[Exercise echocardiography in patients with hypertrophic cardiomyopathy].
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Biomedical subjects
Publications and source records attributed to M Asai.
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DNA sequences complementary to the Torpedo californica electroplax mRNA coding for the alpha-subunit precursor of the acetylcholine receptor were cloned. The nucleotide sequence of the cloned cDNA indicates that the precursor consists of 461 amino acids including a prepeptide of 24 amino acids. Possible sites for acetylcholine binding and antigenic determinants on the alpha-subunit molecule are discussed.
The primary structure of a precursor protein that contains beta-neo-endorphin, dynorphin and a third leucine-enkephalin sequence with a carboxyl extension has been deduced from the nucleotide sequence of cloned DNA complementary to the porcine hypothalamic mRNA encoding it. The three peptides are each bounded by Lys-Arg. This precursor protein, like adrenal preproenkephalin and the corticotropin/beta-lipotropin precursor, comprises multiple repetitive units and a cysteine-containing amino-terminal sequence preceded by a signal peptide.
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Systolic motion of the left ventricular posterior wall (LVPW) was studied by M-mode and long-axis two-dimensional echocardiography in 35 patients (pts) with secundum type of atrial septal defect (ASD), comparing with that of 19 surgically closed ASD (post ASD), 27 with hypertrophic cardiomyopathy (HCM), 15 with old anteroseptal myocardial infarction (a-s MI) and 28 normal subjects. The results obtained were as follows: 1) Excursion of LVPW (PWE) was significantly increased in the pts with ASD compared with normal subjects (P less than 0.001), but there was no significant difference in PWE between the pts with ASD and the pts with HCM or a-s MI. 2) Mean systolic posterior wall velocity (MPWVs) was significantly decreased in the pts with ASD compared with the pts with HCM (p less than 0.05). However, no significant difference could be found in MPWVs between the pts with ASD and a-s MI or normal subjects. 3) End-systolic thickening of LVPW was significantly increased in the pts with ASD compared with normal subjects (p less than 0.05), the pts with a-s MI (p less than 0.05) and the pts with post ASD (p less than 0.01), except for the pts with HCM. There was a significant difference in % end-systolic thickness of lVPW between the pts with ASD and the pts with a-s MI or post ASD (p less than 0:05). 4) Mid-systolic thickening and % mid-systolic thickening of LVPW were significantly increased in the pts with ASD compared with normal subjects, the pts with a-s MI, the pts with post ASD and the pts with HCM (p less than 0.01). This characteristic mid-systolic bulging of LVPW in the pts with ASD was coincident with early-systolic anterior motion of IVS. 5) Basal portion of LVPW indicated the marked inward contraction during end-systole in 30 of 35 pts (86%) with ASD. In these 30 pts, association of mitral valve (MV) prolapse was observed. 6) Following surgical closure of ASD in 19 pts, MV prolapse disappeared following normalization of excessive endsystolic contraction of the LVPW in 16 pts (functional MV prolapse). In 3 pts, however, posterior MV showed multiple abnormal echoes, indicating MV prolapse or mitral regurgitation (organic MV prolapse). In conclusion, these results suggested that mid-systolic bulging of LVPW in ASD is compensatory reaction for systolic anterior IVS motion, and that mechanism of MV prolapse in ASD is related to abnormal left ventricular geometry due to excessive inward contraction of basal portion of LVPW during end-systole.
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Brain content of leucine-enkephalin and methionine-enkephalin changes independently during kindling of the amygdala. Both peptides were measured after 4, 8, 15 and 21 days of stimulation. Leu-enkephalin showed a progressive increase during the kindling: the results on the 4th day did not differ significantly from the controls, whereas those on the 8th day displayed an increase only in the stimulated left hemisphere and those on the 15th day showed an increase in both hemispheres. This increase was also seen after 21 days of stimulation. In contrast, Met-enkephalin was not modified during the early stages of kindling, but was found to be increased after the animals had presented five or more generalized seizures. These results show that Leu-enkephalin is related to the development of kindling, whereas Met-enkephalin levels change only as a consequence of the generalized seizures.
In the long history of screening for antibiotics, fungi and actinomycetes have been the only producers of beta-lactam antibiotics although several phytopathogenic bacteria have been reported to produce toxins with a beta-lactam structure. We report here the first evidence that novel monocyclic beta-lactam antibiotics, sulfazecin and isosulfazecin, are produced by new species of Pseudomonas.
Established amygdaloid kindling causes an increase in the immunoassayable content of both Leuenkephalin and Met-enkephalin in the rat brain. Control and sham-operated (electrode implanted but not stimulated) rats do not show statistically significant differences in brain enkephalin content, while kindled rats show a 40% enkephalin increase in both hemispheres. The present finding is in agreement with several lines of evidence and suggest that enkephalins may play a role in epileptic seizures.
The effect of bilirubin on the temperature dependence of Na,K-ATPase activity was investigated with NaI-treated microsomes prepared from young (13- to 23-day-old) and adult (about 1-year-old) rat cerebra. The Arrhenius plots for the enzymic activities in the young and adult rats showed break temperatures at 26 and 18 degrees C, respectively. In the young rat enzyme, bilirubin caused a shift of the break temperature to 23 and 22 degrees C at concentrations of 60 and 120 microM, respectively, with a significant increase of the activation energy below the break temperature. However, no significant changes in the break temperature and the activation energy were observed in the adult rat enzyme exposed to the same concentrations of the pigment. The results suggest that the lipid environment surrounding the enzyme and modulating its activity in the plasma membranes may differ between the young and adult rat cerebra, and that bilirubin may change the physical state of the lipids related to the activity of the young rat Na,K-ATPase.
A novel beta-lactam antibiotic, isosulfazecin (iSZ), was found to be produced by an acidophilic pseudomonad, Pseudomonas mesoacidophila sp. nov. iSZ was produced in parallel with bacterial growth in nutrient broth containing glycerol and sodium thiosulfate under aerated conditions. iSZ was isolated by chromatography on activated charcoal and anion-exchangers and crystallized from 70% aqueous methanol. The molecular formula was determined to be C12H20N4O9S from physiochemical data. The IR and NMR spectra suggested that iSZ has a beta-lactam ring, methoxyl and sulfonate groups. On acid hydrolysis, it gave L-alanine and D-glutamic acid. iSZ is an epimeric isomer of sulfazecin. iSZ was weakly active against Gram-positive and -negative bacteria, and was strongly active against mutants hypersensitive to beta-lactam antibiotics.
Bacteria, actinomycetes, yeasts, and fungi were screened for their ability to modify the structure of ansamitocins, a group of antitumor ansamycin antibiotics. Many strains, mostly actinomycetes, were found to convert ansamitocin P-3 to one or more products. These products, compounds A, B, C, and D, were prepared using Bacillus megaterium IFO 12108, Streptomyces coelicolor IFO 3807, Streptomyces castaneus IFO 13670 and Streptomyces minutiscleroticus IFO 13361, and were identified as 20-O-demethylansamitocin P-3, maytansinol, 15-hydroxyansamitocin P-3 and N-demethylansamitocin P-3, respectively. Other maytansinoids also underwent these microbial conversions.
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Sulfazecin, a new water-soluble acidic antibiotic, which is active against Gram-negative bacteria, was isolated as crystals from the culture broth of Pseudomonas acidophila G-6302 by use of anion exchange resin and activated charcoal. The molecular formula of sulfazecin was determined to be C12H20N4O9S from physicochemical data. The IR and NMR spectra suggested that this antibiotic has a beta-lactam ring, methoxyl and sulfonate groups. On acidic hydrolysis it gave D-alanine and D-glutamic acid. These chemical and physicochemical data indicated that sulfazecin is a new beta-lactam antibiotic.
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