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Biomedical subjects

Y Katagiri

Publications and source records attributed to Y Katagiri.

At least 55 records · Page 3Linked to original sources

Echocardiographic diagnosis of subepicardial aneurysm ruptured into the right ventricle after inferior myocardial infarction.

A subepicardial aneurysm is a rare complication of myocardial infarction that sometimes causes a left to right shunt at the ventricular level. We report on echocardiographic observations in two recent cases of inferior myocardial infarction complicated by rupture of a subepicardial aneurysm into the right ventricle (RV). Two-dimensional and color flow Doppler images in several planes offered diagnostic characteristics of the lesion, including discontinuity of the myocardium at the neck of the aneurysm, a narrow neck relative to the diameter of the aneurysm, and a back and forth flow at the neck of the aneurysm. These techniques also provided new findings, such as a two-chambered structure of the aneurysm and a circular flow pattern within the inner aneurysmal cavity. In addition, color flow Doppler imaging showed multiple shunt flows from the aneurysm to the RV. Echocardiographically diagnosed abnormalities were verified by and successfully treated with surgery in both cases. In conclusion, echocardiography with color flow Doppler imaging may have the potential to diagnose the anatomic and hemodynamic condition of a subepicardial aneurysm.

Aneurysm, Ruptured↗

Purification and characterization of pranlukast hydrolase from rat liver microsomes: the hydrolase is identical to carboxylesterase pI 6.2.

Two carboxylesterases with pI 6.0 and 6.2 derived from rat liver microsomes were purified. The two isozymes were remarkably different in substrate specificity, but they had equal enzymatic activity for alpha-naphthyl acetate and were inhibited equally by phenylmethylsulfonyl fluoride (PMSF) and bis-(4-nitrophenyl) phosphate (BNPP). Carboxylesterases pI 6.0 and 6.2 are identical to the enzymes referred to as hydrolase A and B, respectively, from the results of amino acid sequence analyses. Pranlukast was effectively hydrolyzed by carboxylesterase pI 6.2 but not by the pI 6.0 enzyme, and the difference in the pranlukast metabolism between the human and the rat could be explained by the substrate specificity of carboxylesterase. Furthermore, prodrugs of angiotensin converting enzyme inhibitors were found to be converted to the active drugs after hydrolysis by the carboxylesterases pI 6.0 and 6.2. Carboxylesterases generally catalyze the hydrolysis of ester-type drugs preferentially rather than amide-type drugs.

Amino Acid Sequence↗

Hydrolytic profile for ester- or amide-linkage by carboxylesterases pI 5.3 and 4.5 from human liver.

Carboxylesterases (EC 3.1.1.1) from human liver were purified using Q-Sepharose, Sephadex G-150, isoelectrofocusing and Con A-Sepharose. The calculated molecular mass of the pI 5.3 enzyme was 120 kDa and 61 kDa from the results of Sephadex G-150 gel filtration and SDS-polyacrylamide gel electrophoresis (PAGE), respectively, suggesting that this enzyme is a dimer. On the other hand, carboxylesterase pI 4.5, with a molecular mass of 64 kDa, was a monomer. The activities of both enzymes were inhibited by typical serine enzyme inhibitors. Amino acid sequence analysis of the purified enzymes pI 5.3 and 4.5 showed high homology with rabbit carboxylesterase form 1 and 2, respectively. The results also suggested that carboxylesterase pI 5.3 is identical to the deduced amino acid sequence from cDNA for HU1, and that carboxylesterase pI 4.5 is identical to the deduced amino acid sequence from the cDNA registered as human carboxylesterase (hCE-2) in GenBank. We first purified carboxylesterase pI 4.5 and investigated its hydrolytic activity upon various drugs. The two enzymes differed in substrate specificity. Prodrugs of angiotensin-converting enzyme inhibitors, such as delapril and imidapril, were converted to active metabolites by carboxylesterase pI 5.3, but not by carboxylesterase pI 4.5. The hydrolysis velocity of temocapril by carboxylesterase pI 5.3 was 12-fold faster than by carboxylesterase pI 4.5. In contrast, aspirin, oxybutynin and procaine were hydrolyzed by only carboxylesterase pI 4.5. We also found that an amide-linkage in drugs, except for that in aniracetam, was not a good substrate for the two enzymes. Consequently, carboxylesterases pI 5.3 and 4.5 may be involved in the metabolism of various drugs containing an ester-linkage.

Amino Acid Sequence↗

[A case of esophageal leiomyoma found as mediastinal tumor, diagnosed with endoscopic ultrasonography].

A 20 year-old female was admitted to our department because of an abnormal shadow in chest roentgenogram on a physical check-up. The barium swallowing study revealed an oppression of the middle of the esophagus. Endoscopy, chest CT and MRI failed to distinguish submucosal tumor from mediastinal tumor. Endoscopic ultrasonography showed the mass originated from the esophagus and a diagnosis of esophageal smooth muscle tumor was obtained. The tumor was tried to resect by thoracoscopic surgery but was failed because of its shape like a tortoise shell. The tumor was resected through the right thoracotomy and the diagnosis was confirmed histopathologically.

Adult↗

Down-regulation of cyclin F levels during nerve growth factor-induced differentiation of PC12 cells.

Treatment with nerve growth factor (NGF) produces a marked decrease of cyclin F levels in PC12EY cells. This decrease is prevented by the simultaneous addition of K-252a. A smaller decrease is observed when the cells are treated with fibroblast growth factor, but the addition of epidermal growth factor has no comparable effect. Time course studies show that the decrease in cyclin F precedes the changes produced by NGF in the distribution of cells within the cell cycle. The data suggest that cyclin F is involved in NGF-mediated cell cycle events during the differentiation of PC12EY cells.

Animals↗

Influence of CO2 tension on hepatic hemodynamics during portal arterialization.

We investigated the effect of portal arterialization (PA) on hepatic energy metabolism and hepatic hemodynamics. Portal perfusion flow rate with arterial blood was 25% of the preperfusion portal flow. During PA up to 120 min, hepatic energy metabolism was maintained from the aspects of ATP, energy charge, and arterial ketone body ratio. However, during this PA, carbon dioxide tension (25-35 mm Hg) in arterial blood was lower than that in normal portal vein blood and portal vein resistance (PVR) was significantly increased during perfusion compared with that at preperfusion. When carbon dioxide tension (50-63 mm Hg) in arterial blood was made equivalent to that in normal portal vein blood by controlling the respiratory conditions, PVR was not increased during PA up to 120 min. It was suggested that PCO2 in perfusion blood should change PVR, while it should not change hepatic energy metabolism when portal perfusion flow rate with arterial blood was 25% of the preperfusion portal flow.

Animals↗

Influence of mosaicism on sexing of human preembryos detected by the polymerase chain reaction.

PURPOSE: Preimplantation sex determination using a single cell by the polymerase chain reaction (PCR) was investigated to elucidate the influence of mosaicism. METHODS: The SRY and ZFX genes were coamplified as target sequences for the Y and X chromosomes, respectively. The sensitivity of the single and nested PCR method was examined initially followed by amplification of single amniocytes by the nested PCR. Then the sex of single blastomeres at the three- and nine-cell stages was determined by the nested PCR. RESULTS: The nested PCR was 10(4)-fold more sensitive than the single PCR. Sex determination was possible in 97.5% (117/120) of the blastomeres tested. However, the correspondence rate for all blastomeres within a single embryo was only 60% (12/20 embryos). Among the remaining embryos for which sexing of all blastomeres was not consistent, only one blastomere showed findings indicating the presence of mosaicism (or pseudomosaicism). CONCLUSIONS: At least two blastomeres need to be assessed when determining the sex of an embryo in order to avoid misdiagnosis due to mosaicism (or pseudomosaicism).

Blastocyst↗

Purification and partial characterization of an indomethacin hydrolyzing enzyme from pig liver.

PURPOSE: Indomethacin is well known to be metabolized via O-demethylation and N-deacylation. In this paper we found an enzyme involved in the hydrolysis of amide-linkage of indomethacin and partially characterized it as well as its substrate specificity. METHODS: An indomethacin hydrolyzing enzyme was purified to homogeneity from pig liver microsomes using columns of Q-Sepharose, Red-Sepharose and Blue-Sepharose. The enzyme activity was assayed by measuring of rho-chlorobenzoic acid liberated from indomethacin by HPLC. RESULTS: The purified enzyme effectively hydrolyzed the amide linkage in indomethacin but not those in alpha-naphthylacetate and rho-nitrophenylacetate, which are typical substates for carboxylesterase. The subunit molecular mass of the enzyme was 65 kDa according SDS-polyacrylamide gel electrophoresis. The Michaelis constant (K(m)) and maximum velocity (Vmax) values for indomethacin were 67.8 microM and 9.02 nmol/min/mg protein, respectively. The amino acid sequence analysis of the enzyme after cyanogen bromide cleavage showed high homology with a mouse carboxylesterase isozyme designated as ES-male. The activity of indomethacin hydrolysis was relatively high in the pig, rabbit and human liver homogenate, but not in those from rat and mouse. On the other hand, purified human liver carboxylesterases pl 5.3 and 4.5, and pig liver carboxylesterases have no catalytic activity for indomethacin. CONCLUSIONS: These results indicate that the hydrolysis of amide-linkage of indomethacin in humans would be associated with an enzyme similar to the indomethacin hydrolyzing enzyme from pig liver microsomes described here.

Animals↗

Specific cross-reaction of IgG anti-phospholipid antibody with platelet glycoprotein IIIa.

To study the pathological functions of anti-phospholipid (anti-PL) antibodies, we have analyzed their effect on platelet function. We identified an IgG anti-PL mAb, designated PSG3, which cross-reacted specifically with glycoprotein (GP) IIIa in human platelets and inhibited platelet aggregation. PSG3 bound also to certain polyanionic substances, such as double-stranded DNA, heparan sulfate, dextran sulfate and acetylated-LDL, but not to other polyanionic substances. The binding of PSG3 to GPIIIa was completely inhibited by heparan sulfate and dextran sulfate, indicating that PSG3 recognizes a particular array of negative charges expressed on both GPIIIa and the specified polyanionic substances. Since neither neuraminidase- nor endoglycopeptidase F-treatment of GPIIIa had any significant effect on the binding of PSG3, this array must be located within the amino acid sequence of GPIIIa but not in the carbohydrate moiety. Reduction of the disulfide bonds in GPIIIa greatly reduced its reactivity, suggesting that the negative charges in the epitope are arranged in a particular conformation. PSG3 inhibited platelet aggregation induced by either ADP or collagen, it also inhibited fibrinogen binding to activated platelets in a dose-dependent fashion. PSG3, however, did not inhibit the binding of GRGDSP peptide to activated platelets. These results suggest that the PSG3 epitope on GPIIIa contains a particular array of negative charges, and possibly affects the fibrinogen binding to GPIIb/IIIa complex necessary for platelet aggregation.

Amino Acid Sequence↗

Association between the extent of sclerotic changes in iliac arteries and long-term prognosis in patients with ischemic heart disease.

Peripheral vascular disease is often complicated with ischemic heart disease and is associated with increased cardiac mortality. Latent progression of sclerotic changes in the arteries supplying the lower extremities is often present but undiagnosed. We examined the influence of sclerotic changes of the iliac arteries on the late outcome in 79 patients with ischemic heart disease. Lower abdominal aortography was performed at the time of cardiac catheterization between December 1989 and January 1991. The degree of sclerotic change in the iliac arteries was assessed according to aortography findings such as stenosis, dilatation or bend, with higher scores representing more advanced sclerosis (aortography score). The mean aortography score of all patients was 5.8 +/- 4.6. The patients were followed up for 4.4 +/- 1.2 years to monitor the occurrence of cardiac events (cardiac death, acute myocardial infarction, coronary bypass surgery, or coronary angioplasty for new lesion). The cardiac event-free rate at 5 years was 76.6% in the high score group (32 patients with scores of 6 or more) and 92.9% in the low score group (47 patients with scores of 5 or less). The difference was significant (p = 0.007) by log-rank test. The hazard rate of the aortography score for predicting risk of cardiac event was 1.11 by the Cox proportional hazards model (95% confidence intervals: 1.01-1.23, p = 0.039). When the analysis was adjusted for coronary bypass surgery as primary therapy, the number of diseased coronary arteries, or the presence of peripheral vascular disease, similar results were obtained. In conclusion, more severe sclerotic change in iliac arteries is associated with a higher incidence of cardiac events in patients with ischemic heart disease.

Aged↗

[A case of catamenial pneumothorax with elevated level of serum CA 125].

A 40-year old woman had experienced repeated spontaneous pneumothorax on the right side at the beginning of each menstrual period for one year. The level of serum CA125 was high at 60 ng/ml. Right thoracotomy revealed the presence of multiple darkly-pigmented spots and several pinhole like perforations near the central tendon of the diaphragm. The partial resection of the diaphragm was done, endometrial tissues were detected histologically. Tha patient has been asymptomatic after operation and the level of serum CA125 is normal.

Adult↗

Involvement of alpha v beta 3 integrin in mediating fibrin gel retraction.

Platelet integrin alpha IIb beta 3 (GPIIb-IIIa) plays important roles in platelet-mediated clot retraction. However, little is known about the mechanisms of clot retraction mediated by nucleated cells. In this report, we demonstrate that another member of the beta 3 integrin family, alpha v beta 3, is involved in clot retraction mediated by nucleated cells. Retraction of fibrin clots was observed using a human melanoma cell line, C32TG, which contains no alpha IIb beta 3 complex. This retraction was inhibited by RGD-containing peptide, monoclonal anti-beta 3, and anti-alpha v beta 3 antibodies. Immunoelectron microscopic studies revealed a direct interaction between beta 3 integrin and fibrin fibers at an early stage of clot retraction. We found that another human embryonal cell line, 293, which is known to express alpha v beta 1, but no alpha v beta 3, lacks fibrin gel retractile activity. Upon transfection of beta 3 DNA into 293 cells, the beta 3 subunit formed a complex with an endogenous alpha v subunit. The beta 3-bearing transfectants were found to retract fibrin gels, which was specifically inhibited by anti-beta 3 antibody. In addition, a point mutation at Asp119 in the beta 3 ligand binding domain abolished the clot retractile activity of 293 transfectants, indicating the requirement of alpha v beta 3 ligand-binding activity. Our findings suggest that alpha v beta 3 is involved in mediating the interaction between the three-dimensional fibrin network and nucleated cells and in promoting "post-receptor occupancy" events.

Antibodies, Monoclonal↗

Salutary effect of disopyramide on left ventricular diastolic function in hypertrophic obstructive cardiomyopathy.

OBJECTIVES: The purpose of this study was to estimate the effect of disopyramide on left ventricular diastolic function in patients with hypertrophic obstructive cardiomyopathy. BACKGROUND: Although disopyramide has been reported to lessen clinical symptoms in patients with hypertrophic obstructive cardiomyopathy, few data exist regarding its effect on diastolic function in these patients. METHODS: Thirteen patients with hypertrophic cardiomyopathy (six with and seven without left ventricular outflow obstruction) were examined. Before and after intravenous disopyramide, hemodynamic and angiographic studies were performed. RESULTS: In patients with outflow obstruction, pressure gradient at the outflow tract decreased from a mean +/- SD of 100 +/- 45 to 26 +/- 33 mm Hg (p < 0.01). Although systolic function was similarly impaired in both groups, the time constant of left ventricular pressure decay (tau) shortened from 56 +/- 10 to 44 +/- 8 ms (p < 0.01) and the constant of left ventricular chamber stiffness (kc) decreased from 0.049 +/- 0.017 to 0.038 +/- 0.014 m2/ml (p < 0.01) only in patients with outflow obstruction. Shortening in tau correlated best with decrease in left ventricular systolic pressure (r = 0.84, p < 0.01). In contrast, tau was prolonged from 52 +/- 10 to 64 +/- 11 ms (p < 0.01) and kc was unchanged in patients without outflow obstruction. CONCLUSIONS: The primary effects of disopyramide on the hypertrophied left ventricle were negative inotropic and negative lusitropic. However, left ventricular diastolic properties in patients with outflow obstruction were improved with a decrease in outflow pressure gradient. Relief of clinical symptoms in hypertrophic obstructive cardiomyopathy with disopyramide might be due in part to improvement of diastolic function, which appears secondary to the reduction in ventricular afterload.

Adult↗