26 resultados para Median Voter Hypothesis

em Scielo Saúde Pública - SP


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Liberal-Institutionalism and Structural Realism expectations about international organizations are confronted by looking at if and how US-controlled international aid is granted, and particularly if it is related or not to political affinity and to United Nations Security Council (UNSC) non-permanent membership. A preliminary assessment suggests that these relations only hold for the period of the Cold War, and, even then, only when UNSC non-permanent membership is in years in which the Security Council was deemed very important.

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OBJECTIVE: To analyze whether the relationship between income inequality and human health is mediated through social capital, and whether political regime determines differences in income inequality and social capital among countries. METHODS: Path analysis of cross sectional ecological data from 110 countries. Life expectancy at birth was the outcome variable, and income inequality (measured by the Gini coefficient), social capital (measured by the Corruption Perceptions Index or generalized trust), and political regime (measured by the Index of Freedom) were the predictor variables. Corruption Perceptions Index (an indirect indicator of social capital) was used to include more developing countries in the analysis. The correlation between Gini coefficient and predictor variables was calculated using Spearman's coefficients. The path analysis was designed to assess the effect of income inequality, social capital proxies and political regime on life expectancy. RESULTS: The path coefficients suggest that income inequality has a greater direct effect on life expectancy at birth than through social capital. Political regime acts on life expectancy at birth through income inequality. CONCLUSIONS: Income inequality and social capital have direct effects on life expectancy at birth. The "class/welfare regime model" can be useful for understanding social and health inequalities between countries, whereas the "income inequality hypothesis" which is only a partial approach is especially useful for analyzing differences within countries.

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Granulomatous inflammation is the morphological substrate of a variety of important infectious diseases such as tuberculosis, leprosy, schistosomiasis and others. Nevertheless, although many aspects of this special type of inflammation are known, fundamental questions concerning granuloma formation, persistence, fate and significance for host-parasite relationships still remain to be elucidated. In this brief review, the basic and more relevant literature related to experimental investigations on granuloma physiopathology is presented. Based on recent investigations performed in our laboratory showing that MDF (Macrophage Deactivating Fator) secreted by epithelioid cells and characterized as the calcium-binding protein protein MRP-14 deactivates activated macrophages, a hypothesis to explain the persistence of granulomatous inflammation is put forward

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This review focuses on studies that support the microvascular hypothesis, as well as on immunological and neurogenic mechanisms, and the role of the parasite itself, to explain further the pathology and clinical course of myocardial involvement in chagasic cardiomyopathy. The salient features of coronary microcirculation and Chagas' disease are discussed.

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In 1989, CONTI DÍAZ & RILLA published a hypothesis concerning the as yet unknown ecological niche of Paracoccidioides brasiliensis. The hypothesis proposed a highly efficient paracoccidioidal ecological strategy based on an important natural reservoir of the parasite, probably in heterothermic animals from fresh water environments. Further, the hypothesis proposed, a transient and variable residence in the soil with a wide aleuriospore dispersion throughout the environment together with an elevated capability of infecting humans, and domestic and wild animals. This paper analyzes scientific publications from the IX International Meeting on Paracoccidioidomycosis held in Águas de Lindoia, São Paulo, Brazil from 2-5 October 2005, providing a comparative study among this articles and with other recently published papers and the hypothesis' postulates. Since various findings and observations appear to agree with the postulates, the pursuit of novel, specific research projects in the supposed reservoirs is recommended partially or fully to confirm the hypothesis using classical laboratorial methods and modern molecular biology techniques.

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The association between depression and cardiovascular disease is well documented. Nevertheless, the process through which they are linked remains unknown, as does the direction of this relationship. Studies have suggested both that depression is a risk factor for heart disease and that heart disease is a risk factor for depression. A number of studies have established that a relationship exists between depression and inflammation, with alterations in the levels of inflammatory markers (IL-1, IL-6, TNF-alpha and others). Depressive symptoms have also been identified in many diseases characterized by inflammatory processes e.g. rheumatoid arthritis, bronchial asthma, diabetes, tuberculosis and cardiovascular diseases. In this brief viewpoint, we explain and propose how to use Chagas disease, a disorder characterized by inflammatory processes and leading to cardiovascular and autonomic problems, as a model for studying the directionality of the relationship between heart disease and depression.

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Stressed plants are generally more attacked by galling insects. In this study we investigated the relationship between population abundance and species richness of galling insects on the tree Alchornea castaneaefolia A. JUSS. (Euphorbiaceae), submited to stress induced by the hemiparasite Psittacanthus sp. (Loranthaceae) in the Amazon, Brazil. Branches of A. castaneaefolia attacked by the hemiparasite were more heavily infested by galling insects than non-attacked branches. The field observations partially corroborate the hypothesis that there would be an optimal level of host-plant stress for galling insect establishment.

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Global scale analyses of soil and foliage δ15N have found positive relationships between δ15N and ecosystem N loss (suggesting an open N cycle) and a negative relationship between δ15N and water availability. We show here that soils and leaves from tropical heath forests are depleted in 15N relative to 'typical' forests suggesting that they have a tight N cycle and are therefore limited by N rather than by, often suggested, water availability.

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Abstract Background: BNP has been extensively evaluated to determine short- and intermediate-term prognosis in patients with acute coronary syndrome, but its role in long-term mortality is not known. Objective: To determine the very long-term prognostic role of B-type natriuretic peptide (BNP) for all-cause mortality in patients with non-ST segment elevation acute coronary syndrome (NSTEACS). Methods: A cohort of 224 consecutive patients with NSTEACS, prospectively seen in the Emergency Department, had BNP measured on arrival to establish prognosis, and underwent a median 9.34-year follow-up for all-cause mortality. Results: Unstable angina was diagnosed in 52.2%, and non-ST segment elevation myocardial infarction, in 47.8%. Median admission BNP was 81.9 pg/mL (IQ range = 22.2; 225) and mortality rate was correlated with increasing BNP quartiles: 14.3; 16.1; 48.2; and 73.2% (p < 0.0001). ROC curve disclosed 100 pg/mL as the best BNP cut-off value for mortality prediction (area under the curve = 0.789, 95% CI= 0.723-0.854), being a strong predictor of late mortality: BNP < 100 = 17.3% vs. BNP ≥ 100 = 65.0%, RR = 3.76 (95% CI = 2.49-5.63, p < 0.001). On logistic regression analysis, age >72 years (OR = 3.79, 95% CI = 1.62-8.86, p = 0.002), BNP ≥ 100 pg/mL (OR = 6.24, 95% CI = 2.95-13.23, p < 0.001) and estimated glomerular filtration rate (OR = 0.98, 95% CI = 0.97-0.99, p = 0.049) were independent late-mortality predictors. Conclusions: BNP measured at hospital admission in patients with NSTEACS is a strong, independent predictor of very long-term all-cause mortality. This study allows raising the hypothesis that BNP should be measured in all patients with NSTEACS at the index event for long-term risk stratification.

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Among the pathophysiological derangements operating in the chronic phase of Chagas disease, parasite persistence is likely to constitute the main mechanism of myocardial injury in patients with chronic chagasic cardiomyopathy. The presence of Trypanosoma cruzi in the heart causes a low-grade, but relentless, inflammatory process and induces myocardial autoimmune injury. These facts suggest that trypanocidal therapy may positively impact the clinical course of patients with chronic Chagas heart disease. However, the experimental and clinical evidence currently available is insufficient to support the routine use of etiologic treatment in these patients. The BENEFIT project - Benznidazole Evaluation for Interrupting Trypanosomiasis - is an international, multicenter, double-blind, placebo-controlled trial of trypanocidal treatment with benznidazole in patients with chronic Chagas heart disease. This project is actually comprised of two studies. The pilot study investigates whether etiologic treatment significantly reduces parasite burden, as assessed by polymerase chain reaction-based techniques and also determines the safety and tolerability profile of the trypanocidal drug in this type of chagasic population. The full-scale study determines whether antitrypanosomal therapy with benznidazole reduces mortality and other major cardiovascular clinical outcomes in patients with chronic Chagas heart disease.

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Human immunodeficiency virus (HIV)-1 infection has an important impact on malaria. Plasmodium falciparum and HIV-1 co-infected patients (Pf/HIV) present with a high degree of anaemia, enhanced parasitaemia and decreased CD4+ T cell counts, which increase the risk of developing severe malaria. In addition, infection with either Pf or HIV-1 alone causes extensive immune activation. Our hypothesis was that lymphocyte activation is potentiated in Pf/HIV co-infected patients, consequently worsening their immunosuppressed state. To test this hypothesis, 22 Pf/HIV patients, 34 malaria patients, 29 HIV/AIDS patients and 10 healthy controls without malaria or HIV/acquired immune deficiency syndrome (AIDS) from Maputo/Mozambique were recruited for this study. As expected, anaemia was most prevalent in the Pf/HIV group. A significant variation in parasite density was observed in the Pf/HIV co-infected group (110-75,000 parasites/µL), although the median values were similar to those of the malaria only patients. The CD4+ T cell counts were significantly lower in the Pf/HIV group than in the HIV/AIDS only or malaria only patients. Lymphocyte activation was evaluated by the percentage of activation-associated molecules [CD38 expression on CD8+ and human leukocyte antigen-DR expression on CD3+ T cells]. The highest CD38 expression was detected in the Pf/HIV co-infected patients (median = 78.2%). The malaria only (median = 50%) and HIV/AIDS only (median = 52%) patients also exhibited elevated levels of these molecules, although the values were lower than those of the Pf/HIV co-infected cases. Our findings suggest that enhanced T-cell activation in co-infected patients can worsen the immune response to both diseases.