Sex and race differences in young people's responsiveness to price and tobacco control policies.
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OBJECTIVE: To determine if there are differences in young people's responsiveness to price and tobacco control policies for population subgroups and to examine whether or not these differences, if they exist, can explain sex and racial differences in trends in the prevalence of smoking in young people in the United States. DESIGN: Use cross-sectional and intertemporal variation in local and state tobacco control policies and prices to calculate demand responses to these policies using regression analysis techniques. SUBJECTS: A nationally representative sample of American eighth grade (ages 13-14 years), 10th grade (15-16 years) and 12th grade (17-18 years) students obtained from the 1992-1994 Monitoring the Future surveys. MAIN OUTCOME MEASURE: Thirty-day smoking prevalence. RESULTS: Young men are much more responsive to changes in the price of cigarettes than young women. The prevalence elasticity for young men is almost twice as large as that for young women. Smoking rates of young black men are significantly more responsive to changes in price than young white men. Significant differences in responsiveness to particular tobacco control policies also exist. These differences, however, explain relatively little of the differences in smoking prevalence among young population subgroups. CONCLUSIONS: Policymakers need to keep in mind that there is not a "one-size fits all" strategy for discouraging smoking among young people. (+info)
High prevalence of pathogenic mutations in patients with early-onset dementia detected by sequence analyses of four different genes.
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Clinical differential diagnosis of early-onset dementia (EOD) includes familial Alzheimer disease (FAD) and hereditary prion disease. In both disease entities, postmortem brain histopathological examination is essential for unambiguous diagnosis. Mutations in the genes encoding the presenilins (PS1 and PS2) and amyloid precursor protein (APP) are associated with FAD, whereas mutations in the prion protein (PrP) gene are associated with prion disease. To investigate the proportion of EOD attributable to known genes, we prospectively (i.e., antemortem) screened these four genes for mutations by sequencing genomic PCR products from patients with EOD before age 60 years. Family history for dementia was positive (PFH) in 16 patients, negative (NFH) in 17 patients, and unknown (UFH) in 3 patients. In 12 patients, we found five novel mutations (in PS1, F105L; in PS2, T122P and M239I; and in PrP, Q160X and T188K) and five previously reported mutations (in APP, in three patients who were most likely unrelated, V717I; in PS1, A79V and M139V; and in PrP, P102L and T183A) that are all considered to be disease causing. Of these 12 patients, 9 had PFH. This indicates a detection rate of 56% (9/16) in patients with PFH. We found two mutations (APP V717I) in two of the three UFH patients, and only one mutation (PrP T188K) in 1 of the 17 patients with NFH. We conclude that because of the lack of specific antemortem diagnostic markers for FAD and hereditary prion disease, all four genes should be included in a molecular diagnostic program in patients with EOD who had PFH. (+info)
Linkage disequilibrium and allele-frequency distributions for 114 single-nucleotide polymorphisms in five populations.
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Single-nucleotide polymorphisms (SNPs) may be extremely important for deciphering the impact of genetic variation on complex human diseases. The ultimate value of SNPs for linkage and association mapping studies depends in part on the distribution of SNP allele frequencies and intermarker linkage disequilibrium (LD) across populations. Limited information is available about these distributions on a genomewide scale, particularly for LD. Using 114 SNPs from 33 genes, we compared these distributions in five American populations (727 individuals) of African, European, Chinese, Hispanic, and Japanese descent. The allele frequencies were highly correlated across populations but differed by >20% for at least one pair of populations in 35% of SNPs. The correlation in LD was high for some pairs of populations but not for others (e.g., Chinese American or Japanese American vs. any other population). Regardless of population, average minor-allele frequencies were significantly higher for SNPs in noncoding regions (20%-25%) than for SNPs in coding regions (12%-16%). Interestingly, we found that intermarker LD may be strongest with pairs of SNPs in which both markers are nonconservative substitutions, compared to pairs of SNPs where at least one marker is a conservative substitution. These results suggest that population differences and marker location within the gene may be important factors in the selection of SNPs for use in the study of complex disease with linkage or association mapping methods. (+info)
Highlights of trends in pregnancies and pregnancy rates by outcome: estimates for the United States, 1976-96.
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OBJECTIVES: This report presents key findings from a comprehensive report on pregnancies and pregnancy rates for U.S. women. The study incorporates birth, abortion, and fetal loss data to compile national estimates of pregnancy rates according to a variety of characteristics including age, race, Hispanic origin, and marital status. Summary data are presented for 1976-96. Data from the National Survey of Family Growth (NSFG) are used to show information on sexual activity and contraceptive practices, as well as women's reports of pregnancy intentions. METHODS: Tabular and graphic data on pregnancy rates by demographic characteristics are presented and interpreted. Birth data are from the birth registration system for all births registered in the United States and reported by State health departments to NCHS; abortion data are from The Alan Guttmacher Institute (AGI) and the National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention (CDC); and fetal loss data are from pregnancy history information collected in the NSFG. RESULTS: In 1996 an estimated 6.24 million pregnancies resulted in 3.89 million live births, 1.37 million induced abortions, and 0.98 million fetal losses. The pregnancy rate in 1996 was 104.7 pregnancies per 1,000 women aged 15-44 years, 9 percent lower than in 1990 (115.6), and the lowest recorded since 1976 (102.7). Since 1990 rates have dropped 8 percent for live births, 16 percent for induced abortions, and 4 percent for fetal losses. The teenage pregnancy rate has declined considerably in the 1990's, falling 15 percent from its 1991 high of 116.5 per 1,000 women aged 15-19 to 98.7 in 1996. Among the factors accounting for this decline are decreased sexual activity, increases in condom use, and the adoption of the injectable and implant contraceptives. (+info)
United States life tables, 1997.
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The life tables in this report are current life tables for the United States based on age-specific death rates in 1997. Beginning with 1997 mortality data, complete U.S. life tables were constructed using a new methodology that replaces the abridged life table methodology used previously. The methodology is similar to that used in the decennial life tables. Also, life expectancy and other life table values are shown for ages 85 to 100 years for the first time as part of the annual U.S. life tables. Data used to prepare these life tables are 1997 final mortality statistics; July 1, 1997, population estimates; and data from the Medicare program. Presented are complete life tables by age, race, and sex. In 1997 the overall expectation of life at birth was 76.5 years, an increase of 0.4 years compared with life expectancy in 1996. Life expectancy increased from 1996 to 1997 for each of the four race-sex groups for which life expectancy is reported. Life expectancy increased for black males by 1.1 year (from 66.1 to 67.2), for black females by 0.5 year (from 74.2 to 74.7), for white males by 0.4 year (from 73.9 to 74.3), and for white females by 0.2 year (from 79.7 to 79.9). (+info)
Limitations in the use of race in the study of disease causation.
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Tremendous variation exists in the rates of many chronic diseases across racial groups. However, serious technical and conceptual limitations hamper the ability of racial comparisons to illuminate the causative pathways. First, race is confounded by social class, which is complex, and like other confounders of race, may not be measured with equal validity across racial groups. Second, statistical "adjustments" for race effects can be misleading since residual confounding may be misconstrued as a genetic effect. Third, the biologic concept of race tempts us to ignore the context dependency of genetic expression. When trying to detect genetic effects, both the environmental and genetic contributions must be measured and potential gene-environment interactions accounted for. Unfortunately, this process is beyond our current technical capabilities. To move forward on the problem of prostate cancer and other diseases distinguished by marked ethnic differentials, investigators need a more comprehensive understanding of the factors that mediate the apparent effect of race combined with valid measures of those factors, as well as novel strategies that can help overcome the technical and interpretive limitations of statistical adjustment. Finally, the "grand" theories of race-based genetic susceptibility must be replaced with rigorous criteria to determine when a trait can be ascribed to some genetic origin. (+info)
Trends in specialized surgical procedures at teaching and nonteaching hospitals.
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Teaching hospitals are the principal site of many specialized surgical procedures. The recipients of these procedures tend to be younger, male, and nonwhite and tend to reside in either the poorest or the most affluent neighborhoods. Although the numbers of these procedures performed at major teaching hospitals increased dramatically between 1989 and 1995, they accounted for only a modest proportion of hospital discharges and patient days. Concentration of specialized surgical procedures in major teaching hospitals will likely continue. This trend has implications not only for these hospitals but for health care purchasers, policymakers, medical educators, and clinical researchers as well. (+info)
Job-based health insurance, 1977-1998: the accidental system under scrutiny.
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This paper highlights changes in employer-based health insurance from 1977 to 1998, based on national household surveys conducted by the Agency for Health Care Policy and Research (AHCPR) in 1977, 1987, and 1996; and surveys of employers by the AHCPR in 1977, by the Health Insurance Association of America in 1988, and by KPMG Peat Marwick/Kaiser Family Foundation in 1998. During the study years, in 1998 dollars, the cost of job-based insurance increased 2.6-fold, and employees' contributions for coverage increased 3.5-fold. The percentage of nonelderly Americans covered by job-based insurance plummeted from 71 percent to 64 percent. This decline occurred exclusively among non-college-educated Americans. An information-based global economy is likely to produce not only greater future wealth but also greater inequalities in income and health benefits. (+info)