[Anesthetic management of a patient with gastric cancer complicated by hypertrophic obstructive cardiomyopathy (HOCM)].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Fukui.
Explore the source record for details and available documents.
To determine the clinical significance of regional left ventricular asynergy in patients with impending myocardial infarction, we recorded two-dimensional echocardiograms (2DE) serially and performed coronary angiography immediately after the hospital admission in nine patients with initial impending infarction and their last anginal attacks were within 48 hours. Left ventricular asynergy on the first 2DE was observed in six of nine patients during symptom-free periods (Group A: LV asynergy group). Five of the six patients had significant coronary artery lesions (greater than or equal to 75% stenosis) in at least one major coronary artery. Intracoronary filling defects were detected in four of the five patients. Another three patients without asynergy (Group B) had significant fixed stenosis. Coronary artery spasm was observed in two patients during coronary angiography, but no patient had intracoronary filling defects. Intracoronary nitroglycerin (0.1-0.3 mg) reduced the severity of coronary artery narrowing in two patients. In addition, urokinase (240,000-480,000 IU) via the corresponding vessel (PTCR) in the remaining seven patients resulted in reduction in the severity of coronary artery stenosis in four patients, but not in the remaining three patients. Left ventricular wall movement in the asynergy group improved rapidly and no asynergy was observed by the seventh hospital day in five of the six patients. Successful PTCR treatment resulted in improvement of left ventricular wall movement. No asynergy was found in the non-asynergy group throughout their hospitalizations. These findings indicated that abnormal left ventricular wall movement is found in patients with impending myocardial infarction, even during symptom-free periods, but the wall movement gradually improves. The 2DE observations are useful for estimating the clinical status and for planning precise therapy for impending myocardial infarction.
Explore the source record for details and available documents.
A new method was developed for the synthesis of 2-(1,2-dihydroxyethyl)thieno[3,2-g]pterin and related 2-substituted thienopterins. A dephosphorylated fluorescent oxidation product of the molybdenum cofactor isolated from xanthine oxidase (EC 1.2.3.2) was identified as 2-(1,2-dihydroxyethyl)thieno[3,2-g]pterin by comparison of electronic and fluorescence spectra and TLC behaviors with those of the synthetic compound.
The immunohistochemical localization of keratins in the oral epithelia of several mammals was investigated using the monoclonal antibodies to keratins, PKK1 (41-56 kilodaltons) and KL1 (55-57 kilodaltons). The staining patterns obtained in different locations of the oral mucosa and of the skin epidermis were compared. In the papillae on the dorsal surface of the tongue, some areas exhibited marked PKK1 staining, while other area were PKK1 negative. In general, rodent oral epithelia were negative for PKK1 in the basal layer, while comparatively strong PKK1 staining was observed in cells of the upper spinous layer. In the epidermis, positive PKK1 reactions were confined to the basal layer, while KL1 staining was occasionally seen in the basal layer of oral epithelia. In cats, dogs, and monkeys, different PKK1 and KL1 binding patterns were observed in oral epithelia. Also, the distribution in oral epithelia differed from that seen in the epidermis of these animals. In the epidermis, the distribution of PKK1 and KL1 was regular, with PKK1 usually being confined to the basal layer, while KL1 binding was found in the spinous and granular cell layers, and was dependent on the degree of keratinization. In the animals studies, keratin expression--as detected by PKK1 and KL1--was different in the skin epidermis and oral epithelia, and the localization of these keratins differed in the various types of oral mucosa.
Most of the positional isomers of mono-, di-, tri- and tetranitrobiphenyls were synthesized and assayed for their mutagenicity in Salmonella typhimurium strains TA98, TA98NR and TA98/1,8DNP6 in the absence of S9 mix. In mono- and dinitrobiphenyls, the structure requirements favoring mutagenic activity are the presence of a nitro group at the 4-position and its absence at the 2-position. TA98 and TA98/1,8DNP6 were reverted by 2-position-free 4-nitro analogues, but TA98NR was not reverted. The results suggest that direct-acting mutagenicity involves the reduction of the nitro group by bacterial nitroreductase but does not involve specific esterification enzymes. Some of the tri- and tetranitrobiphenyls e.g. 3,4,3'-, 3,4,4'-, 3,4,3',4'- and 3,4,2',4'-derivatives reverted not only TA98 and TA98/1,8DNP6 but also TA98NR. Those derivatives commonly have 2 nitro groups at an adjoining position (3,4-dinitro group), whereas 2,4,2',4'-tetranitrobiphenyl, which has strong potency not only in TA98 and TA98/1,8DNP6 but also in TA98NR, possesses 2 nitro groups at the 2-position of each benzene ring.
The effect of quercetin as the comutagen on 2-acetylaminofluorene (AAF) was investigated. AAF was metabolized with mammalian metabolic systems (S9 mix) in the presence or absence of quercetin in vitro, and its metabolites were determined by high-performance liquid chromatography. In the presence of quercetin, the total metabolic rate of AAF decreased compared with that in the absence of quercetin, whereas the formation of N-hydroxy-AAF (N-OH-AAF) and 2-aminofluorene (AF) increased. Since the main metabolic pathway of AAF is aryl-hydroxylation, it is suggested that the decrease of total metabolic rate of AAF is due to the inhibition of aryl-hydroxylation by quercetin. From these results, it seems probable that the comutagenic effect of quercetin on AAF is due to the inhibition of aryl-hydroxylation (the detoxifying pathway) and the promotion of N-hydroxylation and deacetylation (the activating pathway) in the AAF metabolism with S9 mix.
We report the complete nucleotide sequence of two genes encoding major peroxisomal polypeptides (PXPs) of Candida tropicalis. One, POX4, encodes PXP-4, which is the most abundant polypeptide in cells grown on oleic acid, and the other, POX5, is the gene for PXP-5. Each of the two polypeptides was found to be the subunit of a distinct long-chain acyl-coenzyme A oxidase: acyl-CoA oxidase II (PXP-4) or acyl-CoA oxidase I (PXP-5). Both the genes had no intron and gave a single open reading frame. The NH2-terminal sequences, except the initiator methionine, and the calculated molecular weights of the deduced polypeptides were consistent with those of the respective PXPs. Well-conserved sequences of 12 and 16 hydrophobic amino acids were present in the middle of the polypeptide, instead of at the NH2 terminus, and may be internal signal sequences for the peroxisomal location of PXPs. Although the two polypeptides were significantly homologous throughout their sequences, the local homologies in two regions out of five were markedly diverged from the average (63%); the homology in the second region was 93%, whereas that in the fourth one was only 24%. The implications of this finding are discussed in respect to the multiplicity of peroxisomal enzymes and the presence of multifunctional proteins in peroxisomes.
In order to investigate the role of coronary thrombosis as a precipitating factor of acute myocardial infarction (AMI), we examined coronary angiographic findings in 89 patients with AMI taken within 24 hours of the onset and in 42 patients with prolonged angina attack of impending myocardial infarction (impending MI) taken within 50 hours of the last angina attack. Furthermore, in the patients with impending MI, the effects of intracoronary and intravenous thrombolytic therapy and anticoagulant therapy used to prevent impending MI from developing into AMI, were also studied. (1) In 72 of 89 patients (81%) with AMI, coronary thrombi were detected angiographically. The thrombi were detected most frequently (88%) in angiographs taken within 3 hours of onset. (2) In 23 of 42 patients with impending MI, coronary thrombi were detected angiographically. In 6 patients with coronary thrombi who underwent intracoronary thrombolysis during angina attack, occlusive coronary thrombi in ischemia-related vessels were the observed, and recanalization by thrombolysis with intracoronary urokinase infusion relieved chest pain and improved ECG changes. (3) The incidence of AMI in 42 patients with impending MI who were treated with intracoronary and intravenous thrombolytic therapy and anticoagulant therapy was significantly less than in the conventional therapy group (80 patients) (11.9% vs. 27.5%; p less than 0.05). In 4 of 5 patients with developing AMI, coronary thrombi were detected angiographically in the acute phase of impending MI. These results indicate that coronary thrombosis plays an important role not only in the precipitation of impending MI but also in the development of impending MI to AMI.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A simple high-performance liquid chromatographic method has been developed for determining N1-alkylnicotinamides, including C1-C5 alkyl derivatives, in urine. N1-Alkylnicotinamides were reacted with acetophenone in strong alkali medium at 0 degrees C and then formic acid was added. The reaction mixture was heated in acidic medium at above 93 degrees C, and the fluorescent product, 1-alkyl-7-phenyl-1,5-dihydro-5-oxo-1,6-naphthyridine, was chromatographed by HPLC, using a Zorbax SCX-300 column with a mixed mobile phase of acetonitrile-0.04 M ammonium phosphate, monobasic. N1-Alkylnicotinamides can be determined as 1,6-naphthyridine derivatives by a fluorometric detector at a level of 100 pg (signal/noise = 2). Recoveries of N1-alkylnicotinamides in urine were satisfactory. Interfering reaction products from NAD+ and NADP+ were clearly eliminated for determination of N1-alkylnicotinamides without pentyl derivatives.
Holotryptophanase inactivated by oxidation of cysteinyl residues showed a different absorption spectrum from the native enzyme. At pH 8.0, the native enzyme preferentially existed as a 337-nm species (active form), whereas in the inactive enzyme a 420-nm species (inactive form) was dominant. During the reactivation of the enzyme by reduction with dithiothreitol, an increase at 337 nm and a decrease at 420 nm were observed with concomitant increase in enzymatic activity, which was accompanied by the appearance of two cysteinyl residues per monomer. Specific S-cyanylation of cysteinyl residues by nitrothiocyanobenzoic-acid-inactivated apotryptophanase with the modification of one cysteinyl residue per monomer, whereas holotryptophanase was highly resistant to inactivation with nitrothiocyanobenzoic acid. The essential role of the active-site-bound pyridoxal 5'-phosphate in protection against inactivation was confirmed by the agreement of the K1/2 (protection) of 5.0 microM for pyridoxal 5'-phosphate with Km of 2.0 microM in enzyme catalysis. The inactivation by nitrothiocyanobenzoic acid caused a similar shift in the equilibrium between the 337-nm species and 420-nm species, i.e. decrease of the 337-nm species and increase of the 420-nm species. From the pH dependence of the equilibrium between these two species, pKa of 7.9 and 7.4 was obtained for the inactive and the dithiothreitol-activated enzyme, respectively, indicating that cysteinyl residue(s) participated in lowering the pKa of the interconversion between the 337-nm species (active form) and 420-nm species (inactive form). The possible role of cysteinyl residues in the function of tryptophanase is discussed.
The biosynthetic pathway of tremerogen A-10, a polyisoprenyl peptide mating pheromone produced by mating type AB cells of the heterobasidiomycetous yeast Tremella mesenterica, was investigated by immunological techniques with antibody specific to the peptide moiety of the pheromone. Using the biological assay and the radioimmunoassay of the pheromone and its related substances, it was suggested that the peptide is synthesized near the end of logarithmic phase of growth with a temporary accumulation of precursors in the cell. The precursors initially appeared in membrane-bound form and were subsequently converted to soluble forms prior to the secretion. The pheromone acquired its biological activity during the secretion. In the presence of tunicamycin or compactin, pheromone production was blocked with accumulation of membrane-bound precursors. Monensin, however, blocked pheromone production with accumulation of soluble precursors. The molecular species which accumulated in the presence of the antibiotics were analyzed by immunoprecipitation followed by sodium dodecyl sulfate/urea/polyacrylamide gel electrophoresis. In the absence of the inhibitors, membrane-bound precursors with molecular masses of 28 kDa, 12 kDa, 7.8 kDa and 2.8 kDa were found. The precursors which accumulated in the presence of tunicamycin and compactin were the 12-kDa and 28-kDa species, respectively. The results suggested that membrane-bound very high-molecular-mass precursors were initially formed and their extensive modifications, including glycosylation, farnesylation and proteolytic digestion, occur in the membrane. Based on these data, a biosynthetic and secretory pathway was postulated.
The level of carnitine acetyltransferase was markedly increased in harmony with appearance of peroxisomes in alkane-grown cells and propionate-grown cells of Candida tropicalis. From immunochemical studies with antibodies against peroxisomal and mitochondrial carnitine acetyltransferases, it was confirmed that no other type of the enzyme than the peroxisomal and mitochondrial ones was present in alkane-, propionate- and glucose-grown cells of the yeast. The increase in the enzyme level in alkane- and propionate-grown cells was immunochemically proved to result from the increase in the amount of the enzyme protein.
Paget cells from cases of mammary and extramammary Paget's disease were examined for carcinoembryonic antigen (CEA) and CEA-related antigens by the immunoperoxidase method. Paget cells showed a conspicuous positive reaction with antiserum to CEA, but were negative when nonspecific cross-reacting-antigen (NCA)-absorbed antiserum to CEA, or a monoclonal antibody to CEA was used as the detecting agents. Paget cells may contain large amounts of NCA antigen or CEA-related substances.
All positional isomers of mononitro- and monoaminobiphenyls and those of dinitro-, diamino- and aminonitrobiphenyls, which have one substituent on each benzene ring, were assayed for mutagenicity in Salmonella typhimurium by the Ames method. The results suggest that the structural requirements favoring mutagenic activity are the presence of substituents at the 4-position and their absence at the 2'-position. The introduction of an amino group to the 3'- or 4'-position of 4-nitrobiphenyl or a nitro group to 3'- or 4'-position of 4-aminobiphenyl enhanced the mutagenicity. Among the mutagenic compounds, 4-nitro analogues were mutagenic in strains TA98 and TA100 in the absence of a microsomal metabolic activation system. Strain TA98NR was not reverted by the direct-acting mutagens, whereas strain TA98/1,8-DNP6 was as revertible as strain TA98; these results suggest that the direct-acting mutagenicity involves the reduction of the nitro group by bacterial nitroreductase but does not involve specific esterification enzymes.
Explore the source record for details and available documents.