontinuous. Our work suggests that this phenomenon is related to diversity as well as to the environmental disturbance regime, both of which are affected by anthropogenic activities. By introducing new techniques for modeling the aggregate behavior of groups of species, the present approach may provide a new avenue for ecosystem analysis.
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Ecossistema , Modelos Biológicos , Fenótipo , Biomassa , Meio Ambiente , MatemáticaRESUMO
The stochastic logistic model is the simplest model that combines individual-level demography with density dependence. It explicitly or implicitly underlies many models of biodiversity of competing species, as well as non-spatial or metapopulation models of persistence of individual species. The model has also been used to study persistence in simple disease models. The stochastic logistic model has direct relevance for questions of limiting similarity in ecological systems. This paper uses a biased random walk heuristic to derive a scaling relationship for the persistence of a population under this model, and discusses its implications for models of biodiversity and persistence. Time to extinction of a species under the stochastic logistic model is approximated by the exponential of the scaling quantity U=(R-1)(2) N/R(R+1), where N is the habitat size and R is the basic reproductive number.
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Comportamento Competitivo/fisiologia , Demografia , Ecossistema , Modelos Logísticos , Densidade Demográfica , Processos Estocásticos , Animais , Viés , Análise de Elementos Finitos , Reprodução , Seleção Genética , Especificidade da Espécie , Fatores de TempoRESUMO
This paper investigates the possibility of understanding the effects of host heterogeneity on disease levels through the use of moment approximations. The approach is to avoid assumptions about the distribution of mixing rates (or other parameters) in the population, by treating the low-order moments of the distribution as estimable parameters. This approach, while approximate, can greatly reduce the number of parameters needed to explore the effects of population heterogeneity on disease dynamics. This makes the approach useful for both inference and prediction, and also for gaining insight into the qualitative effects of heterogeneity on the spread of disease. This paper focuses on populations with variations in mixing rate and random mixing. It is shown that moment-based approximations can provide good quantitative estimates of disease dynamics, as well as aiding in qualitative under- standing, over a respectable range of parameters. It is hoped that this approach will provide a useful complement to more traditional box models of heterogeneity.
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Doenças Transmissíveis/transmissão , Doenças Endêmicas/estatística & dados numéricos , Modelos Biológicos , Dinâmica Populacional , Suscetibilidade a Doenças , Humanos , Comportamento Sexual , Infecções Sexualmente Transmissíveis/transmissãoRESUMO
In sessile organisms such as plants, interactions occur locally so that important ecological aspects like frequency dependence are manifest within local neighborhoods. Using probabilistic cellular automata models, we investigated how local frequency-dependent competition influenced whether two species could coexist. Individuals of the two species were randomly placed on a grid and allowed to interact according to local frequency-dependent rules. For four different frequency-dependent scenarios, the results indicated that over a broad parameter range the two species could coexist. Comparisons between explicit spatial simulations and the mean-field approximation indicate that coexistence occurs over a broader region in the explicit spatial simulation.
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Ecossistema , Frequência do Gene/genética , Modelos Genéticos , Desenvolvimento Vegetal , Plantas/genética , Genótipo , Dinâmica não Linear , Densidade Demográfica , Probabilidade , Distribuição Aleatória , Especificidade da Espécie , Processos EstocásticosRESUMO
Hierarchical competition-colonization models have been used to explain limiting similarities among species, successional dynamics, and species loss under habitat destruction. This class of models assumes that there is an inverse relationship between competitive ability and colonization ability and that competitively superior species exclude competitively inferior species when both occupy the same site. This hierarchical model of performance trade-offs, however, exhibits some unusual behaviors in the high-diversity limit, including infinitesimally close species packing, pathologically slow dynamics, and fundamentally important regularities in trait-abundance relationships. In particular, under the condition of constant mortality across species, a 3/2-power-law relationship emerges between abundance and fecundity under infinite packing (abundance of a species with fecundity f is inversely proportional to f to the 3/2 power). In this article, we explore the high-diversity limit of the hierarchical competition-colonization model, with particular emphasis on patterns of species packing, species-abundance relationships, and system stability. Because of the potential for pathologically slow dynamics following perturbations and infinitesimally close species packing in the high-diversity limit for this class of models, the models may need to be modified to include more realistic mechanisms governing the extent and timing of interspecific competitive exclusion in order to effectively capture the structure and dynamics of real-world ecosystems.
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Many diseases show important interactions between epidemiology and immunology. Both models and data suggest that epidemiologically controlled variables, like frequency and intensity of exposure, can affect immunological outcomes in a wide variety of diseases. Conversely, the results of the immunological "battle" between host and parasite determine the ability of the parasite to spread. I present a simple model with two possible states of infection, which assumes that higher exposure to infection is correlated with likelihood of acquiring a more severe infection. For some parameter values, this model leads to simultaneous stability of the disease-free equilibrium and an endemic equilibrium, implying that the disease might be able to persist in a population that it could not invade. I also derive a simple and interpretable sufficient condition for multiple stable states. The "cartoon" model presented here shows that interaction between epidemiology and immunology can have important effects on the invasion and persistence of diseases. In particular, it raises the possibility that this mechanism can lead to mathematical "catastrophe" and to long-term cycles in disease prevalence.
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Epidemiologia , Modelos Imunológicos , Modelos Estatísticos , Doenças Parasitárias/transmissão , Humanos , PrevalênciaRESUMO
The incorporation of population heterogeneity is a central issue in theoretical biology, and it has received considerable attention in epidemiology recently. This paper presents general conclusions and interpretations about the effects of heterogeneity, with and without positive assortative mating, on the ability of a disease to establish itself. We show that the invasion of a disease into a population with random mixing is determined by an average of reproductive numbers for each subgroup, weighted by the total amount of mixing activity of the subgroup. In particular, if the mixing rate is constant across the population, invasion occurs if and only if the average reproductive number for the population exceeds 1. In the case of "preferred mixing," one can find a critical number for each subgroup such that invasion occurs if and only if a suitably defined average over subgroups exceeds 1.