[Aluminum and iron deposition in dialysis patients].
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Biomedical subjects
Publications and source records attributed to F Marumo.
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The CT numbers of cortex at the level of 20 cm (CT20) and spongiosa in the lateral condyle at the level of 2 cm (CT20) proximal from the distal end of the femur, and the bone mineral density of spongiosa in the L3 body (BMD), were obtained by QCT. The study included 43 female patients with rheumatoid arthritis (RA), 71 female patients with primary osteoporosis (OP), 20 female nondialyzed patients with chronic renal failure (CRF:nonHD), 37 hemodialyzed patients (CRF:HD), including 13 parathyroidectomized patients (CRF:HD, PTX), and 10 healthy volunteers. CT20 correlated closely with age in RA. CT02 and BMD correlated closely with age in RA and OP. CT20 and CT02 correlated closely with the duration of hemodialysis in CRF:HD, but not with the duration of disease in RA. The values of CT20 and CT02 in the CRF:HD. PTX group were significantly lower than those in the other CRF groups. BMD in the RA groups was not different from that of healthy volunteers. The CT20 values of the one-third of RA patients older than 60 years were extremely low compared with those of the other two-thirds. The results indicated that BMD was useful in assessing bone mineral content in OP, but not in RA. CT02 and CT20 were useful in assessing bone mineral content in these three diseases, CT20 was especially useful for patients in the CRF:HD group and those with RA older than 60 years, but it was not useful in the CRF:nonHD group.
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Eighteen patients with chronic renal failure due to primary glomerular disease undergoing conservative treatment (CRF patients) were studied to evaluate whether coagulation and fibrinolytic activity in plasma are enhanced in the patients. We measured plasma levels of coagulation-fibrinolysis parameters including thrombin-antithrombin III complex (TAT) (an index of thrombin formation), alpha 2-plasmin inhibitor (alpha 2 PI)-plasmin complex (alpha 2 PIC) (an indicator of plasmin production) and cross-linked fibrin degradation products (XL-FDP) (an index of fibrinolysis secondary to coagulation). There was no correlation between plasma levels of TAT, alpha 2PIC and XL-FDP and serum creatinine levels in CRF patients. Both fibrinogen and TAT were found to be significantly higher in CRF patients than in normal controls. TAT was negatively correlated with serum albumin or total protein. Antithrombin III (ATIII) activity was significantly lower in CRF patients than in normal controls. CRF patients showed significantly but slightly higher alpha 2 PIC and XL-FDP when compared to normal controls. These results suggest that TAT, alpha 2PIC and XL-FDP are good indicators of coagulation-fibrinolysis even in patients with decreased renal function. Coagulation activity is significantly increased in CRF patients but fibrinolysis secondary to coagulation is only slightly enhanced.
In cases of heart failure, the plasma level of immunoreactive human brain natriuretic peptide (IR-hBNP) measured by radioimmunoassay increased 6- to 46-fold over normal level (4.1 +/- 1.0 pg/ml), depending upon the severity. These levels did not significantly correlate to the levels of IR-human atrial natriuretic peptide in individuals. A 4-kDa IR-hBNP, corresponding to authentic hBNP (1-32), was predominant in normal plasma. In cases of cardiac disease, larger molecules which were assumed to be precursors of the 4-kDa form were accumulated in plasma. IR-hBNP was detected in spinal cords (7-24 pg/mg protein) and cerebrospinal fluid (8-19 pg/ml) of patients with noncardiac diseases. The major molecular form corresponded to the hBNP (1-32).
To determine the influence of timing on the prognostic value of programmed ventricular stimulation after acute myocardial infarction (AMI), 32 patients were studied on day 19 (early study) and again on day 36 (late study) after AMI using up to 3 extrastimuli. At the early study, sustained monomorphic ventricular tachycardia (VT) was induced in 12 patients (38%), sustained polymorphic VT in 8 (25%), nonsustained monomorphic VT in 1 (3%), nonsustained polymorphic VT in 1 (3%) and no inducible arrhythmia in 10 (31%). At the late study, sustained monomorphic VT, nonsustained monomorphic VT and nonsustained polymorphic VT were induced in 8 patients (25%) each, and no inducible arrhythmia in 8 (25%). Of the 12 patients who had inducible sustained monomorphic VT at the early study, 7 had noninducibility of sustained monomorphic VT at the late study. Of the 20 patients who had noninducibility of sustained monomorphic VT at the early study, 3 had inducible sustained monomorphic VT at the late study. During the follow-up period (mean +/- standard deviation 21 +/- 8 months), there were 2 sudden cardiac deaths and 3 occurrences of sustained VT. Univariate analysis revealed both inducibilities of sustained monomorphic VT at the early study (p = 0.045) and at the late study (p less than 0.001) to be predictive of sudden cardiac death or clinical occurrence of sustained VT. However, inducibility of sustained monomorphic VT at the late study had a higher sensitivity (100%), specificity (89%), positive predictive value (63%) and negative predictive value (100%) than at the early study (80, 70, 33 and 95%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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Autocrine and paracrine regulation of vascular endothelial cells by endothelins has been postulated and has been the target of many recent investigations. In the present study, we demonstrated, by affinity labeling, the presence of endothelin-1- and endothelin-3-specific receptors on cultured bovine endothelial cells that secrete endothelin; the endothelin-3 receptor was the major form. Analysis using the GTP analogue guanosine 5'-O- (thiotriphosphate) indicated that these receptors are coupled to G proteins.
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Cultured bovine endothelial cells (EC) have specific receptors for endothelin (ET)-3 functionally coupled to phosphoinositide breakdown. We studied whether ET-3 stimulates synthesis of nitric oxide (NO), an endothelium-derived relaxing factor that activates soluble guanylate cyclase in EC, and whether the ET-3-induced NO formation involves G-proteins. ET-3 dose-dependently stimulated production of intracellular cGMP in EC, of which effects were abolished by pretreatment with NG-monomethyl L-arginine, an inhibitor of NO synthesis, and methylene blue, an inhibitor of soluble guanylate cyclase. The stimulatory effects of ET-3 on cGMP production, inositol trisphosphate formation and increase in cytosolic free Ca2+ concentration were similarly blocked by pretreatment with pertussis toxin (PTX). These data suggest that ET-3 induces synthesis of NO mediated by phosphoinositide breakdown via PTX-sensitive G-protein in EC.
The presence of a-smooth muscle actin (smA)-positive cells has recently been reported in the fibrotic liver. Lipocytes have been considered to play important roles in hepatic fibrosis. However, the relation of the a-smA-positive cells and lipocytes has not been determined. The biological implication of a-smA expression remains unknown. To study these questions, we carried out double immunofluorescent staining of a-smA and desmin (a marker for lipocytes), or a-smA and collagen, and double immunohistochemical staining of a-smA and 5-bromo-2'-deoxyuridine (BrdUrd) in carbon tetrachloride-induced fibrotic rat livers. In normal and control livers, a-smA-positive cells were not seen in the lobules, whereas scattered desmin-positive cells were present. With the development of hepatic fibrosis, a-smA was expressed only in a portion of desmin-positive cells located predominantly around collagen bundles. A number of a-smA-positive cells in the lobules were labelled with BrdUrd. These results suggest phenotypic modulation in lipocytes and differentiation of lipocytes towards myofibroblast-like cells, since a-smA is expressed with desmin in myofibroblasts in scar tissue. The expression of a-smA may be related to events of the fibrotic process, such as tissue contraction or fibrogenesis per se.
The purpose of this study was to evaluate the usefulness of ratings of perceived exertion (RPE) as an indicator of exercise intensity in patients with chronic obstructive pulmonary disease (COPD). The subjects were ten male patients with COPD, whose mean forced expiratory volume in 1 s was 1.09 1, SD 0.41, and ten healthy middle-aged men. Ramp incremental exercise on a cycle-ergometer was performed and RPE was determined by the Borg 15-point scale. The absolute oxygen uptake at each RPE was significantly greater in the healthy subjects than in the patients with COPD. However, oxygen uptake calculated as a percentage of maximal at any RPE did not differ significantly between the two groups. Arterial blood lactate concentration at points 15 to 19 on the RPE scale was increased in healthy subjects (P less than 0.05-P less than 0.001), while the dyspnoea index at points 11 to 19 on the RPE scale was higher in patients with COPD (P less than 0.05-P less than 0.001). The main complaints on stopping exercise were dyspnoea in the patients with COPD and fatigue in the healthy subjects. Although the nature of RPE may have been different in the two groups, RPE could be a possible indicator of exercise intensity when physicians prescribe exercise to patients with COPD.
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The effects of NADH and cyanide on NADPH-dependent acetaminophen activation in rat and mouse liver microsomes were studied. In both rat and mouse microsomes, NADPH-dependent acetaminophen-glutathione conjugate production was synergistically enhanced by the addition of NADH, whereas NADH alone did not initiate this reaction. The data suggest that the second electron in this reaction may be transferred from NADH. The present findings are different from a previous report in a reconstituted system that NADH decreases covalent binding of acetaminophen to proteins. This reaction was inhibited by low concentrations of sodium cyanide. The role of the cyanide sensitive factor in this reaction in liver microsomes remains to be further clarified.
Mechanisms of the inhibitory effect of ethanol on acetaminophen hepatotoxicity are controversial. We studied the effects of ethanol and acetaldehyde, an oxidative metabolite of ethanol, on NADPH-dependent acetaminophen-glutathione conjugate production in liver microsomes. Ethanol at concentrations as low as 2mM prevented the conjugate production noncompetitively. Acetaldehyde also inhibited acetaminophen-glutathione conjugate production at concentrations as low as 0.1mM that is comparable with those observed in vivo after social drinking. Acetaldehyde may be involved in ethanol-induced inhibition of acetaminophen hepatotoxicity.
The concentration and molecular form of the plasma atrial natriuretic peptide (ANP) in dogs with mitral regurgitation was investigated. Plasma ANP concentration in dogs with mitral regurgitation was significantly increased (29.4 +/- 1.88 pmol litre-1, n = 40) compared to that in the controls (14.5 +/- 0.62 pmol litre-1, n = 20, P less than 0.01). Molecular forms of plasma ANP were determined by the gel permeation chromatogram. A single peak corresponding to alpha-ANP was detected in the plasma from the controls. However, a peak corresponding to beta-ANP and, or, gamma-ANP was detected in the plasma of the dogs with mitral regurgitation in addition to alpha-ANP. These results suggest that the process of ANP synthesis was altered and excretion of ANP from the heart was enhanced in dogs with mitral regurgitation.