Epidemiologic Surveillance of Teenage Birth Rates in the United States, 2006-2012.

OBJECTIVE: To investigate the geographic variation in the average teenage birth rates by county in the contiguous United States. METHODS: Data from the National Center for Health Statistics were used in this retrospective cohort to count the total number of live births to females aged 15-19 years by county between 2006 and 2012. Software for disease surveillance and spatial cluster analysis was used to identify clusters of high or low teenage births in counties or areas of greater than 100,000 teenage females. The analysis was then adjusted for percentage of poverty and high school diploma achievement. RESULTS: The unadjusted analysis identified the top 10 clusters of teenage births. The cluster with the highest rate was a city and the surrounding 40 counties, demonstrating an average teen birth rate of 67 per 1,000 females in the age range, 87% higher than the rate in the contiguous United States. Adjustments for poverty rates and high school diploma achievement shifted the top clusters to other areas. CONCLUSION: Despite an overall national decline in the teenage birth rate, clusters of elevated teenage birth rates remain. These clusters are not random and remain higher than expected when adjusted for poverty and education. This data set provides a framework to focus targeted interventions to reduce teenage birth rates in this high-risk population.

RNA-editing-associated protein 1 null mutant reveals link to mitochondrial RNA stability.

In trypanosomatids, uridylate residues are post-transcriptionally added to or deleted from pre-mRNAs during the complex process of RNA editing. Editing is carried out exclusively in the mitochondrion of these parasites and involves numerous proteins assembled into protein and ribonucleoprotein complexes. Previously we identified RNA-editing-associated protein -1 (REAP-1), an RNA binding protein found in the mitochondrion of Trypanosoma brucei. REAP-1 was shown to specifically recognize and bind to pre-mRNAs that require editing and was proposed to act as a recruitment factor to deliver pre-mRNAs to editing complexes. To help define the role of REAP-1, we have now constructed REAP-1 null mutants. We show that the null mutants, although viable, have a significant growth defect. RNA levels within the mitochondrion were evaluated using reverse transcriptase real-time PCR. Surprisingly, the results show that mitochondrial RNA levels are increased, regardless of the editing status of the RNA. All RNA tested, whether unedited, edited, or never edited were increased in the mutant cell line relative to wild-type levels. This study provides the first evidence for a role of REAP-1 in RNA metabolism.