Increasing Utilization of the Preparticipation Physical Evaluation.

Objective: The American Heart Association and American Academy of Pediatrics endorse the preparticipation physical evaluation (PPE) to screen student athletes for the risk of sudden cardiac arrest. We sought to identify barriers precluding its use and improve utilization.

Methods: We analyzed documentation of PPE elements during well-care visits of patients aged 12 to 18 years from 5 primary care practices.

Assessment of Exercise Function in Children and Young Adults with Hypertrophic Cardiomyopathy and Correlation with Transthoracic Echocardiographic Parameters.

Exercise function is well characterized in adults with hypertrophic cardiomyopathy (HCM); however, there is a paucity of data in children and young adults with HCM. Here we sought to characterize exercise function in young people with HCM, understand limitations in exercise function by correlating exercise function parameters with echocardiogram parameters and identify prognostic value of exercise parameters. We performed a retrospective, single-center cohort study characterizing exercise function in patients < 26 years old with HCM undergoing cardiopulmonary exercise testing (CPET).

Cardiopulmonary stress testing in children and adults with congenital heart disease.

Cardiopulmonary exercise stress testing (CPET) is a vital tool used to assess patients with a history of congenital heart disease. There are several tests in the cardiologist's armamentarium that allow for assessment of cardiac anatomy and function. The majority of these tests are only performed with the body at rest and some even require sedation.

The PTEN/MMAC1 tumor suppressor induces cell death that is rescued by the AKT/protein kinase B oncogene.

PTEN/MMAC1 is a tumor suppressor gene that is mutated in a variety of cancers. PTEN encodes a phosphatase that recognizes phosphoprotein substrates and the phospholipid, phosphatidylinositol-3,4,5-triphosphate. PTEN inhibited cell growth and/or colony formation in all of the epithelial lines tested with one exception.

PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer.

Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN, that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions.