To assess genetic and environmental influences on adult mortality, we followed 960 families that included children born during the period 1924 through 1926 who were placed early in life with adoptive parents unrelated to them. We evaluated the risks of dying from all causes or from specific groups of causes between the ages of 16 and 58 years for adoptees with a biologic or adoptive parent who died of the same cause before the age of either 50 or 70. We compared these risks with the adoptees' risk of dying from the same causes between the ages of 16 and 58 when either the biologic or adoptive parents were still alive at the ages of 50 and 70. The death of a biologic parent before the age of 50 resulted in relative risks of death in the adoptees of 1.71 (95 percent confidence interval, 1.14 to 2.57) for all causes, 1.98 (1.25 to 3.12) for natural causes, 5.81 (2.47 to 13.7) for infections, 4.52 (1.32 to 15.4) for cardiovascular and cerebrovascular causes, and 1.19 (0.16 to 8.99) for cancers. The death of an adoptive parent resulted in relative risks of death in the adoptees that were close to unity for all causes, natural causes, and infections, 3.02 (0.72 to 12.8) for vascular causes, and 5.16 (1.20 to 22.2) for cancers. A similar but weaker pattern was observed when either a biologic or adoptive parent died before the age of 70. We conclude that premature death in adults has a strong genetic background--especially death due to infections and vascular causes.(ABSTRACT TRUNCATED AT 250 WORDS)

Injection speed had no effect on injection pain, whereas higher injection volumes caused more pain. The results of this study may be of value for guiding patients to use the appropriate injection site and technique to reduce their injection pain. Furthermore, these findings may have important implications for the development of new injection devices and drug formulations for clinical practice.

102 patients with myocardial infarction (MI) were examined by three clinicians, who independently recorded the following symptoms and signs: dyspnoea, a displaced apex beat, S3-gallop, rales, neck vein distension, hepatomegaly, and dependent oedema. Chest X-ray, radionuclide ventriculography, and (in 40 patients) right heart catheterization were carried out immediately after the physical examination. The clinicians frequently disagreed as to the presence of physical signs of heart failure in individuals. Moreover, these signs were of limited value in identifying patients with pulmonary vascular congestion on chest X-ray, reduced left or right radionuclide ventricular ejection fractions, enlarged ventricular volumes or haemodynamic evidence of ventricular dysfunction. We conclude that clinicians frequently disagree in the recognition of physical signs of heart failure, and that these signs have an unpredictable relationship to radiographic, radionuclide and haemodynamic measures of ventricular performance in patients with MI. Nevertheless, physical signs are useful in identifying patients with high risk of cardiac death.