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HIV+ individuals with human CMV (HCMV) reactivation have a CD3 receptor-mediated T cell hyporesponsiveness when compared with CD4-matched HIV+ and HCMV- control groups. The impairment of proliferation was not reversed by exogenous IL-2. A typical increase in NFkappaB expression was observed following cross-linking of the CD3 receptor, but did not lead to increased CD25 cell surface expression or cell proliferation. The HCMV-induced non-responsiveness was not observed when cells were stimulated with phorbol esters. Lymphocytes cultured with media collected from cell cultures infected with HCMV showed a dose-dependent inhibition in the total T cell population even though cells staining dually for CD8/57 increased in number. The altered growth factor requirements of CD8/57+ cells may therefore account for their presence in AIDS and patients following bone marrow transplantation.

The relationship between heart rate and cancer mortality was examined in 3 Chicago epidemiologic studies: 1233 white men originally age 40-59 followed 18 years from the Chicago Peoples Gas Company study; 1899 white men originally age 40-55 followed 17 years from the Chicago Western Electric Company study; 5784 white men originally age 45-64 followed 5 years from the Chicago Heart Association Detection Project in Industry. There was a significant association between heart rate and cancer mortality in both univariate and multivariate analyses in men from the Gas Company study and in men from the Chicago Heart Association study, but there was no association between heart rate and cancer mortality in men from the Western Electric study. The relationship persisted in the Gas Company study but not in the Chicago Heart Association study after eliminating deaths within the first 2 years of follow-up. With cancer deaths broken down by the site, mortality from lung and colon cancer in the Gas Company study and mortality from lung cancer in the Chicago Heart Association study were significantly associated with baseline heart rate on univariate analysis and on bivariate analysis controlling for age. Only colon cancer in the Gas Company, however, remained associated with heart rate when other variables were controlled. Thus, in 2 of the 3 studies examined, heart rate appeared to be an independent risk factor for cancer mortality in men.

The associations between heart rate and death from the cardiovascular diseases (CVD), coronary heart disease (CHD) and sudden death from CHD, along with death from all causes and non-cardiovascular causes, are examined for three groups of middle-aged white males: 1233 men aged 40-59 years followed for 15 years from the Chicago Peoples Gas Company study; 1899 men aged 40-55 years followed for 17 years from the Chicago Western Electric Company study; and 5784 men aged 45-64 years followed an average of five years from the Chicago Heart Association Detection Project in Industry. In univariate analyses, mortality from both cardiovascular and non-cardiovascular causes generally increases with increasing heart rate. In bivariate analyses, using the Cox regression model to control for age, heart rate is significantly related to mortality from all causes in each study, with the associations again due to both cardiovascular and non-cardiovascular causes. In multivariate Cox regression, controlling for age, blood pressure, serum cholesterol, cigarettes smoked per day and relative weight, heart rate is a significant risk factor for sudden CHD death and non-CVD death in two of the three studies, with the association with sudden death being U-shaped in one of the studies. Although heart rate may be an independent risk factor for sudden CHD death, the associations with other CVD death and non-sudden CHD death, in general, appear to be secondary to associations between heart rate and other cardiovascular risk factors.

In the Chicago Western Electric Company study, diet was assessed at the initial examination, in 1957-1958, of 1900 middle-aged men and again at their second examination about one year later. At the first examination, lipid composition of the diet, as summarized by a score based on the formula of Keys, Anderson and Grande (Grande, F. Predicting change in serum cholesterol from change in lipid composition of the diet. In: Lauer RM, Shekelle RB, eds. Childhood Prevention of Atherosclerosis and Hypertension. New York: Raven Press, 1980:145-53), was positively associated with level of serum cholesterol. Between the first and second examinations, however, hypercholesterolemic men were more likely than others to have reduced intake of dietary saturated fatty acids and cholesterol. As a result, at the second examination the cross-sectional linear association between the diet score and serum cholesterol concentration was significantly positive for men with initial levels of serum cholesterol less than 250 mg/dl, significantly negative for men with initial levels of 250 mg/dl or higher and not significantly different from zero for all men together. The bias introduced by change in diet among hypercholesterolemic men differs importantly from bias due to unreliability of measurement and to interindividual differences in intrinsic level of serum cholesterol, because it can produce statistically significant but spurious correlations.

The relations between coffee consumption and 19-year mortality from all causes, coronary heart disease, and non-coronary causes were assessed in 1,910 white males aged 40-56 years in 1957-1958 from the Chicago Western Electric Company Study. Mortality rates, adjusted for age, serum cholesterol, diastolic blood pressure, and smoking status, were compared for those consuming 0-1, 2-3, 4-5, and 6+ cups of coffee per day; coffee intake, measured at the first anniversary examination, included both caffeinated and decaffeinated intake. Mortality from all causes was greatest in the highest and lowest intake groups. The increased mortality in the 6+ cups per day group was due to coronary heart disease, while the increased mortality in the lowest intake group was due to noncoronary causes. The adjusted relative risk of coronary heart disease death for those drinking 6+ cups of coffee per day compared with those drinking less was 1.71 (95 per cent confidence limits 1.27, 2.30). This increased risk of coronary heart disease death was present in both smokers and nonsmokers, with adjusted relative risks of 1.62 and 2.21, respectively (95 per cent confidence limits 1.17, 2.24 and 1.06, 4.62). The increased mortality from non-coronary causes in the lowest intake group was due primarily to increased mortality from cancer and cardiovascular diseases other than coronary heart disease. The results of this study support the hypothesis that those who drink 6+ cups of coffee per day may be at an increased risk of death from coronary heart disease.

The interrelationships among education, smoking, and non-cardiovascular (non-CVD) mortality were examined in middle-aged white males from the Chicago Peoples Gas Company Study (PG), the Chicago Western Electric Company Study (WE), and the Chicago Heart Association Detection Project in Industry (CHA). In each study, college graduates had the lowest prevalence of current smokers and the highest prevalence of former smokers. The associations between education and smoking were strongest in CHA, a study with baseline measurements 10-14 years after those of PG and WE and 3-8 years after the US Surgeon General's report on smoking and health in 1964. In PG and WE, the relative risks of non-CVD death for those who did not attend college compared to those who did were 1.50 and 1.38 (95% limits, 1.04 to 2.18 and 0.95 to 2.02). In CHA, the relative risk for those who did not graduate from college compared to those who did was 1.55 (1.17, 2.05). Differences in baseline cigarette smoking could account for only 23-29% of these increased risks. Because the associations between education and non-CVD mortality may have been confounded by changes in smoking status over the course of follow-up in these studies, non-CVD deaths were subdivided into those from causes related to smoking and causes not related to smoking. For smoking-related causes, the relative risk of death for those who did not attend/graduate from college was 1.95 (0.96, 3.95) in WE, 2.13 (1.18, 3.87) in PG, and 2.34 (1.47, 3.84) in CHA, while the relative risks for causes not related to smoking were 1.17, 1.12 and 1.16, respectively. These findings suggest that education is related inversely to non-CVD mortality primarily through smoking and smoking-related causes of death. With smoking becoming increasingly a habit of the less well-educated, these findings underscore the need for smoking prevention and cessation programmes targeted at the lower end of the socioeconomic scale.