Attenders at a contraceptive clinic for single women.
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Adult↗
Biomedical subjects
M Wadsworth
Publications and source records attributed to M Wadsworth.
Psychosocial and developmental antecedents of chest pain in young adults.
OBJECTIVE: The objective of this study was to assess the relationships among chest pain, psychiatric disorder, and early experience of ill health. METHODS: The Medical Research Council National Survey of Health and Development is a population-based birth cohort study established in 1946 (N = 5362). During childhood, several informants (parents, teachers, and school physicians) were interviewed or completed questionnaires. Data were available on the subjects' health, the health of their parents, and subjects' personalities. At the age of 36 years, subjects were asked about chest pain using the Rose Angina Questionnaire and completed the Present State Examination, a semistructured psychiatric interview. Subjects were followed for another 7 years (to age 43 years) to determine the outcome of those with chest pain. RESULTS: Chest pain was reported in 17.2% (95% CI = 15.9-18.5%) of respondents at 36 years. The prevalence of exertional chest pain was 1.0% (95% CI = 0.7-1.3%). There was little evidence of coronary heart disease in those with exertional pain at age 36 years when followed for 7 years. However, there was a powerful cross-sectional relationship between psychiatric disorder and chest pain (OR for psychiatric disorder and all chest pain = 3.55, 95% CI = 2.34-5.37; OR for psychiatric disorder and exertional chest pain = 29.08, 95% CI = 6.65-127.15). Childhood risk factors, including poor health reported in parents at age 15 years and fatigue during childhood, were also associated with chest pain. CONCLUSIONS: Chest pain (especially exertional chest pain) is strongly associated with psychiatric disorders in young adults. Childhood experiences, including illness in parents, are associated with subsequent chest pain.
Adolescent↗
Immunoelectron microscopic localization of plasminogen activator inhibitor type 1 (PAI-1) in smooth muscle cells from morphologically normal and atherosclerotic human arteries.
Vascular wall fibrinolytic system proteins are believed to play a pivotal role in atherogenesis. Tissue-type plasminogen activator (t-PA) and urokinase plasminogen activator (u-PA) influence persistence of luminal thrombi and proteolysis of extracellular matrix, respectively. The major physiologic inhibitor of t-PA and u-PA is plasminogen activator inhibitor type 1 (PAI-1). All three of these fibrinolytic system proteins have been detected in vascular endothelial cells, smooth muscle cells, and macrophages by light microscopic immunohistochemistry. This study was undertaken to delineate, by immunoelectron microscopy, the loci of PAI-1 in smooth muscle cells from intact morphologically normal and atherosclerotic human arteries as well as in isolated and cultured smooth muscle cells from arteries. In intact vessels, PAI-1 immunoreactivity was associated with contractile filaments in cells in both normal and atherosclerotic tissues. Lipid-laden smooth muscle cells in atherosclerotic vessels were mainly of the synthetic phenotype and displayed lesser amounts of PAI-1 associated with rough endoplasmic reticulum and contractile filaments. Isolated smooth muscle cells exhibited either a contractile or synthetic phenotype. In the cells with a contractile phenotype, PAI-1 was associated with the contractile elements, whereas in the cells with a synthetic phenotype, the PAI-1 was associated predominantly with elements of the endoplasmic reticulum. Because PAI-1 is associated predominantly with contractile filaments in smooth muscle cells, the net amount of immunodetectable PAI-1 appears to be greater in contractile compared with synthetic phenotype cells.
Arteriosclerosis↗