914 resultados para infant mortality and life expectancy
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The paradoxically low infant mortality rates for Mexican Americans in Texas have been attributed to inaccuracies in vital registration and idiosyncracies in Mexican migration in rural areas along the U.S.-Mexico border. This study examined infant (IMR), neonatal (NMR), and postneonatal (PNMR) mortality rates of Mexican Americans in an urban, non-border setting, using linked birth and death records of the 1974-75 single live birth cohort (N = 68,584) in Harris County, Texas, which includes the city of Houston and is reported to have nearly complete birth and death registration. The use of parental nativity with the traditional Spanish surname criterion made it possible to distinguish infants of Mexican-born immigrants from those of Blacks, Anglos, other Hispanics, and later-generation, more Anglicized Mexican Americans. Mortality rates were analyzed by ethnicity, parental nativity, and cause of death, with respect to birth weight, birth order, maternal age, legitimacy status, and time of first prenatal care.^ While overall IMRs showed Spanish surname rates slightly higher than Anglo rates, infants of Mexican-born immigrants had much lower NMRs than did Anglos, even for moderately low birth weight infants. However, among infants under 1500 grams, presumably unable to be discharged home in the neonatal period, Mexican Americans had the highest NMR. The inconsistency suggested unreported deaths for Mexican American low birth weight infants after hospital discharge. The PNMR of infants of Mexican immigrants was also lower than for Anglos, and the usual mortality differentials were reversed: high-risk categories of high birth order, high maternal age, and late/no prenatal care had the lowest PNMRs. Since these groups' characteristics are congruent with those of low-income migrants, the data suggested the possibility of migration losses. Cause of death analysis suggested that prematurity and birth injuries are greater problems than heretofore recognized among Mexican Americans, and that home births and "shoebox burials" may be unrecorded even in an urban setting.^ Caution is advised in the interpretation of infant mortality rates for a Spanish surname population of Mexican origin, even in an urban, non-border area with reportedly excellent birth and death registration. ^
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Evaluation of the impact of a disease on life expectancy is an important part of public health. Potential gains in life expectancy (PGLE) that can properly take into account the competing risks are an effective indicator for measuring the impact of the multiple causes of death. This study aimed to measure the PGLEs from reducing/eliminating the major causes of death in the USA from 2001 to 2008. To calculate the PGLEs due to the elimination of specific causes of death, the age-specific mortality rates for heart disease, malignant neoplasms, Alzheimer disease, kidney diseases and HIV/AIDS and life table constructing data were obtained from the National Center for Health Statistics, and the multiple decremental life tables were constructed. The PGLEs by elimination of heart disease, malignant neoplasms or HIV/AIDS continued decreasing from 2001 to 2008, but the PGLE by elimination of Alzheimer's disease or kidney diseases revealed increased trends. The PGLEs (by years) for all race, male, female, white, white male, white female, black, black male and black female at birth by complete elimination of heart disease 2001–2008 were 0.336–0.299, 0.327–0.301, 0.344–0.295, 0.360–0.315, 0.349–0.317, 0.371–0.316,0.278–0.251, 0.272–0.255, and 0.282–0.246 respectively. Similarly, the PGLEs (by years) for all race, male, female, white, white male, white female, black, black male and black female at birth by complete elimination of malignant neoplasms, Alzheimer's disease, kidney disease or HIV/AIDS 2001–2008 were also uncovered, respectively. Most diseases affect specific population, such as, HIV/AIDS tends to have a greater impact on people of working age, heart disease and malignant neoplasms have a greater impact on people over 65 years of age, but Alzheimer's disease and kidney diseases have a greater impact on people over 75 years of age. To measure the impact of these diseases on life expectancy in people of working age, partial multiple decremental life tables were constructed and the PGLEs were computed by partial or complete elimination of various causes of death during the working years. Thus, the results of the study outlined a picture of how each single disease could affect the life expectancy in age-, race-, or sex-specific population in USA. Therefore, the findings would not only assist to evaluate current public health improvements, but also provide useful information for future research and disease control programs.^
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Life expectancy has consistently increased over the last 150 years due to improvements in nutrition, medicine, and public health. Several studies found that in many developed countries, life expectancy continued to rise following a nearly linear trend, which was contrary to a common belief that the rate of improvement in life expectancy would decelerate and was fit with an S-shaped curve. Using samples of countries that exhibited a wide range of economic development levels, we explored the change in life expectancy over time by employing both nonlinear and linear models. We then observed if there were any significant differences in estimates between linear models, assuming an auto-correlated error structure. When data did not have a sigmoidal shape, nonlinear growth models sometimes failed to provide meaningful parameter estimates. The existence of an inflection point and asymptotes in the growth models made them inflexible with life expectancy data. In linear models, there was no significant difference in the life expectancy growth rate and future estimates between ordinary least squares (OLS) and generalized least squares (GLS). However, the generalized least squares model was more robust because the data involved time-series variables and residuals were positively correlated. ^
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Infant Mortality has been made a point of emphasis by the Department of Health and Human Services in the Healthy People 2000, 2010, and 2020 priorities. This study used the Behavioral Model for Vulnerable Populations to consider a number of factors which impact infant mortality in the indigent populations in the State of Texas. The primary focus of this study was the enabling factor of community resources, specifically the program used by each county to provide care to their indigent population. The Legislature of the State of Texas requires that each state have a program set up within a Hospital District, Public Hospital or develop a County Indigent Health Care Program (CIHCP) in order to provide the basic health care needs of their most vulnerable residents. We sought to determine whether the development of a CICHP without an appointed hospital to provide the care would have an adverse effect on residents seeking care and increase infant mortality. A Poisson Regression Analysis was used to analyze incidence rate ratios adjusting for race/ethnicity and wealth/poverty variables. Our study showed that counties using a CIHCP had significantly lower infant mortality rates when compared to counties using a hospital district and were statistically equivalent to counties using a public hospital program or a combination of service programs. This relationship was maintained when adjusted incidence rate ratios were calculated. This may give evidence that counties struggling to fund a public hospital or hospital district may be able to find a more cost-effective alternative in the CIHCP without adversely affecting the health status of their residents. More cost-benefit analysis and controlling analysis must be done to further characterize this relationship. ^
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Congenital anomalies have been a leading cause of infant mortality for the past twenty years in the United States. Few registry-based studies have investigated the mortality experience of infants with congenital anomalies. Therefore, a registry-based mortality study was conducted of 2776 infants from the Texas Birth Defects Registry who were born January 1, 1995 to December 31, 1997, with selected congenital anomalies. Infants were matched to linked birth-infant death files from the Texas Department of Health, Bureau of Vital Statistics. One year Kaplan-Meier survival curves, and mortality estimates were generated for each of the 23 anomalies by maternal race/ethnicity, infant sex, birth weight, gestational age, number of life-threatening anomalies, prenatal diagnosis, hospital of birth and other variables. ^ There were 523 deaths within the first year of life (mortality rate = 191.0 per 1,000 infants). Infants with gastroschisis, trisomy 21, and cleft lip ± palate had the highest first year survival (92.91%, 92.32%, and 87.59%, respectively). Anomalies with the lowest survival were anencephaly (5.13%), trisomy 13 (7.41%), and trisomy 18 (10.29%). ^ Infants born to White, Non-Hispanic women had the highest first year survival (83.57%; 95% CI: 80.91, 85.88), followed by African-Americans (82.43%; 95% CI: 76.98, 86.70) and Hispanics (79.28%; 95% CI: 77.19, 81.21). Infants with birth weights ≥2500 grams and gestational ages ≥37 weeks also had the highest first year survival. First year mortality drastically increased as the number of life-threatening anomalies increased. Mortality was also higher for infants with anomalies that were prenatally diagnosed. Slight differences existed in survival based on infant's place of delivery. ^ In logistic regression analysis, birth weight (<1500 grams: OR = 7.48; 95% CI: 5.42, 10.33; 1500–2499 grams: OR = 3.48; 95% CI: 2.74, 4.42), prenatal diagnosis (OR = 1.92; 95% CI: 1.43, 2.58) and number of life-threatening anomalies (≥3: OR = 22.45; 95% CI: 11.67, 43.18) were the strongest predictors of death within the first year of life for all infants with selected congenital anomalies. To achieve further reduction in the infant mortality rate in the United States, additional research is needed to identify ways to reduce mortality among infants with congenital anomalies. ^
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Acknowledgements We thank Ms Katie Wilde, Data Management Team, University of Aberdeen and Lynsey Waugh, Information and Services Division of NHS Scotland for their help with data extraction and linkage. Funding sources This work was supported by funding from the Chief Scientist Office, Scotland. We also acknowledge support from Tommy’s and the British Heart Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. None of the authors are related to any of the funders
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Sandhoff disease is a neurodegenerative disorder resulting from the autosomal recessive inheritance of mutations in the HEXB gene, which encodes the β-subunit of β-hexosaminidase. GM2 ganglioside fails to be degraded and accumulates within lysosomes in cells of the periphery and the central nervous system (CNS). There are currently no therapies for the glycosphingolipid lysosomal storage diseases that involve CNS pathology, including the GM2 gangliosidoses. One strategy for treating this and related diseases is substrate deprivation. This would utilize an inhibitor of glycosphingolipid biosynthesis to balance synthesis with the impaired rate of catabolism, thus preventing storage. One such inhibitor is N-butyldeoxynojirimycin, which currently is in clinical trials for the potential treatment of type 1 Gaucher disease, a related disease that involves glycosphingolipid storage in peripheral tissues, but not in the CNS. In this study, we have evaluated whether this drug also could be applied to the treatment of diseases with CNS storage and pathology. We therefore have treated a mouse model of Sandhoff disease with the inhibitor N-butyldeoxynojirimycin. The treated mice have delayed symptom onset, reduced storage in the brain and peripheral tissues, and increased life expectancy. Substrate deprivation therefore offers a potentially general therapy for this family of lysosomal storage diseases, including those with CNS disease.
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Thioredoxin (Trx) is an intracellular redox protein with extracellular cytokine-like and chemokine-like activities. We show here that, although plasma Trx levels are unrelated to survival of HIV-infected individuals with CD4 cell counts above 200/μl blood, survival is significantly impaired (P = 0.003) when plasma Trx is chronically elevated in HIV-infected subjects with CD4 T cell counts below this level (i.e., with Centers for Disease Control (CDC)-defined AIDS). Relevant to the mechanism potentially underlying this finding, we also present data from experimental studies in mice showing that elevated plasma Trx efficiently blocks lipopolysaccharide (LPS)-induced chemotaxis, an innate immune mechanism that is particularly crucial when adaptive immunity is compromised. Thus, we propose that elevated plasma Trx in HIV-infected individuals with low CD4 T cell counts directly impairs survival by blocking pathogen-induced chemotaxis, effectively eliminating the last (innate) barrier against establishment of opportunistic and other infections in these immunodeficient individuals.
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Mode of access: Internet.
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Mode of access: Internet.
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Published also in the author's A familiar explanation of the nature, advantages, and importance of assurance upon lives ... London, 1842. 19 1/2 cm. p. 183-221.
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"May 2000."
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Cover title.
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Description based on: 1988.