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Biomedical subjects

M R Malinow

Publications and source records attributed to M R Malinow.

At least 73 records · Page 4Linked to original sources

Synthesis and transsulfuration of homocysteine in blood.

Interest in total plasma homocysteine (homocyst[e]ine) as a risk factor for atherosclerosis is expanding. However, the origin of plasma homocyst(e)ine has not been defined. Our studies examined the metabolism of homocyst(e)ine by blood cells as a potential contributor to the homeostasis of homocyst(e)inemia. Incubation of blood for 24 hours at 37 degrees C produced a threefold increase in the level of plasma homocyst(e)ine. In samples of fractionated blood cells incubated in vitro, increases in total plasma homocysteine were limited to incubated erythrocyte fractions and were influenced by addition of methionine. Anticoagulants had no significant effect. Incubation of blood in the presence of methionine tagged with sulfur 35 demonstrated incorporation of label into homocysteine and transsulfuration products. Similar incubations of blood cell fractions suggested that synthesis of homocysteine occurred in erythrocytes, whereas leukocytes both synthesized and transsulfurated homocysteine. These findings demonstrated a possible interaction of different blood cells in the metabolism of methionine, as well as their potential role as a source of total plasma homocysteine in plasma.

Adult↗

Carotid artery intimal-medial wall thickening and plasma homocyst(e)ine in asymptomatic adults. The Atherosclerosis Risk in Communities Study.

BACKGROUND: Plasma levels of homocyst(e)ine are elevated in certain patients with occlusive arterial diseases. We extended these findings to asymptomatic adults. METHODS AND RESULTS: We determined plasma homocyst(e)ine levels in 287 pairs of asymptomatic adults. Cases and controls were defined on the basis of intimal-medial thickness of the carotid wall as measured by B-mode ultrasound. Study subjects had no history of atherosclerotic disease and were selected from a probability sample of 15,800 men and women between 45 and 64 years old. Subjects with thickened intimal-medial carotid walls (cases) had higher plasma homocyst(e)ine levels than controls (p < 0.001). The odds ratio for having a thickened carotid artery wall was 3.15 (p < 0.001) for subjects in the top quintile of plasma homocyst(e)ine levels (> 10.5 mumol/L) compared with those in the bottom quintile (< 5.88 mumol/L). CONCLUSIONS: The present study as well as observations on the common occurrence of elevated plasma homocyst(e)ine levels in patients with occlusive arterial diseases suggest that clinical trials should be conducted to determine whether normalization of hyperhomocyst(e)inemia may prevent progression of atherosclerosis.

Arteriosclerosis↗

Total homocysteine in plasma or serum: methods and clinical applications.

Total homocysteine is defined as the sum of all homocysteine species in plasma/serum, including free and protein-bound forms. In the present review, we compare and evaluate several techniques for the determination of total homocysteine. Because these assays include the conversion of all forms into a single species by reduction, the redistribution between free and protein-bound homocysteine through disulfide interchange does not affect the results, and total homocysteine can be measured in stored samples. Total homocysteine in whole blood increases at room temperature because of a continuous production and release of homocysteine from blood cells, but artificial increase is low if the blood sample is centrifuged within 1 h of collection or placed on ice. Different methods correlate well, and values between 5 and 15 mumol/L in fasting subjects are considered normal. Total homocysteine in serum/plasma is increased markedly in patients with cobalamin or folate deficiency, and decreases only when they are treated with the deficient vitamin. Total homocysteine is therefore of value for the diagnosis and follow-up of these deficiency states and may compensate for weaknesses of the traditional laboratory tests. In addition, total homocysteine is an independent risk factor for premature cardiovascular diseases. These disorders justify introduction of the total homocysteine assay in the routine clinical chemistry laboratory.

Blood Chemical Analysis↗

Pharmacologic consequences of cholesterol absorption inhibition: alteration in cholesterol metabolism and reduction in plasma cholesterol concentration induced by the synthetic saponin beta-tigogenin cellobioside (CP-88818; tiqueside).

Natural and synthetic saponins inhibit cholesterol absorption and reduce plasma cholesterol levels in experimental animals and are therefore of potential pharmacologic utility in the treatment of hypercholesterolemia. To determine the effects of this class of compounds on cholesterol absorption and metabolism, we evaluated the effects of the synthetic saponin, beta-tigogenin cellobioside (tiqueside; CP-88818), on male golden Syrian hamsters. When administered as either a single oral bolus or as a dietary supplement for up to 2 weeks, tiqueside inhibited cholesterol absorption in a dose-dependent manner in both the presence and absence of dietary cholesterol. Administration of tiqueside to chow-fed hamsters as a 0.2% dietary supplement (150 mg/kg per day) for 4 days resulted in a 68% decrease in intestinal cholesterol absorption with no change in either bile absorption or cholesterol 7 alpha-hydroxylase activity, suggesting that tiqueside inhibits cholesterol absorption without interfering with enterohepatic bile acid recirculation. Under these conditions, hepatic cholesterol levels were also reduced in a dose-dependent manner. Hepatic cholesterol reduction was highly correlated with cholesterol absorption inhibition, and induced compensatory increases in both hepatic HMG-CoA reductase activity and hepatic low density lipoprotein (LDL) receptor levels. Compensatory increases in intestinal HMG-CoA reductase activity were also noted after tiqueside administration, and are consistent with a luminal mechanism for tiqueside action. As a consequence of these changes to cholesterol metabolism, tiqueside administration induced plasma cholesterol reductions that were highly correlated with both hepatic cholesterol reduction and cholesterol absorption inhibition. Tiqueside also produced comparable plasma cholesterol lowering in a variety of other species fed either cholesterol-free diets (hamster, rat, mouse, dog) or cholesterol-containing diets (hamster, rat, rabbit, mouse, cynomolgus monkey, rhesus monkey, SEA quail) indicating the ubiquity of tiqueside action. For all species evaluated except the dog, the reduction in plasma cholesterol was due primarily to a reduction in circulating non-HDL cholesterol levels with little or no change in HDL cholesterol levels. Taken together, these results indicate that inhibition of cholesterol absorption by tiqueside produces profound effects on cholesterol metabolism without affecting bile acid metabolism, and that these changes lead to reductions primarily in plasma non-HDL cholesterol concentrations. The synthetic saponin, tiqueside, may thus represent a prototypical form of therapy for the treatment of hypercholesterolemia.

Amino Acid Sequence↗

A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians.

OBJECTIVE: To assess prospectively the risk of coronary heart disease associated with elevated plasma levels of homocyst(e)ine. DESIGN: Nested case-control study using prospectively collected blood samples. SETTING: Participants in the Physicians' Health Study. PARTICIPANTS: A total of 14,916 male physicians, aged 40 to 84 years, with no prior myocardial infarction (MI) or stroke provided plasma samples at baseline and were followed up for 5 years. Samples from 271 men who subsequently developed MI were analyzed for homocyst(e)ine levels together with paired controls, matched by age and smoking. MAIN OUTCOME MEASURE: Acute MI or death due to coronary disease. RESULTS: Levels of homocyst(e)ine were higher in cases than in controls (11.1 +/- 4.0 [SD] vs 10.5 +/- 2.8 nmol/mL; P = .03). The difference was attributable to an excess of high values among men who later had MIs. The relative risk for the highest 5% vs the bottom 90% of homocyst(e)ine levels was 3.1 (95% confidence interval, 1.4 to 6.9; P = .005). After additional adjustment for diabetes, hypertension, aspirin assignment, Quetelet's Index, and total/high-density lipoprotein cholesterol, this relative risk was 3.4 (95% confidence interval, 1.3 to 8.8) (P = .01). Thirteen controls and 31 cases (11%) had values above the 95th percentile of the controls. CONCLUSIONS: Moderately high levels of plasma homocyst(e)ine are associated with subsequent risk of MI independent of other coronary risk factors. Because high levels can often be easily treated with vitamin supplements, homocyst(e)ine may be an independent, modifiable risk factor.

Adult↗

Hyperhomocyst(e)inemia, anti-estrogen antibodies and other risk factors for thrombosis in women on oral contraceptives.

Hyperhomocyst(e)inemia was shown to be associated with vascular occlusion in atherosclerotic patients. We have conducted a study to determine if hyperhomocyst(e)inemia was also related to the vascular events observed in women on oral contraceptives, presumably having little or no atherosclerosis. Two hundred women receiving oral contraceptives were included in the study: 100 were healthy controls and 100 had documented vascular occlusion. Determination of serum homocyst(e)ine and anti-estrogen antibody levels wore performed under blind conditions. They were evaluated in logistic regression models in which age and smoking were also included. Women with vascular occlusion had higher levels of homocyst(e)ine (P less than 0.001) and of anti-estrogen antibodies (P less than 0.001) when compared to controls. They were also older (P less than 0.001) and more frequently smokers (P less than 0.05). The above mentioned variables were, in isolation, independent predictors of vascular occlusion. Moreover, a model assessing those variables and their interactions indicated that the levels of anti-estrogen antibodies and smoking increased the predictability in older women, as well as the levels of age-adjusted homocyst(e)ine. The study suggests that the above factors can identify women at risk and that determination of anti-estrogen antibodies and homocyst(e)ine levels may help to detect women predisposed to vascular occlusions when taking oral contraceptives.

Adult↗

Hyperhomocysteinaemia in stroke: prevalence, cause, and relationships to type of stroke and stroke risk factors.

Moderate hyperhomocysteinaemia is a frequent finding in atherothrombotic cerebrovascular disease. This study confirms and extends this observation. Hyperhomocysteinaemia was present in 57 of 142 survivors with stroke (40%) and in four of 66 controls (6%). Plasma homocysteine concentrations were increased not only in carotid artery disease or lucunar stroke but also in haemorrhagic or embolic strokes. Homocysteine values were unrelated to the presence of hypertension, smoking, or hypercholesterolaemia, or to the concentrations of blood glucose, glycosylated haemoglobin, and plasma fibrinogen. Multiple regression analysis of the patient data showed that about 40% of the variation in plasma homocysteine concentrations could be predicted by the values for the homocysteine metabolism cofactors, blood folate and plasma pyridoxal 5-phosphate and by renal function as reflected in the values for serum creatinine. In patients, urine excretion of homocysteine per unit creatinine was significantly increased and strongly correlated both to the plasma homocysteine concentration and to the values for blood folate, plasma pyridoxal 5-phosphate, and serum vitamin B12. We conclude that moderate hyperhomocysteinaemia is frequently present in cases of stroke, is independent of other stroke risk factors or the type of stroke, and is partly related to renal function and the concentrations of homocysteine metabolism cofactors.

Adult↗

Hyperhomocyst(e)inaemia: an independent risk factor for intermittent claudication.

The aim of this study was to test the question of hyperhomocyst(e)inaemia as a risk factor for intermittent claudication (IC) independent of other important risk factors for peripheral atherosclerotic disease, such as smoking, hypertension, diabetes mellitus, hypercholesterolaemia, hypertriglyceridaemia, low levels of high-density-lipoprotein (HLD) cholesterol and age. The study population was recruited from an epidemiological study in Linköping County, Sweden, where all middle-aged men (n = 15,253, 45-69 years of age) were screened for IC. Seventy-eight subjects with verified IC and 98 healthy sex- and age-matched controls were randomly selected. Plasma levels of homocyst(e)ine (including the sum of free and bound forms of homocysteine and their disulphide oxidation products, homocystine, and homocysteine-cysteine mixed disulphide) were significantly higher (16.74 +/- 5.45 mumol l-1, mean value +/- SD, P = 0.0002) in IC subjects than in controls (13.80 +/- 3.21 mumol l-1), with 23% of the claudicants above the 95th percentile for controls. Stepwise logistic regression analysis revealed that the difference in plasma homocyst(e)ine was independent of the other above-mentioned risk factors. Moreover, the elevation of plasma homocyst(e)ine in claudicants was mainly confined to subjects with serum folate levels of less than or equal to 11.0 nmol l-1. The results suggest that folic acid supplementation should be tried in IC subjects with hyperhomocyst(e)inaemia.

Aged↗

Population variation and genetics of plasma homocyst(e)ine level.

A high level of plasma homocyst(e)ine (H(e)) has been reported to be an independent risk factor for coronary heart disease (CHD), at least in some populations. We have determined the H(e) concentration in the plasma of two series of Norwegians in order to establish a baseline for future analysis of people with CHD. The mean sex- and age-adjusted homocyst(e)ine level was 10.6 (range 4.84-29.88) in one series and 10.5 (range 3.76-40.57) in the other. The H(e) level appeared to be independent of other proven or potential risk factors or protective factors with respect to CHD. The intraclass correlation coefficient in monozygotic (MZ) twins is a (possibly inflated) estimate of heritability. We have examined two series of MZ twins. The intraclass correlation coefficient was significant in both series. In one series, the Pearson correlation coefficient was 0.53 and the Kendall correlation coefficient 0.38. In the other, the values were 0.56 and 0.46, respectively. We conclude that in the population examined, H(e) levels exhibit significant heritability.

Adult↗

Estimates of heritability of plasma homocyst(e)ine levels in aging adult male twins.

Plasma homocyst(e)ine level was determined for 96 identical (MZ) and 92 fraternal (DZ) adult male twins aged 59-69. There was no difference in mean between MZ (10.31 nmol/ml) and DZ (10.36 nmol/ml) twins. The intraclass correlation coefficient of the log-transformed homocyst(e)ine level in 43 complete MZ and 39 complete DZ pairs was 0.55 and 0.19, respectively. The MZ correlation was significantly (p less than 0.05) greater than the DZ correlation, suggesting that the level of plasma homocyst(e)ine is genetically influenced.

Aged↗

Community cholesterol screening: medical follow-up in subjects identified with high plasma cholesterol levels.

Population screening or plasma cholesterol is an effective method of detecting hypercholesterolemia; however, follow-up and treatment are essential components of such a program. After a city-wide screening in 1987 of more than 19,872 persons, using a mailed survey with a response rate of 48%, we evaluated subsequent actions of 3,078 individuals with high plasma cholesterol levels. Slightly more than half the population was aware of high blood cholesterol levels prior to the time of screening and apparently used the program for follow-up. Overall, after the screening, 65% consulted a physician within 5 months of screening and blood cholesterol levels were remeasured in 80% of the sample. Procrastination and expense were cited as the primary reasons for failing to consult a physician. If screening is to be effectively utilized as a means of reducing the prevalence of high plasma cholesterol levels, diligent follow-up must be made of all individuals identified to be at increased risk on the basis of their initial values.

Adult↗

Plasma homocyst(e)ine levels in men with premature coronary artery disease.

Plasma homocyst(e)ine (that is, the sum of free and bound homocysteine and its oxidized forms, homocystine and homocysteine-cysteine mixed disulfide) levels were determined in 170 men (mean age +/- SD 50 +/- 7 years) with premature coronary artery disease diagnosed at coronary angiography and in 255 control subjects clinically free of coronary artery disease (mean age 49 +/- 6 years). Patients with coronary artery disease had a higher homocyst(e)ine level than control subjects (13.66 +/- 6.44 versus 10.93 +/- 4.92 nmol/ml, p less than 0.001). High density lipoprotein (HDL) cholesterol levels were lower (32 +/- 10 versus 46 +/- 13 mg/dl, p less than 0.001) and triglycerides levels were higher (193 +/- 103 versus 136 +/- 106 mg/dl, p less than 0.001) in the coronary disease group. Plasma total cholesterol and low density lipoprotein (LDL) cholesterol levels were not significantly different between patients with coronary disease and control subjects. The presence of hypertension, smoking or diabetes mellitus did not significantly alter homocyst(e)ine levels in the patient or the control group. Patients who were not taking a beta-adrenergic blocking drug (n = 70) had a nonsignificantly higher homocyst(e)ine level than did patients taking this class of drugs (n = 100) (14.67 +/- 8.92 versus 12.95 +/- 3.77 nmol/ml, p = 0.087). By design, none of the control subjects were taking a beta-blocker. No significant correlations were observed between homocyst(e)ine and age, serum cholesterol, LDL cholesterol, HDL cholesterol or triglyceride levels. It is concluded that an elevated plasma homocyst(e)ine level is an independent risk factor for the development of premature coronary atherosclerosis in men.

Cholesterol↗

Elevated plasma homocyst(e)ine concentration as a possible independent risk factor for stroke.

Homocyst(e)ine refers to the sulfur-containing amino acids homocysteine, homocystine, and homocysteine-cysteine mixed disulfide, which normally exist in plasma in both the free and protein-bound forms. Marked hyperhomocyst(e)inemia is associated with well-recognized complications of occlusive thrombotic events and a characteristic syndrome. It is less clear whether mild to moderate elevations in plasma homocyst(e)ine concentrations (i.e., 1.5-5-fold increases) also represent a risk factor for stroke and, if so, whether it is independent of other recognized risk factors. To examine these questions we compared the plasma homocyst(e)ine levels in 41 patients with acute strokes, 27 patients with transient ischemic attacks, 31 patients with recognized risk factors for but no recent symptoms of cerebrovascular disease, and 31 normal volunteers (controls). Plasma homocyst(e)ine concentration was moderately but significantly higher in the patients than in the controls (p less than 0.0001). Approximately 30% of the patients had homocyst(e)ine levels higher than the controls. No relation was found between homocyst(e)ine concentration and other recognized stroke risk factors or stroke type; however, a positive correlation was found between serum uric acid and plasma homocyst(e)ine levels. These data suggest that a moderately elevated plasma homocyst(e)ine concentration may be an independent risk factor for cerebrovascular disease.

Cerebrovascular Disorders↗

Detection of experimental atherosclerosis with indium-111 radiolabelled hematoporphyrin derivative.

It has been observed that atherosclerotic lesions (AL) concentrate certain porphyrins. We evaluated the usefulness of 111In-labelled Photofrin II (PFII), a porphyrin derived from haematoporphyrin derivative, for detection of experimental AL in cholesterol fed rabbits. Three groups of rabbits were studied: non-atherosclerotic (n = 3), 6 and 12 week cholesterol fed (n = 4, 3). 111In-PFII was injected intravenously and gamma camera images were obtained at 24 and 48 h. At 48 h, explanted aortas were also imaged. Aortic arch (AA) to background (BKG) count ratios were calculated from images of the whole body and explanted aortas. AA/BKG ratios were significantly higher in the 12 week cholesterol fed rabbits (3.9 +/- 0.72 at 24 h) and (4.0 +/- 0.67 at 48 h) than in the non-atherosclerotic rabbits (2.2 +/- 0.07 at 24 h) and (2.3 +/- 0.18 at 48 h) (p less than 0.05). The AA/BKG ratio for the explanted aortas showed similar results. Additionally, in two of three 12 week cholesterol fed rabbits, focal count deposition was visible on the whole animal images at the site of aortic arch atherosclerosis. We conclude that 111In-PFII concentrates in AL as early as 24 h after injection and has the potential to be used as an imaging agent for experimental atherosclerosis.

Animals↗

Cigarette smoke extract increases albumin flux across pulmonary endothelium in vitro.

Cigarette smoking causes lung inflammation, and a characteristic of inflammation is an increase in vascular permeability. To determine if cigarette smoke could alter endothelial permeability, we studied flux of radiolabeled albumin across monolayers of porcine pulmonary artery endothelium grown in culture on microporous membranes. Extracts (in either dimethylsulfoxide or phosphate-buffered saline) of cigarette smoke in a range estimate of concentrations simulating cigarette smoke exposure to the lungs in vivo caused a dose-dependent increase in albumin flux that was dependent on extracellular divalent cations and associated with polymerization of cellular actin. The effect was reversible, independent of the surface of endothelial cells exposed (either luminal or abluminal), and due primarily to components of the vapor phase of smoke. The effects occurred without evidence of cell damage, but subtle morphological changes were produced by exposure to the smoke extracts. These findings suggest that cigarette smoke can alter permeability of the lung endothelium through effects on cytoskeletal elements.

Actins↗