Response to health insurance by previously uninsured rural children.
OBJECTIVE: To examine the healthcare utilization and costs of previously uninsured rural children. DATA SOURCES/STUDY SETTING: Four years of claims data from a school-based health insurance program located in the Mississippi Delta. All children who were not Medicaid-eligible or were uninsured, were eligible for limited benefits under the program. The 1987 National Medical Expenditure Survey (NMES) was used to compare utilization of services. STUDY DESIGN: The study represents a natural experiment in the provision of insurance benefits to a previously uninsured population. Premiums for the claims cost were set with little or no information on expected use of services. Claims from the insurer were used to form a panel data set. Mixed model logistic and linear regressions were estimated to determine the response to insurance for several categories of health services. PRINCIPAL FINDINGS: The use of services increased over time and approached the level of utilization in the NMES. Conditional medical expenditures also increased over time. Actuarial estimates of claims cost greatly exceeded actual claims cost. The provision of a limited medical, dental, and optical benefit package cost approximately $20-$24 per member per month in claims paid. CONCLUSIONS: An important uncertainty in providing health insurance to previously uninsured populations is whether a pent-up demand exists for health services. Evidence of a pent-up demand for medical services was not supported in this study of rural school-age children. States considering partnerships with private insurers to implement the State Children's Health Insurance Program could lower premium costs by assembling basic data on previously uninsured children. (+info)
Reduced beta-cell compensation to the insulin resistance associated with obesity in members of caucasian familial type 2 diabetic kindreds.
OBJECTIVE: Both obesity and a family history of diabetes reduce insulin sensitivity, but the impact of obesity on insulin secretion among individuals predisposed to diabetes is uncertain. We used a pedigree-based approach to test the hypothesis that beta-cell compensation to the insulin resistance associated with obesity is defective among individuals predisposed to diabetes by virtue of a strong family history of type 2 diabetes before the development of diabetes or glucose intolerance. RESEARCH DESIGN AND METHODS: A total of 126 members of 26 families ascertained for at least a sib pair with type 2 diabetes with onset before age 65 years underwent a tolbutamide-modified frequently sampled intravenous glucose tolerance test (FSIGT). Family members included 26 individuals with impaired glucose tolerance and 100 individuals with normal glucose tolerance (NGT). The acute insulin response to glucose (AIRglucose) was determined and insulin sensitivity (S(I)) estimated by minimal model analysis of FSIGT data. The beta-cell compensation for insulin sensitivity was estimated from the disposition index (DI), calculated as the product of S(I) and AIRglucose. Obesity was measured by BMI. RESULTS: Among all individuals, BMI was a significant predictor of both S(I) and AIRglucose, as expected. However, BMI also significantly predicted DI (P = 0.002) after correcting for age, sex, family membership, and glucose tolerance status. The relationship of BMI and DI was confirmed in 85 individuals with NGT who were aged <45 (P = 0.002) but not in 91 unrelated control individuals without a family history of diabetes. When normoglycemic individuals aged <45 were separated into three classes by BMI (< or =27, 27-30, >30), S(I) decreased progressively and significantly with obesity whereas AIRglucose rose significantly from lean to most obese classes. In contrast to the expectation of complete beta-cell compensation with obesity D1 fell significantly (P = 0.004) among obese family members. This relationship was not observed in control subjects. CONCLUSIONS: Individuals with a genetic predisposition to diabetes show a reduced beta-cell compensatory response to the reduced insulin sensitivity associated with obesity. We propose that this impaired compensation may be one manifestation of the underlying genetic defect in susceptible individuals. This finding helps explain the multiplicative effects of family history and obesity on risk of type 2 diabetes. (+info)
Spoligotyping and polymorphic GC-rich repetitive sequence fingerprinting of mycobacterium tuberculosis strains having few copies of IS6110.
Several genetic loci have been utilized to genotype isolates of Mycobacterium tuberculosis. A shortcoming of the most commonly used method, IS6110 fingerprinting, is that it does not adequately discriminate between isolates having few copies of IS6110. This study was undertaken to compare pTBN12 fingerprinting of polymorphic GC-rich repetitive sequence genes and spoligotyping of the direct repeat locus as secondary typing procedures for M. tuberculosis isolates having fewer than six copies of IS6110. A total of 88 isolates (100% of the isolates with fewer than six copies of IS6110 isolated in Arkansas during 1996 and 1997) were included in this study. Among the 88 isolates, 34 different IS6110 patterns were observed, 10 of which were shared by more than 1 isolate, involving a total of 64 isolates. The 64 isolates were subdivided into 13 clusters (containing 37 isolates) and 27 unique isolates based on a combination of IS6110 and pTBN12 fingerprinting and into 11 clusters (containing 51 isolates) and 13 unique isolates based on a combination of IS6110 fingerprinting and spoligotyping. Identical spoligotypes were found among isolates having different IS6110 patterns, as well as among isolates showing different pTBN12 patterns. In contrast, all isolates that had different IS6110 patterns were found to be unique by pTBN12 typing. The clustering rate was 73, 58, and 42%, respectively, for IS6110 fingerprinting alone, IS6110 fingerprinting and spoligotyping combined, and IS6110 and pTBN12 combined fingerprinting. The data indicate that the pTBN12 method has greater discriminating power among low-copy-number isolates than does spoligotyping. (+info)
Anatomy of a successful K-12 educational outreach program in the health sciences: eleven years experience at one medical sciences campus.
The Department of Anatomy and Neurobiology, College of Medicine, University of Arkansas for Medical Sciences (UAMS) is the administrative home of a nationally recognized educational outreach program in the health sciences for K-12 teachers (includes school nurses, counselors, etc.) and students. This program is called the Partners in Health Sciences (PIHS) program. It began in the summer of 1991 and is based on an annual needs assessment of the state's teachers. PIHS is a program available to all teachers and students in the state. It has several different components: (1) a cafeteria of 21 days of mini-courses offered in the summer to meet the professional development needs of K-12 biology/health teachers and other school personnel; (2) weekly, interactive telecommunication broadcasts for students during the academic year; (3) intensive, 5-day workshops that train five selected teachers at a time (10 per year) to use an authoring software program to develop grade-appropriate interactive, computer-assisted, instructional (CAI) modules for Internet (http://k14education.uams.edu) use by teachers and students; (4) a monthly science night for students and their parents at a local science magnet high school; (5) field trips to the UAMS campus for teachers and their students; (6) community-requested presentations by program faculty; and (7) availability of earning undergraduate and graduate credit for science education majors in the College of Education, University of Arkansas at Little Rock. The data presented in this report span the period from 1991 through 2001. For all program activities, 14,084 different participants have consumed a total of 50,029 hours of education. (+info)
Molecular subtype analyses of Campylobacter spp. from Arkansas and California poultry operations.
Campylobacter isolates from diverse samples within broiler production and processing environments were typed by using flaA short variable region DNA sequence analysis. Sixteen flocks from four different farms representing two broiler producers in Arkansas and California were analyzed. Fourteen of the flocks (87.5%) were Campylobacter-positive; two remained negative throughout the 6-week rearing period. In general, multiple clones were present within a flock. Additionally, clones found within a flock were also present on the final product, although the diversity of Campylobacter spp. on the final product appeared to be reduced relative to that observed within the flock. Comparison of clones between flocks on the same farm revealed that some clones of Campylobacter persisted in multiple flocks. Furthermore, some clones were identified across the two farms that were under the same management. In two sampling periods, environmental isolates were positive for Campylobacter prior to flock shedding. Environmental samples associated with five additional flocks were positive for Campylobacter concomitantly with recovery of Campylobacter from the birds. Analysis of the environmental isolates that were positive prior to flock shedding demonstrated that in some instances the environmental isolates possessed genotypes identical to those of isolates originating from the flock, while in other cases the environmental isolates possessed genotypes that were distantly related to isolates obtained from the flock. Analyses of environmental isolates that tested positive concurrently with the positive isolates from the flocks demonstrated varied results; in some instances the environmental isolates possessed genotypes identical to those of isolates originating from the flock, while in other cases the environmental isolates possessed genotypes that were distantly related to isolates obtained from the flock. These data suggest that the external environment may contribute to Campylobacter contamination during poultry production and processing. However, environmental contamination with Campylobacter does not appear to be the sole contributing factor. (+info)
Transmission of Mycobacterium tuberculosis in a rural community, Arkansas, 1945-2000.
A cluster of tuberculosis cases in a rural community in Arkansas persisted from 1991 to 1999. The cluster had 13 members, 11 linked epidemiologically. Old records identified 24 additional patients for 40 linked cases during a 54-year period. Residents of this neighborhood represent a population at high risk who should be considered for tuberculin testing and treatment for latent tuberculosis infection. (+info)
Mycobacterium tuberculosis transmission between cluster members with similar fingerprint patterns.
Molecular epidemiologic studies provide evidence of transmission of Mycobacterium tuberculosis within clusters of patients whose isolates share identical IS6110-DNA fingerprint patterns. However, M. tuberculosis transmission among patients whose isolates have similar but not identical DNA fingerprint patterns (i.e., differing by a single band) has not been well documented. We used DNA fingerprinting, combined with conventional epidemiology, to show unsuspected patterns of tuberculosis transmission associated with three public bars in the same city. Among clustered TB cases, DNA fingerprinting analysis of isolates with similar and identical fingerprints helped us discover epidemiologic links missed during routine tuberculosis contact investigations. (+info)
Racial differences in the outcome of patients with colorectal carcinoma.
BACKGROUND: African-American (AA) patients with colorectal carcinoma have a worse prognosis compared with Caucasians. To analyze the causes of this disparity in survival, a retrospective study of patients with colorectal carcinoma was undertaken. The impact of treatments received and the role of socioeconomic factors such as income, education, and poverty levels were studied. METHODS: A retrospective analysis of patients with colorectal carcinoma at a single institution was conducted. The overall survival of AA and Caucasians, stage at presentation, treatment received, and socioeconomic factors were analyzed using the institutional tumor registry and 1990 census data. RESULTS: The overall survival of AA patients was worse compared with Caucasians, both due to all causes (P < 0.001) and cancer-related deaths (P < 0.001). The relative risk of death due to all causes was 1.4 (95% confidence interval [CI] 1.2-1.8) for AA, 4.3 for patients with Stage IV disease (95% CI 3.2-5.7), and 2.3 for patients not undergoing surgery (95% CI 1.7-3.1). After multivariate adjustment for gender, site, socioeconomic factors, and therapeutic modalities, the relative risks for death were 1.5 (95% CI 1.2) for AA, 1.4 (95% CI 1.1-1.7) for patients 60 years of age or older, and 4.2 (95% CI 3.4-5.2) for Stage IV disease. The survival difference between AA and Caucasians was not influenced by income, poverty level, and education. African Americans were treated less frequently with chemotherapy and radiation therapy compared with their Caucasian counterparts. CONCLUSIONS: African American patients with colorectal carcinoma have a poorer prognosis compared with Caucasians. This discrepancy may be due to decreased utilization of chemotherapy and radiation therapy. Socioeconomic factors and lack of access to health care do not entirely explain the worse prognosis of AA. These factors should be identified and dealt with to improve the health care of AA patients with various malignant disorders. (+info)