Search PubMed⌕ Search

Biomedical subjects

K Saku

Publications and source records attributed to K Saku.

At least 109 records · Page 6Linked to original sources
PubMed1990

[O5-antigenic classification of Salmonella typhimurium isolated from outbreaks of Salmonella enteritis].

S. typhimurium (STM) were isolated from outbreaks of Salmonella enteritis and were studied for their reactivity to monoclonal antibody TMY1 specific for Salmonella O5-antigen with the following results; By using the bacterial agglutination test with TMY1, STM were classified into O5-antigenic molecule positive and negative (copenhagen type) strains, suggesting the usefulness of TMY1 as an exquisite epidemiologic tool for Salmonella enteritis.

Antigens, Bacterial↗
PubMed1990

Cardiac function of WHHL rabbit, an animal model of familial hypercholesterolemia.

To investigate the cardiac function of WHHL rabbit (WHHL), an animal model of familial hypercholesterolemia, electrocardiography (ECG) and echocardiography (UCG) were taken from this species of homozygous type and normolipidemic Japanese White rabbits (controls). In WHHL, two of four had intraventricular conduction disturbances (IVCD) in ECG. UCG study showed that the ejection fraction significantly increased (p less than 0.05) and deceleration time was shortened (p less than 0.01) in WHHL compared to normal controls.

Animals↗
PubMed1989

Plasma fibrinogen levels as an independent indicator of severity of coronary atherosclerosis.

The relationship between plasma fibrinogen levels and the severity of coronary atherosclerosis was examined in 229 patients, aged 25-82 years (162 men and 67 women), undergoing coronary angiography. Severity of coronary atherosclerosis was assessed in terms of the number of vessels with a 75% or greater stenosis and Gensini's severity score. Fibrinogen levels increased progressively with the severity of coronary atherosclerosis, determined by both the number of involved vessels and Gensini's severity score in men, and the relationships were statistically significant. Similar patterns were noted among women, but the trends were not statistically significant. The association was evident even after adjustment for age, hypertension, total cholesterol, cigarette smoking, alcohol intake, high density lipoprotein cholesterol and body mass index. These results provide evidence that in the Japanese also plasma fibrinogen levels can serve as an independent indicator of the progression of coronary atherosclerosis.

Adult↗
PubMed1989

Kinetics of HDL-apo A-I in the WHHL rabbit, an animal model of familial hypercholesterolemia.

Plasma high density lipoproteins (HDL) and their major protein, apolipoprotein (apo) A-I, are deficient in homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits. As the pathophysiology of subnormal HDL-apo A-I is unclear, we examined kinetic parameters of HDL-apo A-I in WHHL rabbits and normolipidemic Japanese White (control) rabbits. The total plasma mass of HDL-apo A-I was significantly smaller (P less than 0.01) in WHHL rabbits than in controls (less than one-third). Mean fractional catabolic rates (FCR) computed from the specific radioactivity decay curves of HDL-apo A-I were significantly greater (P less than 0.01) in WHHL rabbits than in controls (0.874 +/- 0.052 vs. 0.502 +/- 0.060/day, respectively). Mean synthetic rates of HDL-apo A-I were significantly lower (P less than 0.01) in WHHL rabbits than in controls (8.67 +/- 0.59 vs. 18.14 +/- 3.75 mg/kg body weight/day, respectively). We conclude that the deficiency of plasma HDL-apo A-I in the WHHL rabbits resulted from an increase in FCR and a decrease in apo A-I synthesis.

Animals↗
PubMed1989

Lipoprotein and apolipoprotein losses during continuous ambulatory peritoneal dialysis.

The daily loss of apolipoproteins into the dialysate from 5 patients on continuous ambulatory peritoneal dialysis (CAPD) was measured. The mean excretion of apolipoprotein (apo) AI and apo AII, major proteins of high-density lipoproteins (HDL), were 84 and 17 mg/day, respectively, while that of apo B, a major protein of low-density lipoproteins (LDL) was 39 mg/day. The peritoneal clearance of apo AI and apo AII were similar; both being significantly greater than that of apo B. The fractional catabolic rates of various proteins found in the CAPD dialysate showed molecular sieving effects of the peritoneal membrane and indicated that the apolipoproteins were excreted as lipoproteins. These findings suggest that there is continuous and selective loss of HDL compared to LDL which may also indicate an increased predisposition of these patients to atherosclerosis.

Adult↗
PubMed1989

Abdominal aortic aneurysm of unknown origin and renovascular hypertension in a 25 year old male.

A 25 year old male had an abdominal aortic aneurysm involving bilateral renal arteries. Aortography revealed no irregularity in the aortic wall but a slight kinking at the tenth thoracic level followed by a fusiform aneurysm. Computed tomography (CT) showed an enlarged aortic lumen with an intraluminal thrombus. Plasma renin activity (PRA) was markedly increased (11 ng/ml/h), and the administration of captopril caused a further increase in PRA with a significant reduction in blood pressure, indicating the presence of renovascular hypertension. Abdominal aneurysm in a young adult is very rare. The etiology of the aneurysm appears to be idiopathic.

Adult↗
PubMed1989

Lack of effect of chlorpromazine and haloperidol on serum lipid levels and on atherogenesis in cholesterol fed rabbits.

Effects of chlorpromazine and haloperidol on serum lipid levels and on atheromotous plaques of aortae were studied in 1% cholesterol fed rabbits. To three different groups, subcutaneous injections of saline, chlorpromazine and haloperidol were given daily, following a cholesterol fed diet for twelve weeks. Serum total cholesterol and triglyceride levels were similar at 0, 6, 12 weeks among the three groups. No significant differences in the area with atheromatous plaque of aorta were noted among the three groups. Therefore, chlorpromazine and haloperidol have no preventive action against cholesterol-induced atherosclerosis in rabbits.

Animals↗
PubMed1988

"Torsades de pointes" and atrioventricular block.

In order to elucidate the trigger factor of the production of torsades de pointes (TdP), electrophysiological study was conducted in 15 patients with atrioventricular (AV) block; 6 with TdP (TdP group) and 9 without TdP (control group). In the TdP group, all had an episode of syncope and frequent ventricular premature beats (VPBs) on routine ECG, while four (44%) had syncope and three (33%) had VPBs in the control group. Aging, QRS width, ventricular cycle length, QT interval, and block site from His bundle electrogram were similar in both groups, however the QTc interval was significantly (p less than 0.01) longer in the TdP group than in the control group (580 +/- 112 vs. 459 +/- 37, respectively). Furthermore, four patients (67%) in the TdP group showed advanced AV block in which a slow ventricular rate and an irregular rhythm were characteristic, whereas only one control (11%) showed advanced AV block and all other control patients (89%) had complete AV block. These data indicate that patients with advanced atrioventricular block associated with prolonged QTc interval and frequent ventricular premature beats might induce torsades de pointes.

Aged↗
PubMed1988

Apolipoproteins in human biopsied nephrotic kidneys.

Using monospecific antibodies to purified human apolipoproteins, immunofluorescence microscopy of renal biopsies from 4 patients with nephrotic syndrome revealed apolipoprotein (apo) AI, apo CIII and apo B (LDL) in lysosomes of the proximal tubular cells. This supports the hypothesis that there is increased filtration of both high density lipoproteins (HDL) and low density lipoproteins (LDL) with partial reabsorption by the tubules, thus affecting the serum lipoprotein levels.

Adolescent↗
PubMed1988

High-density lipoprotein apolipoprotein AI and AII turnover in moderate and severe proteinuria.

The kinetic parameters of high-density lipoprotein (HDL) and its major apolipoproteins (Apo) AI and Apo AII were studied in 2 patients with moderate and severe proteinuria and 2 normal controls after intravenous injection of autologous 125I-HDL. The fractional catabolic rates (FCR) of HDL estimated by urine/plasma radioactivity ratio, and FCR of Apo AI and Apo AII calculated from the radioactivity decay curves were higher in the patients. These results support the concept that high-density lipoproteinuria and renal parenchymal sequestration of HDL found in the nephrotic syndrome contribute to accelerated HDL catabolism.

Adult↗
PubMed1987

Small, bilateral, calcified intrarenal aneurysms--a case report.

With increased use of renal angiography and ultrasonography, intrarenal aneurysms and arteriovenous malformations have been easily diagnosed. The authors report a case of small, bilateral intrarenal aneurysms with calcifications that were associated with a visible pulsatile wall motion recorded by M-mode ultrasonography. The finding of selective renal angiography was consistent with bilateral intrarenal aneurysms. Accelerated atherosclerosis and long-term history of hypertension were thought to have caused them.

Aged↗
PubMed1985

Activation of fibrinolysis by apolipoproteins of high density lipoproteins in man.

The effects on fibrinolysis of purified normal human plasma lipoproteins and their apolipoproteins (apo) were assessed in an in vitro system containing urokinase, plasminogen, and fibrin. High and very low density lipoproteins (HDL and VLDL, respectively) but not low density lipoproteins (LDL) significantly increased lysis of radiolabeled fibrin or lysis area of plated fibrin compared to controls. Apo HDL, apo HDL2, apo HDL3, apo VLDL (buffer soluble apo), apo AI and AII activated fibrinolysis by 1.3-1.4 fold of control values, whereas apo B (as a narrow density cut of LDL) and non-lipoprotein control proteins (albumin and myoglobin) did not. Addition of HDL in the absence of urokinase failed to activate fibrin lysis. These data demonstrate that the major proteins of HDL - apo AI and apo AII - and possibly certain minor constituent(s) common to HDL and VLDL participate in the fibrinolytic process.

Apolipoproteins↗
PubMed1985

Apolipoprotein AI and AII metabolism in patients with primary high-density lipoprotein deficiency associated with familial hypertriglyceridemia.

Plasma high-density lipoproteins (HDL) and their major proteins--apolipoprotein (apo) AI and apo AII--are subnormal in most patients with familial hypertriglyceridemia. However, the pathophysiology of low-plasma apo AI and apo AII is unclear. The kinetic parameters (turnover) of HDL apo AI and apo AII were studied in six lean patients with primary HDL deficiency associated with familial hypertriglyceridemia and five normolipidemic controls. Autologous 125I labeled HDL were injected intravenously (IV; 25 microCi) and blood samples drawn ten minutes after the injection and periodically thereafter for 12 days. Urine samples were collected daily and their radioactivity measured. Kinetic parameters were calculated from the area under the decay curve using three exponentials. Mean plasma apo AI and apo AII were significantly lower (P less than 0.001) in patients than normals (70.4 +/- 2.7 v 106.9 +/- 7.0; 24.2 +/- 1.6 v 39.2 +/- 0.9 mg/dL, respectively). The mean fractional catabolic rates (FCR) obtained from plasma 125I-HDL, apo AI, apo AII radioactivity decay curves and by Berson and Yalow's method (urine/plasma radioactivity ratios) were significantly greater (P less than 0.05) in patients than in controls (0.387 v 0.299; 0.391 v 0.309; 0.361 v 0.275; 0.272 v 0.207/d; respectively). The mean synthetic rates (SR) of apo AI and apo AII were significantly lower in patients than in controls (11.12 v 14.17 mg/kg body weight/d, P less than 0.05; 3.53 v 4.68 mg/kg body weight/d, P less than 0.05, respectively). In vitro lipolysis of triglyceride (TG) rich lipoproteins by bovine lipoprotein lipase, and measurement of hepatic TG lipase and lipoprotein lipase in postheparin plasma were similar in patients and controls, indicating no abnormality in these factors that are linked to HDL and TG catabolism. However, a significant positive correlation between hepatic TG lipase and the FCR of apo AI and apo AII was found. The data suggest that in this series of patients with HDL deficiency the low plasma HDL-cholesterol, apo AI, and apo AII levels resulted from decreased synthesis and an increased fractional catabolic rate of apo AI and apo AII, the major proteins of HDL.

Adult↗
PubMed1985

Effect of desialylation of very low-density lipoproteins on their catabolism by lipoprotein lipase.

Very low-density lipoproteins (VLDL) contain sialylated apolipoproteins (apo) (eg, apo CIII1-3) that inhibit apo CII activation of lipoprotein lipase (LPL) and also uptake of triglyceride (TG)-rich lipoproteins by the liver. Hypertriglyceridemic patients can have an excess of sialylated apo CIII (apo CIII1 or apo CIII2) in VLDL. These observations have prompted the notion that sialic acid in VLDL may impede LPL or receptor-mediated clearance of VLDL and thus result in hypertriglyceridemia. The aim of this study was to determine whether desialylation of VLDL altered their property as a substrate for LPL. VLDL isolated from five hypertriglyceridemic patients was desialylated with neuraminidase, labeled with a fluorescent probe, dansyl phosphatidylethanolamine and 600 micrograms of labeled VLDL TG were incubated with a constant amount of purified bovine LPL. The change in fluorescence against time was monitored on a recorder to yield curves representing continuous lipolysis of VLDL by LPL. Mean initial velocity of reaction (Vi) and extent of lipolysis measured as total increase in fluorescence over baseline at 30 minutes (F30/FO) were similar (Vi = 10.2 +/- 0.37 control v 10.2 +/- 0.42 u/min desialylated VLDL; F30/FO = 4.1 +/- 0.15, control v 4.1 +/- 0.07 desialylated VLDL; n = 5). Thus, sialic acid does not influence VLDL catabolism by LPL. Our study does not exclude a possible role of the sialic acid in receptor mediated uptake of remnants produced by initial catabolism of VLDL by LPL.

Adult↗