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Biomedical subjects

M Ando

Publications and source records attributed to M Ando.

At least 379 records · Page 21Linked to original sources
PubMed1997

Assessment of hepatic vitamin E status in adult patients with liver disease.

No published reports compare hepatic alpha-tocopherol (adjusted for hepatic lipid content) with indicators of blood alpha-tocopherol in adult patients with various liver diseases. alpha-Tocopherol was simultaneously measured in liver biopsy tissues and blood from 66 subjects (9 comparison patients hospitalized for biliary tract surgery, 13 with chronic persistent hepatitis, 9 with chronic aggressive hepatitis, 10 with acute hepatitis, 10 with cirrhosis, 7 with both cirrhosis and hepatic cell carcinoma, and 8 with fatty liver). Hepatic, erythrocyte, and plasma alpha-tocopherol concentrations were measured, as were hepatic and serum lipids. The ratios of alpha-tocopherol to total lipid concentrations (Toc/TL ratios) in plasma and liver were calculated. In both comparison patients and patients with chronic persistent hepatitis and fatty liver, hepatic alpha-tocopherol concentrations were strongly correlated with hepatic triglyceride and total lipid concentrations (r = .72, P < .001; and r = .75, P < .001, respectively); the relationships (slopes) when hepatic alpha-tocopherol concentrations were compared with hepatic triglyceride and total lipid concentrations were similar in these patients and in all subjects. No strong correlations were found between hepatic and blood alpha-tocopherol parameters in all subjects. These results suggest that hepatic alpha-tocopherol is present at similar concentrations in triglycerides as well as total cholesterol and phospholipids and that neither plasma Toc/TL ratios nor erythrocyte alpha-tocopherol concentrations are useful indicators of hepatic vitamin E status. The hepatic Toc/TL ratio may be useful to assess total hepatic vitamin E status.

Adult↗
PubMed1997

Flexor digitorum profundus avulsion with associated fracture of the distal phalanx.

Two unusual cases of flexor digitorum profundus avulsion with an associated fracture of the distal phalanx are reported. In one case the injury consisted of avulsion of a large bone fragment from the distal phalanx and an associated profundus avulsion from the fragment. The other case showed simultaneous shaft fracture of the distal phalanx with avulsion of the profundus tendon, which could not be included in the existing classification of profundus injuries. The latter injury was misdiagnosed initially.

Adult↗
PubMed1997

Attritional flexor tendon ruptures after a malunited intra-articular fracture of the distal radius.

Rupture of the flexor tendon following Colles fracture is uncommon. In all reported cases it occurred as a complication of an extra-articular, displaced fracture of the distal radius. We report a case in which flexor tendon rupture occurred 30 years after a comminuted intra-articular fracture of the distal end of the radius. There have been no reports of delayed flexor tendon rupture after an intra-articular fracture of the distal radius in young adults.

Colles' Fracture↗
PubMed1997

Vascularized fibular grafts for the reconstruction of segmental tibial bone defects.

Free vascularized fibular grafts were employed in seven patients with large tibial defects following trauma or resection of tumour. All patients were followed for more than 5 years. Tibial union and excellent functional results were achieved in all seven patients. Free vascularized fibular transfer seems to be an effective method of treatment for massive segmental bone defects.

Adolescent↗
PubMed1997

Hepatotoxicity of diisopropyl ester of malonic acid and chloromalonic acids, disinfection by-products of the fungicide isoprothiolane.

The fungicide isoprothiolane (diisopropyl 1,3-dithiolane-2-ylidenemalonate) decomposes to the diisopropyl esters of malonic acid (DM), chloromalonic acid (DCM) and dichloromalonic acid (DDCM) upon aqueous chlorination. In this study, the cytotoxicity of these compounds was examined using rat hepatocytes cultured on Matrigel. DCM and DDCM caused hepatocellular death at concentrations > 0.5 mM, while DM had no effect on the cell viability even at the maximum concentration examined (4 mM). Significant lipid peroxidation, measured as 2-thiobarbituric acid reactive substances, was observed in both DCM- and DDCM-treated hepatocyte cultures, and was significantly enhanced by pretreatment with 0.1 mM bis(p-nitrophenyl)phosphate (BNPP), a carboxylesterase inhibitor. When both BNPP and SKF-525A, a cytochrome P450 inhibitor, were present in the medium, DCM-induced cytotoxicity and lipid peroxidation were significantly suppressed compared to cultures with BNPP-treatment alone. By contrast, the DDCM-induced cytotoxicity was not affected by the combined pretreatment of SKF-525A and BNPP. These results indicate that DCM is metabolically activated by cytochrome P450 in an ester form, while DDCM is activated by a mechanism other than one involving cytochrome P450. To further elucidate the cytochrome P450 isozyme involved in the metabolic activation of DCM, microsomal lipid peroxidation was studied in vitro using microsomes from rats treated with beta-naphthoflavone, musk xylene, phenobarbital, pyrazole, or dexamethasone. Among these preparations, the microsomes from dexamethasone-treated rats showed the most extensive lipid peroxidation in the presence of DCM, and the lipid peroxidation was enhanced by BNPP as observed in hepatocyte cultures. These findings suggest the possible involvement of cytochrome P450 3A in the metabolic activation of DCM.

Animals↗
PubMed1997

Changes in cytochrome P450 enzymes by 1,1-dichloroethylene in rat liver and kidney.

We examined the effect of 1,1-dichloroethylene (1,1-DCE) on microsomal cytochrome P450 (P450) enzymes in rat liver and kidney. Rats were treated intraperitoneally with 1,1-DCE daily for 4 days, at doses of 200, 400, and 800 mg/kg. Among the P450-dependent monooxygenase activities in liver microsomes, testosterone 2alpha-hydroxylase (T2AH), which is associated with CYP2C11 activity, was remarkably decreased by 800 mg/kg 1,1-DCE. The level relative to control activity was < 10%. Furthermore, immunoblotting showed that 1,1-DCE (> or = 400 mg/kg) significantly decreased CYP2C11/6 protein levels in liver microsomes. In addition, 7-methoxyresorufin O-demethylase (MROD), 7-ethoxycoumarin O-deethylase (ECOD), benzphetamine N-demethylase (BZND), chlorzoxazone 6-hydroxylase (CZ6H), and testosterone 6beta-hydroxylase (T6BH) activities were significantly decreased by the highest dose of 1,1-DCE (by 40-70%). However, the activities of other P450-dependent monooxygenases, namely 7-ethoxyresorufin O-deethylase (EROD), 7-benzyloxyresorufin O-debenzylase (BROD), aminopyrine N-demethylase (APND), erythromycin N-demethylase (EMND), lauric acid omega-hydroxylase (LAOH), and testosterone 7alpha-hydroxylase (T7AH) were not affected by 1,1-DCE at any dose. Immunoblotting showed CYP1A1/2, CYP2B1/2, CYP2E1, and CYP3A2/1 protein levels were significantly decreased by 60-66% by 1,1-DCE (800 mg/kg), whereas that of CYP4A1/2 was not affected by any dose of 1,1-DCE. By contrast, among the P450-dependent monooxygenase activities in kidney microsomes, only CZ6H activity was increased by 1,1-DCE (1.6-fold at 800 mg/kg). Also, it was observed that 1,1-DCE (800 mg/kg) significantly increased CYP2E1 protein levels by immunoblotting (approximately 1.5-fold). These results suggest that 1,1-DCE changes the constitutive P450 isoforms in the rat liver and kidney, and that these changes closely relate to the toxicity of 1,1-DCE.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1997

Fluoride mediates apoptosis in osteosarcoma UMR 106 and its cytotoxicity depends on the pH.

Although an excess intake of fluoride has been reported to cause skeletal fluorosis, very little is known about the mechanism of adverse effects of fluoride on bone. In the present study cytotoxic effects of fluoride were studied using the osteosarcoma cell line, UMR 106. The DNA ladder formation upon agarose electrophoresis and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed that UMR 106 underwent apoptosis following exposure to 5 mM fluoride for 8 h. On the other hand exposure to A23187, a calcium ionophore, caused necrosis while co-exposure to fluoride and A23187 inhibited fluoride-mediated apoptosis in UMR 106. The proliferation of UMR 106 cells cultured for 6 days in the presence of 0.5 mM fluoride was significantly decreased compared to the control culture. The cytotoxic effects of fluoride were modulated by both the cell density and the pH of the culture medium. The fluoride-induced viability loss in UMR 106 was enhanced in culture of high cell-density and inversely correlated with pH of the culture medium. Enhancement of fluoride cytotoxicity at acidic pH was also observed in rat alveolar macrophages and RAW 264, a macrophage cell line. The results suggest that fluoride-mediated apoptosis and culture conditions, including pH of the medium, should be taken into consideration to evaluate toxicity of fluoride in vitro.

Animals↗
PubMed1997

Fate of trileaflet equine pericardial extracardiac conduit used for the correction of anomalies having pulmonic ventricle-pulmonary arterial discontinuity.

BACKGROUND: External conduits used for the repair of congenital heart diseases having discontinuity between the pulmonic ventricle and the pulmonary artery still carries a high risk of reoperation. Between June 1983 and June 1992, handmade equine pericardial conduit with fabricated trileaflet valve had been the conduit of choice in our institute. The aim of this study is to clarify the temporal sequence of conduit obstruction in this material and to formulate the optimal surgical strategies for this disease entity. METHODS: One hundred forty-three patients have undergone extracardiac conduit repair using this conduit. Postoperative catheterization performed within 2 months showed pulmonary to systemic ventricular systolic pressure ratio of 0.57 +/- 0.17 with the pressure gradient between pulmonic ventricle and pulmonary artery of 21.1 +/- 17.2 mm Hg. In 63 patients among the survivors, a series of Doppler two-dimensional echocardiographic images could be clearly obtained. RESULTS: Moderate-to-severe degree of pulmonary insufficiency represented only 3.2% of all cases within 3 months, which rapidly increased to 14.3% at 1 to 3 years and 32.8% at 3 to 5 years. However, the rate of increase of pulmonary insufficiency diminished beyond 5 years with 34.9% at 5 to 7 years and 40.0% at 7 to 9 years. Estimated pressure gradient calculated by Bernoulli's equation applied in the same patient subset was 4.1 +/- 7.9 mm Hg within 3 months, which progressively increased to 7.1 +/- 11.8 mm Hg at 1 to 3 years, 21.0 +/- 24.0 mm Hg at 3 to 5 years, 40.2 +/- 25.9 mm Hg at 5 to 7 years, and 71.3 +/- 34.0 mm Hg at 7 to 9 years. Among patients with a pressure gradient across the conduit of more than 40 mm Hg at follow-up catheterization, the primary cause of the obstruction was attributed to degeneration of the valve in 7 patients, whereas sternal compression was strongly suspected as the primary cause in the other 8 patients. Intimal peel was not obvious in the excised specimens. CONCLUSIONS: Degeneration of the valve in the equine pericardial conduit became prominent at 3 to 5 years after the operation, whereas the pressure gradient across the conduit continued to progress thereafter. A thick and hardened valve from degeneration and varying degrees of external compression by the sternum were delineated at the site of stenosis.

Animals↗
PubMed1997

Surgical management of Behçet's aortitis: a report of eight patients.

BACKGROUND: Behçet's aortitis is one of the most severe manifestations of Behçet's disease. However, there have been few reports of this rare entity. This article we describe our experience with surgical treatment of Behçet's aortitis in 8 patients. METHODS: From May 1978 to February 1995, we operated on 8 patients with Behçet's aortitis. All patients were followed up for a total of 54.4 patient-years (mean, 6.8 years). RESULTS: There were no operative deaths, but 1 patient died in the hospital of ventricular fibrillation. Another death occurred as a result of pseudoaneurysm rupture 10 months after operation. Fourteen operations were performed on eight patients: a second operation was performed on four patients, and a third operation was performed on two patients. The translocated Bentall procedure, a modified Bentall procedure, was performed six times. One patient required a second operation for graft detachment, but the others have done well without further surgical intervention. Aortic valve replacement was performed six times, and three reoperations were needed after aortic valve replacement. CONCLUSIONS: The translocated Bentall procedure may be effective for Behçet's aortitis, but further investigation is necessary.

Adult↗
PubMed1997

Effect of 2,4,4'-trichloro-2'-hydroxydiphenyl ether on cytochrome P450 enzymes in the rat liver.

We examined the effect of 2,4,4'-trichloro-2'-hydroxydiphenyl ether (Irgasan DP300) on microsomal cytochrome P450 (P450) enzymes in rat liver. Rats were treated intraperitoneally with Irgasan DP300 daily for 4 days, at doses of 0.2, 0.4 and 0.8 mmol/kg. Among the P450-dependent monooxygenase activities, 7-benzyloxyresorufin O-debenzylase (BROD) and 7-pentoxyresorufin O-depentylase (PROD) in rats, which are associated with CYP2B1, were remarkably induced by all doses of Irgasan DP300. The relative induction to each control activity were from 5.6- to 22.3-fold and 4.9- to 20.2-fold, respectively. Furthermore, immunoblotting showed that CYP2B1/2 protein level in rat liver microsomes was increased from 10.8- to 34.4-fold by Irgasan DP300. In addition, 7-ethoxycoumarin O-deethylase (ECOD) and p-nitrophenol hydroxylase (PNPH) activities were significantly increased by Irgasan DP300 at all doses (from 1.4- to 4.9-fold). Although the activities of other P450-dependent monooxygenases, namely aminopyrine N-demethylase (APND), aniline p-hydroxylase (ANPH), erythromycin N-demethylase (EMND), lauric acid omega-hydroxylase (LAOH) and testosterone 6 beta-hydroxylase (TS6BH) were increased at high doses (> or = 0.4 mmol/kg) of Irgasan DP300, the relative level was lower than those of the CYP2B1-dependent monooxygenases such as BROD and PROD. However, 7-ethoxyresorufin O-deethylase (EROD), 7-methoxyresorufin O-demethylase (MROD), testosterone 2 alpha-hydroxylase (TS2AH) and testosterone 7 alpha-hydroxylase (TS7AH) activities were not affected by any doses of Irgsan DP300. Immunoblotting showed that CYP3A2/1 and CYP4A1 protein levels were significantly induced from 1.3- to 2.2-fold by Irgasan DP300 (> or = 0.4 mmol/kg), whereas those of CYP1A1/2, CYP2C11/6 and CYP2E1 were not affected by any doses of Irgasan DP300. These results suggest that Irgasan DP300 induces the P450 isoforms of CYP2B subfamily in the rat liver, and that the induced P450 isozymes closely relates to the toxicity of Irgasan DP300 or its chlorinated derivatives.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1997

Isolated volar displaced fracture of the ulnar condyle at the base of the index metacarpal: a case report.

A case involving a displaced fracture of the ulnar condyle at the base of the second metacarpal without concomitant dislocation of the second carpometacarpal joint is described. It seems probable that the fracture was produced by simultaneous volar subluxation of the base of the third metacarpal that reduced spontaneously. Open reduction and internal fixation of the fracture with Kirschner wires achieved satisfactory results.

Adolescent↗
PubMed1997

Large volar plate avulsion fracture of the base of the middle phalanx with rotational displacement: a report of three cases.

Three cases of large volar plate avulsion fracture at the base of the middle phalanx with significant displacement are reported. In each case, the fracture fragment involved about 30% of the articular surface and was rotated 90 degrees. The proximal interphalangeal (PIP) joint showed loss of volar stability with hyperextension stress. This unusual variant of volar plate injury is thought to be caused by subluxation of the PIP joint. All patients underwent open reduction and internal fixation. The fracture healed in anatomic alignment without articular incongruity or instability in all cases.

Adolescent↗
PubMed1997

Changes in the volume of marginal cells induced by isotonic 'Cl- depletion/restoration': involvement of the Cl- channel and Na+-K+-Cl- cotransporter.

Marginal cells constitute the endolymph-facing epithelium responsible for the secretion of endolymph by the stria vascularis in the inner ear. We have studied the possible involvement of Cl- conductance and Na+-K+-Cl- cotransport in the mechanism of changes in cell volume upon isotonic Cl- depletion/restoration. Changes in cell volume were estimated from video-microscopic images with the aid of an image processor. Marginal cells shrank to approximately 80% of their original volume in 30 s and to 65-70% in 90 s upon total replacement of [Cl]o (approximately 150 mM) by gluconate-, and the original volume of the shrunken cells was restored within 2 min after restoration of Cl-. The order of potency of anions to induce isotonic shrinkage was gluconate > I- > F- > Br-. The cell shrinkage caused by Cl- depletion was partially inhibited by 5-Nitro-2-(3-phenyl-propylamino)-benzoic acid (NPPB, 0.2 mM), but not by either 4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid (SITS, 0.5 mM), bumetanide (10 microM) or ouabain (1 mM). The cell shrinkage caused by a reduction of [Cl]o from approximately 150 mM to 7.5 mM was not affected by [K]o in the range of 3.6 mM to 72 mM. These results suggest that the main efflux pathway(s) responsible for the 'Cl removal'-induced shrinkage depends on volume-correlated Cl- conductance (Takeuchi and Irimajiri, J. Membrane Biol. 150, 47-62, 1996) and that this pathway(s) is essentially independent of the Na+-K+-Cl- cotransporter, the Na+,K+-ATPase, and the K+-Cl- cotransporter. With regard to volume recovery after isotonic shrinkage, its critical dependence on the simultaneous presence of Na+, K+ and Cl- in the bath and its substantial inhibition by bumetanide (10 microM) both indicate a major role for Na+-K+-Cl- cotransport. The strong influence on cell volume of solute fluxes working through the Cl- channel and the Na+-K+-Cl- cotransporter implies an essential role for these pathways in the ion transport mechanism(s) of the marginal cell.

Animals↗
PubMed1997

Marginal cells of the stria vascularis of gerbils take up glucose via the facilitated transporter GLUT: application of autofluorescence.

Strial marginal cells are known to take up and metabolize glucose as their main source of metabolic energy. The membrane transport mechanisms for glucose uptake into strial marginal cells, however, are largely unknown. Two types of glucose transporters in mammalian cells have been described, the facilitated glucose transporter GLUT and the sodium/glucose cotransporter SGLT. The goal of the present study was to determine which of these represent the main glucose uptake mechanism in strial marginal cells. Glucose uptake into strial marginal cells was assessed by monitoring the cellular concentration of the reduced form of nicotinamide adenine dinucleotide (NADH) fluorometrically. The relation between the autofluorescence from marginal cells and cellular metabolism was verified as follows. The autofluorescence (excitation: 340 nm, emission: 450-490 nm) decreased when oxidative phosphorylation in the mitochondria was uncoupled with carbonyl cyanide 3-chlorophenylhydrazone (CCCP) and increased when cytochrome oxidase was inhibited with cyanide. These effects indicate that the autofluorescence is dependent on the mitochondrial metabolic state, and more specifically on the level of NADH in mitochondria. Glucose removal from the bath solution elicited a 39% decrease in the autofluorescence intensity within 5 min. Similarly, cytochalasin B (10 microM) reduced the fluorescence intensity by 34% in 5 min. In contrast, neither phlorizin (0.1 mM) nor Na+ removal from the bath solution caused any appreciable change in the autofluorescence intensity. These results indicate that glucose depletion affects the metabolic state of the marginal cell within a few minutes, and that marginal cells take up glucose via GLUT, but not via SGLT. Since the excitation and emission wavelengths of several fluorescent dyes used in physiological studies (e.g., Fura-2 and SBFI) are similar to those of NADH, possible effects of autofluorescence on recording signals should always be taken into account when these dyes are utilized.

Animals↗
PubMed1997

Truncus arteriosus communis associated with chromosome 22q11 deletion.

OBJECTIVES: The purpose of this study was to clarify characteristics of truncus arteriosus communis associated with chromosome 22q11 deletion (del 22q11). BACKGROUND: DiGeorge syndrome and conotruncal anomaly face syndrome are associated with del 22q11 (hemizygosity). In 30% of cases, truncus arteriosus communis is associated with the deletion. METHODS: Fifteen consecutive patients with truncus arteriosus communis were checked for 22q11 with fluorescent in situ hybridization using an N25 probe (Oncor). Cardiovascular anomalies were studied with cardiac catheterization, cineangiography and echocardiography. RESULTS: Five patients had del 22q11. Two had a rare type of truncus arteriosus: type A3 of Van Praagh and Van Praagh with major aortopulmonary collateral arteries and pulmonary ostial stenosis. The other three had type A1 truncus arteriosus and pulmonary artery stenosis. One of them had major aortopulmonary collateral arteries. Ten patients with truncus arteriosus had no del 22q11. The types of truncus arteriosus in these 10 patients were type A1 in 7, type A2 in 2 and type A3 with closed ductus in 1. None of nine patients with type 1 or type 2 truncus arteriosus had pulmonary stenosis. CONCLUSIONS: In truncus arteriosus communis, the rare type A3 with major aortopulmonary collateral arteries and pulmonary ostial stenosis and type A1 with pulmonary artery stenosis are associated with del 22q11.

Abnormalities, Multiple↗
PubMed1997

Emergency extracorporeal life support for patients with near-fatal status asthmaticus.

Extracorporeal life support (ECLS) was used to treat three patients with near-fatal status asthmaticus who did not respond to aggressive medical therapies and mechanical ventilation under controlled permissive hypercapnia. ECLS was instituted in patient 1 because PaCO2 was excessively high and pH was excessively low, in patient 2 because hypoxemia and shock were not responsive to treatment, and in patient 3 because of sustained severe hypotension. ECLS supported adequate gas exchange until pulmonary function improved, diminishing the need for mechanical ventilation and preventing pulmonary complications. Pulmonary dysfunction improved markedly after only 21 to 86 hours of ECLS. Aggressive medical treatments were continued during ECLS. Our findings indicate that ECLS is a useful method for preventing death in patients with near-fatal status asthmaticus.

Adolescent↗