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In the News |
Recent Advances from the NHLBI |
At a hearing on July 19, NIH Director Dr. Elias Zerhouni and members of the House Committee on Energy and Commerce discussed draft legislation to reauthorize the NIH. The proposed bill included a provision to establish within the NIH Director’s office a Division of Program Coordination, Planning, and Strategic Initiatives, which would coordinate research on topics that do not have a “home” under the present NIH structure and would develop new trans-NIH programs.
On June 24, 2005, the House of Representatives passed its version of the Departments of Labor, Health and Human Services, and Education 2005 appropriations act (H.R. 3010). As requested in the President’s budget, the bill includes $2,951,270,000 for the NHLBI. This is an increase of 0.3 percent over the $2,941,201,000 that the NHLBI received in FY 2005. The Senate version, which the appropriations committee approved on July 14, includes $3,023,381,000 for the NHLBI.
House Report 109 143 and Senate Report 109 103 mention numerous diseases of
interest to the NHLBI, including alpha-1 antitrypsin deficiency, aplastic anemia,
asthma, chronic obstructive pulmonary disease (COPD), Cooley’s anemia,
cystic fibrosis, diabetes, Diamond-Blackfan anemia, Duchenne muscular dystrophy,
heart failure, hemophilia, hereditary hemorrhagic telangiectasia, lupus, lymphangioleiomyomatosis
(LAM), lymphedema, Marfan syndrome, pulmonary fibrosis, pulmonary hypertension,
scleroderma, stroke, thrombophilia, and thrombosis. Blood safety, gene therapy,
obesity, sleep, stem cells, and transplantation research also are addressed.
Several bills relevant to the NIH were introduced this summer, including the Pulmonary Hypertension Research Act of 2005 (H.R. 3005), the Family Asthma Act (S. 1489), and the Lupus Research, Education, Awareness, Communication, and Healthcare Amendments of 2005 (H.R. 3307). New resolutions of interest to the NHLBI address topics such as congenital heart defects (H.Res. 305), idiopathic pulmonary fibrosis (H.Con.Res. 178), and bone marrow failure diseases (H.Con.Res. 179).
New results from the NHLBI Programs for Genomic Applications may change prescribing practices of clinicians who order blood thinners to prevent dangerous blood clots. Physicians have been giving warfarin to patients since the 1950s, but they still use trial-and-error to determine the appropriate dose. In search of a way to predict the amount of warfarin that would adequately protect a patient from excessive blood clotting without causing uncontrolled bleeding, investigators analyzed blood samples from patients who were being treated with warfarin. They were able to identify genetic markers that correlated with whether a patient responded best to a low, intermediate, or high dose of the drug. This observation may pave the way for development of a blood test to guide physicians in prescribing safe and effective doses of blood thinners.
In the first study to link clusters of genes to specific forms of childhood asthma, researchers supported by the NHLBI used “gene-chip” microarray technology to compare respiratory epithelial cells from normal children, children with controlled (stable) asthma, and children with asthma exacerbations (acute asthma). They sifted through over 54,000 genes for each child studied and found eight distinct gene clusters that were differentially regulated in stable and acute asthma. One cluster was exclusively linked to acute asthma, while another was linked to stable asthma, suggesting that children with an active asthma exacerbation have a gene expression profile that is clearly different from that of controlled asthma. The findings open the door for molecular subclassification of asthma and the possibility of developing precisely targeted treatments based on unique genetic profiles in patients.