PubMed Health⌕ Search

Biomedical subjects

D Chiu

Publications and source records attributed to D Chiu.

At least 37 records · Page 2Linked to original sources
PubMed1995

Combined effects of HDL cholesterol, triglyceride, and total cholesterol concentrations on 18-year risk of atherosclerotic disease.

BACKGROUND: Whether the combination of a low level of HDL cholesterol (HDL-C) and high level of triglyceride (TG) confers increased risk of cardiovascular disease and whether risk varies across levels of total cholesterol (TC) are not well established. Combined effects of HDL-C, TG, and TC on the incidence of atherosclerotic disease were examined prospectively in Japanese-American men from the Honolulu Heart Program. METHODS AND RESULTS: Among 1,646 men aged 51 to 72 years who were free of coronary heart disease (CHD), stroke, and cancer and were not taking lipid-lowering medication, 318 developed atherosclerotic events (angina, coronary insufficiency, aortic aneurysm, definite CHD, or thromboembolic stroke) and 170 developed definite CHD between 1970 and 1988. Subjects were stratified by TC level (desirable, < 200 mg/dL; borderline high, 200 to 239 mg/dL; high, > or = 240 mg/dL), HDL-C level (< 35 and > or = 35 mg/dL), and TG level (< 200 and > or = 200 mg/dL). With Cox regression with high HDL-C and low TG as reference, age-adjusted relative risks (RR) of atherosclerotic events were significantly elevated in men with low HDL-C and high TG at borderline-high (RR, 2.46; 95% CI, 1.48 to 4.09) and high (RR, 2.21; 95% CI, 1.34 to 3.66) TC levels but not in men with desirable TC levels (RR, 0.89; 95% CI, 0.38 to 2.09). Elevated risks were independent of blood pressure, obesity, fat distribution, diabetes, smoking, and alcohol. Results were not materially altered by exclusion of subjects with angina alone and were similar but somewhat weaker for CHD. CONCLUSIONS: Risk of atherosclerotic disease appears elevated in subjects with low HDL-C and high TG levels when TC is borderline high or high, independent of other cardiovascular risk factors. These findings support recent cholesterol screening recommendations and suggest that joint effects of HDL-C and TG may be important to consider.

Aged↗
PubMed1995

Sudden death, impaired glucose tolerance, and diabetes in Japanese American men.

BACKGROUND: Diabetes and glucose intolerance have been shown to increase the risk of cardiovascular mortality in a number of different populations. Most studies have been based on short follow-up periods, and few have had sufficient numbers to allow researchers to look at sudden death as an outcome. METHODS AND RESULTS: The relation of sudden death, defined as unexpected death occurring within either 1 or 24 hours of first symptoms, to glucose intolerance measured by a nonfasting 1-hour postload measurement made in 1965 or history of diabetes was examined by use of 23 years of follow-up on the 8006 participants enrolled in the Honolulu Heart Program. After adjustment for baseline body mass index, hypertension, cholesterol, triglycerides, smoking, alcohol consumption, and left ventricular hypertrophy or strain, the relative risks for sudden death within 24 hours in individuals with high-normal (151 to 224 mg/dL), asymptomatic high glucose values (> or = 225 mg/dL), and diabetes compared with those with lower glucose values (< 151 mg/dL) were 1.59, 2.22, and 2.76, respectively. All these relative risks were statistically significant (P < or = .05). Trends for sudden death in 1 hour were similar. Among men with sudden death < 1 hour after onset of symptoms, the strength of the association between diabetes and sudden death was stronger among those classified as having died of unknown causes who thus were more likely to have died of an arrhythmia than among those classified as having died of coronary heart disease. CONCLUSIONS: The relations seen in these analyses indicate that individuals with glucose intolerance or diagnosed diabetes are at increased risk for sudden death.

Aged↗
PubMed1995

Lifestyle and biologic factors associated with atherosclerotic disease in middle-aged men. 20-year findings from the Honolulu Heart Program.

OBJECTIVES: To examine the association between a variety of baseline lifestyle and biologic factors in a middle-aged cohort of Japanese-American men and the 20-year incidence rates of total atherosclerotic end points and each of the initial clinical manifestations of this disease, including fatal and nonfatal coronary heart disease, angina pectoris, thromboembolic strokes, and aortic aneurysms. DESIGN: Prospective epidemiologic study. POPULATION: Japanese-American men (N = 2710) between the ages of 55 and 64 years at the time of the initial clinical examination of the Honolulu Heart Program (1965 through 1968) free from evidence of coronary heart disease, cerebrovascular disease, cancer, or aortic aneurysms. RESULTS: Among the men studied, 602 atherosclerotic events developed during the 23-year period of follow-up (1965 through 1988). After adjustment for each of the baseline characteristics examined, significant positive associations between quartile cutoffs of body mass index, systolic blood pressure, serum levels of cholesterol, triglycerides, glucose, and uric acid, as well as cigarette smoking, and the occurrence of any atherosclerotic end point were seen, while an inverse association with alcohol consumption was observed. Characteristics associated with the development of other fatal and nonfatal clinical events in this cohort, including coronary heart disease, thromboembolic stroke, and aortic aneurysms are presented with accompanying relative and attributable risks. CONCLUSIONS: The results of this prospective epidemiologic study provide insights to the long-term predictive utility of the commonly accepted risk factors for coronary heart disease in relation to the different clinical manifestations of atherosclerosis in a middle-aged male cohort followed up for approximately 20 years. These results provide additional support for risk factor modification in middle-aged men and for the encouragement of positive long-term lifestyle changes.

Arteriosclerosis↗
PubMed1994

The Cognitive Abilities Screening Instrument (CASI): a practical test for cross-cultural epidemiological studies of dementia.

The Cognitive Abilities Screening Instrument (CASI) has a score range of 0 to 100 and provides quantitative assessment on attention, concentration, orientation, short-term memory, long-term memory, language abilities, visual construction, list-generating fluency, abstraction, and judgment. Scores of the Mini-Mental State Examination, the Modified Mini-Mental State Test, and the Hasegawa Dementia Screening Scale can also be estimated from subsets of the CASI items. Pilot testing conducted in Japan and in the United States has demonstrated its cross-cultural applicability and its usefulness in screening for dementia, in monitoring disease progression, and in providing profiles of cognitive impairment. Typical administration time is 15 to 20 minutes. Record form, manual, videotape of test administration, and quizzes to qualify potential users on the administration and scoring of the CASI are available upon request.

Aged↗
PubMed1994

A prospective study of the health effects of alcohol consumption in middle-aged and elderly men. The Honolulu Heart Program.

BACKGROUND: The study objective was to determine the association between reported alcohol consumption and total mortality, mortality from selected causes, and incident nonfatal chronic disease events in middle-aged (51 to 64 years old) and elderly (65 to 75 years old) men during an approximate 15-year follow-up period. METHODS AND RESULTS: We conducted a prospective epidemiological study of Japanese-American men who were participating in the Honolulu Heart Program and were free from coronary heart disease, cerebrovascular disease, and cancer at baseline examination and at subsequent reexamination 6 years later. Self-reported alcohol consumption was determined twice: at the baseline examination in 1965 through 1968 and at reexamination approximately 6 years later (1971 through 1974). Four primary alcohol consumption groups who reported similar alcohol intake at the time of these two clinical examinations were considered: abstainers and light (1 to 14 mL of alcohol per day), moderate (15 to 39 mL of alcohol per day), and heavy (> or = 40 mL of alcohol per day) drinkers. Study end points were also determined in very light (1 to 4.9 mL of alcohol per day) drinkers and in men who reported a change in their alcohol intake between examinations. Longitudinal follow-up was carried out through the end of 1988 with determination of selected fatal and nonfatal events according to alcohol intake. After controlling for several potentially confounding factors, total mortality exhibited a J-shaped pattern in relation to alcohol consumption in middle-aged and elderly men. There was a trend for lower rates of occurrence of combined fatal and nonfatal coronary heart disease events with increasing alcohol consumption in both middle-aged and elderly men. Increasing alcohol consumption was related to an increased risk of fatal and nonfatal strokes in middle-aged men, whereas elderly light and moderate drinkers were at increased risk for fatal and nonfatal strokes. Heavy drinkers were at increased risk for fatal and nonfatal malignant neoplasms in the two age groups examined. CONCLUSIONS: The results of this long-term prospective study provide a balanced perspective of the health effects of alcohol consumption in middle-aged and elderly men. High levels of alcohol consumption were shown to be related to an increasing risk of diseases of considerable public health importance. These findings suggest that caution be taken in formulating population-wide recommendations for increases in the population levels of alcohol consumed given the associated significant social and biological problems of high consumption levels.

Aged↗
PubMed1994

Physical activity and 23-year incidence of coronary heart disease morbidity and mortality among middle-aged men. The Honolulu Heart Program.

BACKGROUND: The purpose of the study was to examine the association between physical activity and 23-year incidence of coronary heart disease morbidity and mortality. This cohort study continues to follow 8006 Japanese-American men who were 45 to 68 years of age and living on Oahu, Hawaii, in 1965, for the development of coronary heart disease morbidity and mortality. METHODS AND RESULTS: The Framingham physical activity index was calculated by summing the product of average hours spent at each activity level and a weighting factor based on oxygen consumption. Study subjects were divided into tertiles of physical activity index at baseline. Relative risks and 95% confidence intervals (CI) for incidence of coronary heart disease morbidity and mortality were obtained using the Cox model. After age adjustment and using the lowest physical activity index tertile as a reference group, the relative risk for coronary heart disease incidence for the highest tertile of physical activity was 0.83 (CI, 0.70 to 0.99). After adjusting for age, hypertension, smoking, alcohol intake, diabetes, cholesterol, and body mass index, the relative risk was 0.95 and CI included 1 (CI, 0.80 to 1.14). For coronary heart disease mortality, the age-adjusted relative risk was 0.74 (CI, 0.56 to 0.97) and 0.85 (CI, 0.65 to 1.13) after risk factor adjustment. CONCLUSIONS: The results suggest that the impact of physical activity index on coronary heart disease is mediated through its effects on hypertension, diabetes, cholesterol, and body mass index. These findings support the hypothesis that physical activity is inversely associated with coronary heart disease morbidity and mortality and suggest that physical activity interventions in middle-aged men, by improving cardiovascular risk factor levels, may have significant public health implications in the prevention of coronary heart disease.

Aged↗
PubMed1994

Glucose intolerance and 22-year stroke incidence. The Honolulu Heart Program.

BACKGROUND AND PURPOSE: This study was conducted to determine whether glucose intolerance and diabetes increase the risk of thromboembolic, hemorrhagic, and total stroke independent of other risk factors. METHODS: Among 7549 Japanese-American men aged 45 to 68 years and free of coronary heart disease and stroke during 1965 to 1968, history of diabetes, diabetic medication, and nonfasting glucose 1 hour after a 50-g load were used to classify subjects into four glucose tolerance categories. Incidence of stroke over 22 years was ascertained using comprehensive hospital-based surveillance. Age- and risk factor-adjusted relative risks of stroke were determined using a Cox proportional hazards model. RESULTS: A total of 374 thromboembolic, 128 hemorrhagic, and 36 type-unknown strokes occurred. Incidence of thromboembolic but not hemorrhagic stroke increased with worsening glucose tolerance category. Compared with the "low-normal" (glucose < 151 mg/dL) group, subjects in the "high-normal" (151 to 224 mg/dL), "asymptomatic high" (> or = 225 mg/dL), and "known diabetes" groups all had significantly elevated age-adjusted relative risks of thromboembolic stroke. After adjustment for other risk factors, relative risks remained significantly elevated for the asymptomatic high and known diabetes groups (1.43 and 2.45; 95% confidence intervals, 1.00 to 2.04 and 1.73 to 3.47, respectively). Associations were the same in hypertensive and nonhypertensive subjects and similar but slightly stronger in younger (aged 45 to 54 years) than in older (aged 55 to 68 years) men. CONCLUSIONS: Subjects with diabetes and elevated glucose appear to be at increased risk of thromboembolic but not hemorrhagic stroke. These associations were largely independent of other cardiovascular disease risk factors. Excess risk is apparent in older as well as younger diabetic individuals and in hypertensive and nonhypertensive subjects with diabetes.

Aged↗
PubMed1990

Lability of red blood cell membranes to lipid peroxidation: application to humans fed polyunsaturated lipids.

Red blood cell membranes (RBCM) were used to estimate human red blood cell lability to lipid peroxidation in vitro. RBCM were prepared from blood collected from humans fed diets with either 3 or 15% polyunsaturated fatty acids for 80 days. RBCM were isolated by centrifugation, and oxidative stress was induced by in vitro incubation with 0.1 or 0.5 mM tert-butyl hydroperoxide (t-BOOH) in the presence of 0.5 mg added hemoglobin. Lipid Peroxidation was evaluated by measurement of thiobarbituric acid-reactive substances (TBARS). Lipid peroxidation correlated with the protein content of RBCM in both noninduced and t-BOOH-induced lipid peroxidation systems. TBARS production was dependent on the amount of t-BOOH added to the RBCM. The production of TBARS by RBCM incubated with 0.5 mM t-BOOH was correlated with arachidonic acid content in the red blood cells (RBC) from which RBCM were prepared. The methodology developed was useful for comparative estimations of the lability of RBCM to lipid peroxidation.

Adult↗
PubMed1990

Vitamin C deficiency in patients with sickle cell anemia.

Because peroxidative damage to red cell membranes may contribute to the pathophysiology of sickle cell disease, deficiency of fat- and water-soluble antioxidants could be a determinant in the pathogenesis of this disease. We have previously reported a deficiency of vitamin E in sickle cell disease. The present study was undertaken to see if a deficiency in vitamin C might also be detected. Leukocyte vitamin C, which reflects total body vitamin C reserve, was measured by a modified 2,4-dinitrophenylhydrazine method. Sickle cell patients (N = 18) had lower leukocyte vitamin C levels (18.3 +/- 9.4 micrograms/10(8) cells) than normal controls (N = 12; 30.3 +/- 7.5 micrograms/10(8) cells; p less than 0.01). Furthermore, 50% of the patients had vitamin C levels below 15 micrograms/10(8) cells, a value consistent with vitamin C deficiency. A statistically significant correlation (r = -0.62 with 0.01 less than p less than or equal to 0.025) was found between leukocyte vitamin C levels and serum ferritin concentration. Because dietary vitamin C intake appeared to be adequate, increased vitamin C utilization may account for this deficiency. However, the mechanisms for this deficiency as well as its pathophysiologic consequences remain to be established.

Anemia, Sickle Cell↗
PubMed1989

Lipid alterations and cellular properties of sickle red cells.

Taken together, our studies and those in other laboratories demonstrate a number of membrane lipid changes in sickle erythrocytes. These include (1) changes in membrane phospholipid dynamics, (2) perturbation of the translocase protein that translocates aminophospholipids from the exterior leaflet to the interior leaflet, (3) perturbation of the interaction between membrane phospholipids and skeletal proteins, and (4) abnormal phospholipid molecular species compositions. The mechanism underlying these alterations may involve several independent effects. Included in these will be the oxidative damage that occurs to these membranes and the dissociation of lipids and proteins that accompanies the sickling process.

Anemia, Sickle Cell↗
PubMed1989

Oxidative hemoglobin denaturation and RBC destruction: the effect of heme on red cell membranes.

In this article, we have reviewed evidence to indicate that hemoglobin denaturation can cause sufficient membrane damage to contribute to red cell destruction. We have attempted to explain how hemoglobin denaturation may affect red cell membrane properties at the molecular level. Current information is consistent with the possibility that hemin, in addition to Heinz bodies, is an important factor contributing to red cell membrane damage following hemoglobin denaturation. The initial step in hemin-induced membrane damage appears to involve the oxidation of membrane protein sulfhydryl groups as well as lipids. Structural and functional membrane properties are likely to be altered. Further studies on the role of hemin in the process of red cell aging and in the pathophysiology of red cell disorders characterized by hemoglobin oxidation should yield new information regarding the role of hemin in these conditions.

Erythrocytes↗
PubMed1989

Lipid peroxidation in human red cells.

In this review we have discussed the chemistry and biochemistry of lipid peroxidation as well as lipid repair mechanisms in human RBCs. We have presented findings relating to the effect of lipid peroxidation on the RBC membrane and on several properties that are determinants of RBC survival in vivo. Since we have not discussed how oxidative damage to membrane proteins or hemoglobin may affect RBC survival, the role of lipid oxidation must be considered in a broader perspective. Considerable evidence has recently been reported to indicate that oxidative hemoglobin denaturation plays an extremely important role in RBC survival. Since all cellular components are susceptible to peroxidative damage, it is likely that multiple reactions will be important with regard to RBC oxidant injury, just as they have been implicated in many degenerative processes, and that certain "compartments" of the membrane may be more susceptible than others due to congenital or acquired defects in membrane structure.

Acylation↗
PubMed1988

The use of cis-parinaric acid to determine lipid peroxidation in human erythrocyte membranes. Comparison of normal and sickle erythrocyte membranes.

The recently developed parinaric acid assay is shown to offer possibilities for studying peroxidation processes in biological membrane systems. Taking the human erythrocyte membrane as a model, several initiating systems were investigated, as well as the effect of residual hemoglobin in ghost membrane preparations. The effectivity of a radical generating system appeared to be strongly dependent upon whether radicals are generated at the membrane level or in the water phase. Thus, cumene hydroperoxide at concentrations of 1.0-1.5 mM was found to be a very efficient initiator of peroxidation in combination with submicromolar levels of hemin-Fe3+ as membrane-bound cofactor. In combination with cumene hydroperoxide, membrane-bound hemoglobin appeared to be about 6-times more effective in promoting peroxidation than hemoglobin in the water phase. Results comparing the behaviour of normal and sickle erythrocyte ghost suspensions in the peroxidation assay suggest that the increased oxidative stress on sickle erythrocyte membranes could be due to enhanced membrane binding of sickle hemoglobin, but also partly to a characteristically higher capability of sickle hemoglobin to promote peroxidation. The order of peroxidation-promoting capabilities that could be derived from the experiments was hemin greater than sickle hemoglobin greater than normal hemoglobin.

Anemia, Sickle Cell↗
PubMed1988

Diet-induced asymmetry of the phosphatidylcholine fatty acyl composition in rat erythrocyte membranes.

The effect of dietary fat on the distribution of fatty acids within the bilayer of red cell membrane phosphatidylcholine was determined after feeding young female rats semipurified diets containing 10% of either hydrogenated cottonseed oil, menhaden oil, or corn oil for 4 days. Changes in fatty acyl composition of both plasma and erythrocyte phosphatidylcholine were noted. The composition of the fatty acids in phosphatidylcholine in the outer leaflet of the bilayer was determined after hydrolysis of outer leaflet phospholipids, first with phospholipase A2 and subsequently with sphingomyelinase. The distributions of acyl constituents of phosphatidylcholine in the inner and the outer monolayers of the membrane were found to be distinctively different, regardless of the dietary fat intake. For example, palmitic acid and oleic acid were predominantly present in the phosphatidylcholine of the inner monolayer, and arachidonic acid and docosahexaenoic acid were present in that of the outer monolayer. Despite such diet-induced changes in phosphatidylcholine fatty acid composition, no alteration in erythrocyte integrity was observed when monitored by either morphology or ektacytometry.

Animals↗