PubMed · 14188812
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D S MARTIN. 1964. TEACHING MATERIALS: CDC RESOURCES.. https://pubmed.ncbi.nlm.nih.gov/14188812/
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A multistate Centers for Disease Control and Prevention (CDC) study was designed to investigate the etiology of congenital hearing loss in infants ascertained through state-mandated hearing screening or early hearing loss detection and intervention (EHDI) programs. At least 50% of permanent childhood-onset hearing loss is due to genetic causes, and approximately 20% of all infants with congenital hearing loss have mutations in the GJB2 gene. Another 1% of childhood hearing loss is due to mitochondrial DNA (mtDNA) mutations. The specific aims of this study are to 1) classify the etiology of congenital hearing loss in infants by doing prospective genetic evaluations of all newborns with permanent hearing loss from defined geographic areas, 2) determine the frequency of mutations in GJB2 and two common mitochondrial mutations in these populations, and 3) establish a model infrastructure linking genetic services to statewide EHDI programs. As of April 2003, Utah is the only center evaluating patients. Study subjects identified through the Utah Department of Health EHDI program are contacted by letter and offered a comprehensive medical genetics evaluation with DNA testing for GJB2 and mitochondrial mutations A1555G and A7445G. To date, 25 probands and their immediate family members have been evaluated. We have identified 20 cases with nonsyndromic hearing loss (7 multiplex and 13 simplex), 4 with syndromic hearing loss, and 1 with presumed cytomegalovirus (CMV)-induced hearing loss. Six of 19 (32%) nonsyndromic cases with sensorineural hearing loss have mutations of one or both alleles of the GJB2 gene, and 21% are homozygous or compound heterozygotes for the 35delG mutation. No A1555G or A7445G mtDNA mutations have been found. Data reported to date include only children born in Utah, but EHDI programs in Hawaii, Rhode Island, and designated areas of Georgia have begun enrolling children in what is now a multistate collaborative study. This is the first comprehensive investigation to determine the etiology of hearing loss from populations ascertained through EHDI programs. The results of this study will facilitate the incorporation of genetic services into EHDI programs.
Each year, thousands of preventable deaths and hospitalizations result from complications of influenza and pneumococcal disease, mostly in elderly persons, despite the availability of vaccines. Obtaining signed consent prior to administering the vaccines represents an obstacle to achieving the Healthy People 2010 goals for vaccinating individuals against influenza and pneumococcal disease. Signed consent is neither legally mandated nor a guarantee that the patient (or proxy) has given informed consent. Nonetheless, many health care providers and institutions currently require signed consent before administering these vaccines. Rather, health care providers should use the Vaccine Information Sheets developed by the Centers for Disease Control and Prevention to inform patients about the risks and benefits associated with these vaccines. Requiring signed consent before administering these low-risk, high-benefit vaccines is inconsistent with the current practice of not requiring signed consent before prescribing other common treatments, eg, antibiotic treatment, whose risk levels are the same or higher.
BACKGROUND: Social capital has been related to a number of important public health variables such as overall mortality, health status, and sexually transmitted infections (including AIDS case rates). However, the relationship of social capital to tuberculosis has received little attention. Because social capital may be related to the constructs of poverty and income inequality, any exploration of the correlation between social capital and tuberculosis should include examination of the interrelationships with poverty and income inequality as well. OBJECTIVE: This study examined the state-level relationship between social capital, poverty, income inequality, and tuberculosis case rates. METHODS: The design was state-level, correlational analysis (including bivariate linear correlational analysis, and multivariate linear stepwise regression analysis). Main outcome measures were 1999 state-level case rates of tuberculosis. RESULTS: In bivariate analyses, poverty, income inequality, and social capital were all significantly correlated with tuberculosis case rates. In stepwise multiple regression analyses predicting tuberculosis case rates from this set of three predictor variables, social capital and income inequality entered the regression equation (with social capital being the strongest predictor variable). CONCLUSIONS: These results suggest that social capital is highly predictive of tuberculosis at the state level. The results indicate the need for further research into this potentially causal relationship, including the examination of structural interventions designed to increase social capital.