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Biomedical subjects

Y Masuda

Publications and source records attributed to Y Masuda.

At least 343 records · Page 19Linked to original sources
PubMed1996

[Bronchiolitis obliterans in a patient with chronic graft-versus-host disease after bone marrow transplantation].

A 25-year-old with acute lymphoblastic leukemia (FAB:L2) received an allogeneic bone marrow transplant from an HLA-identical sibling during the first remission. Despite administration of adequate immunosuppressant drugs, active chronic graft-versus-host disease developed and continued. The patient complained of progressive dry coughing and breathlessness on exertion 18 months after the transplant and severe hyperlucency and multiple bullae were observed on a chest X-ray film. Three years after the transplant, recurrent bilateral pneumothorax developed and lung cysts were resected twice. Histological examination revealed bronchiolitis obliterans. We speculate that post-transplant bronchiolitis obliterans caused multiple bullae to form by a check-valve mechanism, which then led to recurrent bilateral pneumothorax.

Adult↗
PubMed1996

[Fatty acid metabolic disorder detected by 123I-BMIPP SPECT shortly after elective percutaneous transluminal coronary angioplasty].

UNLABELLED: Decreased or unchanged BMIPP uptake is often observed in the repeated SPECT imaging soon after successful angioplasty, although coronary flow remarkably recovers. To evaluate clinical significance of this phenomenon, 23 patients underwent BMIPP SPECT before elective PTCA (BM-1), soon after PTCA (72 hours, BM-2), and 3 months later (BM-3). SPECT imagings were divided into 7 segments and were semiquantitatively evaluated by 2 cardiologists in the blinded fashion. Decreased uptake at BM-2 compared with BM-1 was evaluated by comparing with stress Thallium-201 SPECT performed in the same schedule but on the different date (TI-1, 2, 3), ischemic manifestation at PTCA, and wall motion change of LVG. Patients with restenosis were excluded from this study. RESULTS: BM-2 showed decreased uptake in 14 (61%), unchanged in 2 (9%), and increased in 7 (30%) patients, while stress TI showed increased perfusion in all patients. Among 91 myocardial segments correspondent to PTCA vessels, 30 (33%) showed overt uptake reduction, and only 13 (14%) segments showed increased uptake. BM-2 uptake reduction was significantly associated with the absence of collateral artery (odds ratio, OR = 3.1, p <0.01), multi vessel disease (OR = 2.0, p = 0.01), total balloon inflating time (p <0.05), ST elevation on ECG (OR = 3.6, p = 0.01), chest pain during PTCA (OR = 3.1, p <0.1), while pre-dilatation by using small size balloon catheter prevented BM-2 uptake reduction (OR = 6.0, p = 0.01). Multiple logistic regression analysis showed that chest pain, balloon inflating time and pre-dilatation were independently associated with BM-2 uptake reduction. Three months after PTCA. the segments with BM-2 reduction had stress TI uptake similar to the segments without BM-2 reduction, however, they showed poorer recovery of BM-3 uptake and LV wall motion. CONCLUSION: BMIPP uptake reduction shortly after angioplasty was associated with ischemic manifestation and poor LV motion recovery, thus, it may be a sensitive representation of the stunned myocardium.

Aged↗
PubMed1996

Effects of efonidipine, nicardipine and captopril on proteinuria in aged spontaneously hypertensive rats.

Previous studies have shown that antihypertensive drugs attenuate the progression of proteinuria by their treatments from young age, but few have examined their effects on impaired renal function in older age. In the present study the calcium antagonists efonidipine ((+/-)-2-[benzyl (phenyl)amino]ethyl 1,4-dihydro-2,6-dimethyl-5-(5,5-dimethyl-2-oxo-1,3, 2-dioxaphosphorinan-2-yl)-4-(3-nitrophenyl)-3-pyridinecarboxyla te hydrochloride ethanol, CAS 111011-76-8, NZ-105) and nicardipine, and an angiotensin-converting enzyme inhibitor, captopril, were examined for their effects on heavy proteinuria in aged spontaneously hypertensive rats (SHR). Efonidipine (20 mg/kg), nicardipine (20 mg/kg) and captopril (30 mg/kg) were orally administered once a day for 4 weeks. The urinary protein excretion (UproE) increased with age (54.9 mg/kg/day at 24 weeks of age to 170.8 mg/kg/day at 36 weeks). The increased UproE was significantly suppressed by daily administration of efonidipine or captopril as compared to that in the non drug treated control group. The UproE in the nicardipine group was maintained at a slightly lower level than in the control. The histological examination showed that the damages of the kidneys were slightly suppressed by efonidipine and captopril. These findings indicate that efonidipine as well as captopril reduce proteinuria in aged SHR and the effect was stronger than that of nicardipine. This beneficial effect of efonidipine on proteinuria suggests its usefulness in antihypertensive therapy.

Aging↗
PubMed1996

The effects of a long-term powdered diet on the amounts of two principal neurotransmitters in the major salivary glands and on stimulated salivary secretion in mice.

The amounts of 2 principal neurotransmitters, acetylcholine (ACh) and norepinephrine (NE) in the 3 major salivary glands, and pilocarpine-, isoproterenol- and phenylephrine-induced salivation in male mice fed a powdered diet for 16 weeks were compared with those in mice fed a standard pellet diet (as control). There were no significant differences in the final body weights of mice fed the powdered diet and the control diet. The only salivary gland in the powdered diet fed mice to increase significantly in weight was the sublingual gland. Mice fed the powdered diet had significantly increased ACh concentrations and contents, but had decreased amounts of NE, in the submandibular and sublingual, but not the parotid glands. The salivation stimulated by pilocarpine was markedly decreased in mice fed the powdered diet, whereas the salivation stimulated by phenylephrine or isoproterenol was not. These findings indicate that reduced mastication affects not only the secretory function but also the amounts of these neurotransmitters in the salivary glands of mice.

Acetylcholine↗
PubMed1996

[Effect of amiloride on the early and late stage of postischemic recovery in isolated perfused rat hearts--possible involvement of Na+/H+ and Na+/Ca2+ exchange].

To investigate whether Na+/H+ exchange or Na+/Ca2+ exchange involves in the ischemic-reperfusion injury, we examined the effect of amiloride, a potent inhibitor of Na+/H+ exchange, on the ischemic reperfused rat heart. When, the hearts were loaded with 0.1 mM amiloride preischemically, the recovery of left ventricular developed pressure was significantly improved than that of the control group, whereas the recovery of heart rate was not influenced by amiloride pretreatment at 30 min of reperfusion. Measurement of intracellular cations revealed that intracellular Na+ accumulation in the early stage (within 5 min) of reperfusion was inhibited by amiloride pretreatment. On the other hand, in the late stage (from 5 min to 30 min) of reperfusion, Ca2+ overload was inhibited by amiloride. These results suggest that Na+/H+ exchange mainly participates in the early stage of reperfusion injury and Na+/Ca2+ exchange system, secondary to the Na+/H+ exchange, participates in the late stage of the reperfusion injury. Moreover, pretreatment with amiloride also decreased creatine phosphokinase activity in the coronary effluent and completely abolished the incidence of ventricular arrhythmia during reperfusion. It is assumed that the improvement of postischemic cardiac dysfunction induced by amiloride pretreatment may be attributable to its inhibition on the resultant Ca2+ accumulation during ischemia.

Amiloride↗
PubMed1996

Receptor binding and antagonist properties of a novel endothelin receptor antagonist, TAK-044 [cyclo[D-alpha-aspartyl-3-[(4-phenylpiperazin-1-yl) carbonyl]-L-alanyl-L-alpha-aspartyl-D-2-(2-thienyl) glycyl-L-leucyl-D-tryptophyl]disodium salt], in human endothelinA and endothelinB receptors.

Receptor binding and antagonist properties of an endothelin (ET) receptor antagonist, TAK-044 ¿cyclo[D-alpha-aspartyl-3-[(4-phenylpiperazin-1-yl) carbonyl]-L-alanyl-L-alpha-aspartylD-2-(2-thienyl) glycyl-L-leucyl-D-tryptophyl]disodium salt¿, were investigated using recombinant human ETA and ETB receptors expressed in Chinese hamster ovary cells. The membranous ETA receptor was shown to be heterogeneous in ET-3 binding affinity (Hill coefficient = 0.54, Kd1 = 390 pM and Kd2 = 8.1 nM). This heterogeneity disappeared upon the addition of guanosine-5'-O-3-thiotriphosphate (Hill coefficient = 0.95, Kd = 7.8 nM). The Kd (from a computer program LIGAND analysis) and Ki (from Dixon plot analysis) values of TAK-044 were 95 and 120 pM for the membranous ETA receptor and 41 and 60 nM for the ETB receptor, respectively. The Kd values of TAK-044 for the ETA receptor was comparable to that of ET-1. The Ki values of TAK-044 for the cellular ETA and ETB receptors were 130 pM and 130 nM at 5,000 cells/well and 1.3 and 590 nM at 50,000 cells/well, respectively. Dixon plot analysis indicated that TAK-044 is a competitive inhibitor of ET-1 binding. TAK-044 inhibited ET-1-induced phosphatidylinositol hydrolysis and arachidonic acid release at 50,000 cells/well in a competitive manner with respective pA2 values of 8.5 and 8.7 in the ETA-expressing cells and 7.4 and 6.6 in the ETB-expressing cells. TAK-044 suppressed ET-1-induced transient increase in intracellular Ca+2 concentration in the ETA- and ETB-expressing cells with respective IC50 values of 2.8 and 230 nM. TAK-044 is a potent and competitive ETA receptor antagonist which simultaneously exhibits definite antagonist activity at the ETB receptor.

Animals↗
PubMed1996

[Natural history and prognosis of medical treatment for the patients with aortic dissections].

The natural history of patients with acute aortic dissections in extremely poor. In 1958, Hirst et al reported 21% of such patients died within a 24 hours, 80% died within a 4 weeks and 93% died with in a 1 year if not treated aggressively. However, there has been a dramatic improvement in the prognosis of patients with aortic dissections since the introduction of surgical treatment by DeBakey et al, and that of medical treatment by Wheat et al. We studied the long-term results of medical treatment for aortic dissections and evaluated the risk factors that determine the prognosis of medically treated patients. The survival rates of medically treated patients with type A dissections at 24 hours, 1 week, 1 month, 1 year, and 10 years after the onset of the disease were 74, 41, 36, 34, 23%, respectively, and the survival rates in type B dissections were 100, 94, 92, 85, 60%, respectively. The risk factors in the acute phase of dissections were type A and serious complications. These in the chronic phase were increasing age, the large diameter of the dissecting aorta and serious complications in acute phase, excluding shock and pericardial tamponade. These results show that emergency surgical intervention is indicated in the patients with acute type A dissections and in those who had acute type B dissections with serious complications.

Acute Disease↗
PubMed1996

Superoxide dismutases in human palatine tonsils.

In order to investigate the protective system of human palatine tonsils against the cytotoxic superoxide radicals (O(-)(2)) generated from the oxygen-related bactericidal system, immunohistochemistry and electron spin resonance (ESR) spectrometry were used to detect the distribution and activities of superoxide dismutases (SODs) in tonsils of different related systemic diseases. Immunohistochemistry showed that SODs distribute in extrafollicular lymphatic tissue and crypt epithelium. No distribution difference could be found between tonsils of different related systemic diseases. ESR revealed no significant difference between SODs activities in tonsils of different related systemic diseases. However, the mitochondrial SOD activity was found to constitute approximately 50%-60% of the total tonsillar cellular SODs activity. The results suggest: i)tonsils possess the ability to control cytotoxic O(-)(2), ii) crypt epithelium and extrafollicular lymphatic tissue may encounter more O(-)(2) threat, iii) SODs may be important in protecting germinal centers from O(-)(2) injury, and iv) systemic diseases are less related to the local expression of tonsillar SODs.

Adult↗
PubMed1996

Effect of cromakalim on ischemic and reperfused immature heart: experiments with isolated neonatal New Zealand white rabbit hearts.

To elucidate whether K+ channels are involved in the ischemia-reperfusion injury in immature heart, we examined the effect of cromakalim, a potent opener of ATP-sensitive K+ channel (KATP channel), on the ischemic and reperfused neonatal New Zealand white rabbit heart. The experiments were divided into control group and cromakalim pretreated group. When, the heart was loaded with 10 microM cromakalim preischemically, the recovery of heart rate and left ventricular developed pressure were significantly improved than those of the control group. Pretreatment with cromakalim also decreased lactate excretion in the coronary effluent. Measurements of cation contents with atomic absorption method revealed that intracellular K+ content was lower in cromakalim pretreated group at preischemia, end of ischemia and 20 min after ischemia. Intracellular accumulation of Na+ and Ca2+ at reperfusion period was inhibited by cromakalim pretreatment. From these results, it is assumed that cromakalim might act on KATP channels of plasma membrane and reduces the K+ content of the cardiomyocytes which in turn inhibits Na+ and Ca2+ accumulation during the reperfusion period. Prevention of Na+ and Ca2+ accumulation after ischemia might be a reason for cardioprotective effect of cromakalim on neonatal New Zealand white rabbit heart.

Animals↗
PubMed1996

Effect of (+/-)-(E)-1-(3-fluoro-6,11-dihydrodibenz[b,e]-oxepine-11 -yl)-4-(3-phenyl-2-propenyl)-piperazine dimaleate on cerebral vasospasm and impairment of cerebral circulation in subarachnoid hemorrhage model in rats.

A subarachnoid hemorrhage (SAH) model in rats was produced by the injection of homologous blood into the cisterna magna. Effects of AJ-3941 ((+/-)-(E)-1-(3-fluoro-6,11 -dihydrodibenz[b,e]-oxepine-11-yl)-4-(3-phenyl-2-propenyl)-p iperazine dimaleate, CAS 143110-70-7) on the development of cerebral vasospasm and the change of regional cerebral blood flow (rCBF) following SAH was investigated in this model. Cerebral vasospasm following SAH showed a biphasic pattern with an early phrase at 10 min and a late phrase on 1 day after blood injection. The physiological parameters (blood pressure, heart rate and blood gas contents) remained stable within the physiological range throughout the course of the experiment. AJ-3941 (0.01 mg/kg i.v. or 0.3 mg/kg p.o.) significantly prevented the development of late phase cerebral vasospasm. Cisternal injection of homologous blood significantly reduced rCBF immediately after the injection and the reduction lasted during the observation period (30 min). Reduction in rCBF after the injection of homologous blood was prevented by AJ-3941 (0.01 mg/kg i.v.). rCBF in AJ-3941-treated rats completely returned to the basal values after 30 min. The present suggest that AJ-3941 may be useful in the prevention of late spasm and in the improvement of cerebral circulation impaired with SAH.

Animals↗
PubMed1995

Cloning and characterization of the POX2 gene in Candida maltosa.

To study the function of acyl-CoA oxidase in an n-alkane-assimilating yeast, Candida maltosa, we isolated the POX2 gene which is a member of the acyl-CoA oxidase gene family. POX2 had a 2172-bp open reading frame (ORF) encoding an approx. 84-kDa polypeptide (724 amino acids (aa)) and was contiguous to POX4, another member of the acyl-CoA oxidase gene family on the same chromosomal DNA in a convergent arrangement. Northern blot analysis revealed that the expression of POX2 was induced in cells grown on oleic acid, n-tetradecanol and n-tetradecane. By using a gene-disruption technique, we constructed strains (termed P2DD and P4DD) in which both alleles of POX2 and POX4 were disrupted. The P2DD strain was normal in assimilation of various hydrophobic carbon sources, such as n-tetradecane, n-tetradecanol and oleic acid. In contrast, the P4DD strain was defective in its ability to grow on such hydrophobic carbon sources.

Acyl-CoA Oxidase↗
PubMed1995

Neural activity of chorda tympani mechanosensitive fibers during licking behavior in rats.

The chorda tympani nerve, supplying the anterior two-thirds of the tongue, contains gustatory and mechanosensitive afferent fibers. We have analyzed discharge patterns in rats of various fibers recorded from dissected nerve filaments during licking behavior of which 4 were taste-sensitive and 12 mechanosensitive. The incidence of these two types were estimated electrophysiologically under anesthesia and their conduction velocity measured. Recordings in freely moving animals showed that the mechanosensitive fibers innervating the dorsal part of the tongue gave two burst discharges per lick, suggesting that contact of the tongue with the upper incisors and/or lip occurred during tongue protrusion and retraction. The fibers from the tip of the tongue showed one burst discharge per lick, which was the response to contact with a drinking spout. No rhythmical discharges synchronized with lick signals were observed in the fibers from the lateral part of the tongue or the taste-sensitive fibers. Such mechanoreceptor discharges were difficult to detect in recordings from the whole chorda tympani nerve. This masking of responses was due mainly to activation of a small number of mechanosensitive fibers by licking-induced mechanical stimulation. The lubricating action of saliva also decreased mechanoreceptor sensitivity. Despite their small number, the mechanosensitive fibers had axons with faster conduction velocities (larger diameter) than the taste-sensitive fibers. This was probably the reason why dissected nerve bundles more frequently showed mechanical than taste responses in conscious rats.

Action Potentials↗
PubMed1995

Cloning and sequencing of a cDNA encoding a taste-modifying protein, miraculin.

A cDNA clone encoding a taste-modifying protein, miraculin (MIR), was isolated and sequenced. The encoded precursor to MIR was composed of 220 amino acid (aa) residues, including a possible signal sequence of 29 aa. Northern blot analysis showed that the mRNA encoding MIR was already expressed in fruits of Richadella dulcifica at 3 weeks after pollination and was present specifically in the pulp.

Amino Acid Sequence↗
PubMed1995

Anticholinergic effects of class III antiarrhythmic drugs in guinea pig atrial cells. Different molecular mechanisms.

BACKGROUND: It is well known that vagal stimulation increases the vulnerability to atrial fibrillation via muscarinic receptor-mediated shortening of refractory period. Recently it has been reported that some class III antiarrhythmic drugs effectively terminate or prevent atrial flutter and fibrillation by prolonging atrial effective refractory period. However, effects of class III antiarrhythmic drugs on the muscarinic acetylcholine receptor-operated K+ current (IK.ACh), which is important for the repolarization phase of the action potential in atrial cells, have not been thoroughly examined. METHODS AND RESULTS: Effects of three class III antiarrhythmic drugs, d,l-sotalol, E-4031, and MS-551, on the carbachol (1 mumol/L)-induced action potential shortening and outward K+ current were examined in guinea pig atrial cells by conventional microelectrode and patch clamp techniques. In isolated left atria, d,l-sotalol (100 mumol/L), E-4031 (3 mumol/L), and MS-551 (30 mumol/L) partially reversed the carbachol-induced action potential shortening. In isolated single atrial cells, IK.ACh was activated by extracellular application of carbachol (1 mumol/L) or adenosine (10 mumol/L) or by intracellular loading of GTP gamma S (100 mumol/L). Sotalol (3 to 1000 mumol/L), E-4031 (1 to 100 mumol/L), and MS-551 (1 to 100 mumol/L) inhibited the carbachol-induced IK.ACh in a concentration-dependent manner, and their IC50 (half-maximal inhibition) values were 35.5, 7.8, and 11.4 mumol/L, respectively. However, the GTP gamma S-induced and adenosine-induced IK.ACh were inhibited by high concentrations of E-4031 and MS-551 but not by sotalol. CONCLUSIONS: Sotalol may inhibit IK.ACh by the blockade of the atrial muscarinic receptors, whereas E-4031 and MS-551 may inhibit the current not only by blocking the muscarinic receptors but also by depressing the function of the K+ channel itself and/or G proteins. These drugs may potentially be useful for the prevention and termination of atrial flutter and fibrillation through their inhibitory action on IK.ACh.

Acetylcholine↗
PubMed1995

Induction of hepatic microsomal drug-metabolizing enzymes by methylsulphonyl metabolites of polychlorinated biphenyl congeners in rats.

The effect of methylsulphonyl (MeSO2) metabolites of 2,3',4',5-tetrachlorobiphenyl (tetraCB) (IU-70), 2,2',3',4',5-pentachlorobiphenyl (pentaCB) (IU-87), 2,2',4',5,5'-pentaCB (IU-101) and 2,2',3',4',5,5'-hexachlorobiphenyl (hexaCB) (IU-141), on the hepatic microsomal drug-metabolizing enzyme system was investigated in rats. The administration of 3-MeSO2-2,3',4',5-tetraCB (10 mumol/kg), 3-MeSO2-2,2',3',4',5-pentaCB (0.5 mumol/kg), 3-MeSO2-2,2',4',5,5'-pentaCB (0.5 mumol/kg) and 3-MeSO2-2,2',3',4',5,5'-hexaCB (2 mumol/kg) to rats significantly increased the contents of cytochromes P-450 and b5 and the activities of aminopyrine N-demethylase, 7-ethoxycoumarin O-deethylase and benzo[a]pyrene hydroxylase. From these results, it is suggested that the 3-MeSO2 derivatives studied are possibly potent phenobarbital-like inducers of microsomal drug-metabolizing enzymes. On the other hand, 4-MeSO2-2,3',4',5-tetraCB, 4-MeSO2-2,2',3',4',5-pentaCB, 4-MeSO2-2,2',4',5,5'-pentaCB and 4-MeSO2-2,2',3',4',5,5'-hexaCB had almost no effect on both cytochrome contents and these enzyme activities. After 96 h, following administration of 2,3',4',5-tetraCB, 2,2',3',4',5-pentaCB, 2,2',4',5,5'-pentaCB and 2,2',3',4',5,5'-hexaCB (342 mumol/kg each), significant increases in contents of these two cytochromes and in activities of these enzymes were observed. The relationship between liver concentrations of 3-MeSO2-PCBs after administration of four PCB congeners and that after administration of their 3-MeSO2 derivatives, and increases in the contents of both cytochromes and activities of drug-metabolizing enzyme suggests that the 3-MeSO2 metabolites derived from PCBs studied play an important role in the induction of the drug-metabolizing enzymes by the parent PCB congeners.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1995

Characterization of hepatic microsomal cytochrome P-450 from rats treated with methylsulphonyl metabolites of polychlorinated biphenyl congeners.

The inducing potency of 3-methylsulphonyl(MeSO2)-2,2',4',5,5'-pentachlorobiphenyl (pentaCB), which was one of the major MeSO2 metabolites of polychlorinated biphenyls (PCBs) present in seal blubber, on the hepatic drug metabolizing enzyme activities was examined in comparison with that of the parent compound and phenobarbital (PB). The inducing fashion of the above enzymes and changes in the contents of PB-inducible P-450 forms by 2,3',4',5-tetrachlorobiphenyl (tetraCB) (IU-70), 2,2',3',4',5-pentaCB (IU-87), 2,2',4',5,5'-pentaCB (IU-101) and 2,2',3',4',5,5'-hexachlorobiphenyl (hexaCB) (IU-141), and their MeSO2 metabolites were investigated in rats. Administration at various doses (0.2-1.0 mumol/kg) of 3-MeSO2-2,2',4',5,5'-pentaCB produced nearly dose-related increases in the hepatic concentration of this methyl sulphone, in the contents of cytochromes P-450 and b5, and in activities of aminopyrine N-demethylase, 7-ethoxycoumarin O-deethylase and benzo[a]pyrene hydroxylase of liver microsomes. Major PB-inducible forms, CYP2B1, CYP2B2, CYP3A2 and CYP2C6 were induced with four PCBs (342 mumol/kg) and their 3-MeSO2 metabolites (0.5-10 mumol/kg), indicating that 3-MeSO2 metabolites were strong PB-type inducers of hepatic drug-metabolizing enzymes. 3-MeSO2-2,2',4',5,5'-pentaCB was an especially strong inducer. On the other hand, four PB-inducible forms of cytochrome P-450 were not induced with the 4-MeSO2 isomers. The relation between liver concentrations of the corresponding 3-MeSO2 derivatives and induction of four PB-inducible forms of cytochrome P-450 after administration of four PCBs and their 3-MeSO2 derivatives further confirmed that the 3-MeSO2 metabolites played an important role in the induction which parent PCB congeners caused on the hepatic drug-metabolizing enzyme system.

Animals↗