Disease surveillance and population surveys of risk characteristics in a northeast rural community of Japan (1965 census population, 7,030) are combined in an attempt to relate morbidity and risk factor trends for coronary heart disease and stroke during the last 2 decades. Between 1964 and 1983, the incidence of coronary heart disease (i.e., combined myocardial infarction, angina pectoris, and sudden death) did not change significantly among men and women ages 40-69, and was lower than that for stroke. The incidence of all stroke declined about 60% for both men and women, ages 40-69, with a significant decrease in cerebral hemorrhage for both sexes and in cerebral infarction for men. Between 1963Between -1966Between and 1980Between -1983 upward shifts occurred in the means and distributions of serum total cholesterol and serum total protein in every age and sex group, primarily during the 1st decade. Age-adjusted mean cholesterol levels rose 22 mg/dl to the 1980-1983 mean of 179 mg/dl in men ages 40-69. In women ages 40-69, the mean rose 29 mg/dl to 192 mg/dl. Among nutrients, animal fat intake doubled in men ages 40-59 from 4.5% of daily calories in 1969 to 9.6% in 1980-1983. Animal protein intake also increased, from 5.8% to 7.1%. Most of this increase occurred between 1969 and 1972-1975 and may be attributable to an increased intake of meat, eggs and dairy products. From 1963From -1966From to 1980From -1983 relative weight index rose significantly for all age-sex groups except men ages 50-69. Mean systolic and diastolic blood pressure levels declined for every age-sex group, with a 15-mm Hg age-adjusted decrease in systolic, 4-mm Hg decrease in diastolic pressure among men ages 40-69, and a 11-mm Hg systolic and 4-mm Hg diastolic decrease for women. Two cohorts of men and women ages 40-69 at baseline were followed for disease incidence: an early cohort (2,257 persons) followed from 1963-1966 to 1973 and a later cohort (2,711 persons) followed from 1972-1975 to 1983. In these cohorts, significant risk prediction for cerebral hemorrhage and infarction was obtained with blood pressure level and end organ effects in the electrocardiogram and fundus photographs. Serum cholesterol was inversely associated with cerebral hemorrhage in the early cohort but not in the later. The reduced association of serum cholesterol in the later cohort may be due in part to the marked upward shift in means and distributions of serum cholesterol between these two periods and the lower power of the later analysis. (Circulation 1989;79:503-515) The frequency of coronary heart disease (CHD) and stroke in populations is strongly related to the prevalence of hypertension and atherosclerosis, which are greatly influenced, in turn, by risk characteristics, related behaviors, and associated environmental factors.' Japan has recently experienced rapid change in living and eating patterns.2 This provides a unique opportunity to observe a natural experiment in which population risk may change.In an attempt to relate morbidity t...

The present study examined the inhibitory eects of N-Hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine (HET0016) on the renal metabolism of arachidonic acid by cytochrome P450 (CYP) enzymes. HET0016 exhibited a high degree of selectivity in inhibiting the formation of 20-hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE) in rat renal microsomes. The IC 50 value averaged 35+4 nM, whereas the IC 50 value for inhibition of the formation of epoxyeicosatrienoic acids by HET0016 averaged 2800+300 nM. In human renal microsomes, HET0016 potently inhibited the formation of 20-HETE with an IC 50 value of 8.9+2.7 nM. Higher concentrations of HET0016 also inhibited the CYP2C9, CYP2D6 and CYP3A4-catalysed substrates oxidation with IC 50 values of 3300, 83,900 and 71,000 nM. The IC 50 value for HET0016 on cyclo-oxygenase activity was 2300 nM. These results indicate that HET0016 is a potent and selective inhibitor of CYP enzymes responsible for the formation of 20-HETE in man and rat.

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HRQOL decreases with progression of CKD stage and/or presence of anemia, undernutrition, hypertension, diabetes, or history of CVD.

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