Isolation and characterization of sporeamicin C.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Ishizawa.
Explore the source record for details and available documents.
Sporeamicin A, a novel antibiotic, was isolated from the culture filtrate of an actinomycete. The producing organism, strain L53-18, was taxonomically assigned as a species of the genus Saccaropolyspora. The antibiotic was extracted with chloroform and was then purified by crystallization. It was obtained as colorless prisms from ethanolic solutions. Sporeamicin A exhibited a strong UV absorption peak at 276 nm. The molecular formula of sporeamicin A was determined to be C37H63NO12.
Structure of a novel antibiotic, sporeamicin A (SRM-A), was determined by a combination of spectroscopic and X-ray crystallographic studies. SRM-A has a unique structure containing a 2,3-dihydro-3-oxofuran moiety as part of a 14-membered macrolide ring.
Sporeamicin A is a new erythromycin-type antibiotic isolated from a species of Saccharopolyspora. It was active in vitro against a wide variety of Gram-positive bacteria. In vitro studies indicated that the sporeamicin A was stable in the presence of human serum, although it was bound to serum proteins. Sporeamicin A was effective in the mouse protection test against Staphylococcus aureus, Streptococcus pyogenes and Streptococcus pneumoniae. Sporeamicin A attained higher plasma and tissue levels in the rat than did erythromycin stearate.
Explore the source record for details and available documents.
The characterisation and purification of the ethylene binding protein from developing cotyledons of Phaseolus vulgaris is described. Polyclonal antibodies to this protein recognise homologous proteins in peas, tomatoes and Arabidopsis. Direct binding assays and results from immunological studies indicate that more binding protein is present in abscission zones of Phaseolus than in petioles; ethylene treatment increases binding site abundance in abscission zones. Binding sites for ethylene in peas. Arabidopsis and rice are described indicating that there exist two classes differing only in their rate constants of association and dissociation. Arabidopsis mutants wholly insensitive to ethylene may be receptor deficient and their possible use in receptor studies is assessed. It is proposed that those binding sites with high rate constants of association are functional receptors. The sites with low rate constants of association may be receptors but may also represent receptor precursors or internalised receptors.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In a patient with intermittent type A Wolff-Parkinson-White (WPW) syndrome, the echocardiogram revealed late "double peaked" anterior motions (the former in the late systole, the latter in the early diastole) of left ventricular posterior wall during WPW conduction. In the same condition, phonocardiographic and mechanocardiographic observations indicated a prolonged electromechanical interval, but the external isovolumic contraction time (EICT) and left ventricular ejection time/EICT ratio remained unaltered. In addition, definite but slight alteration in the spatial ventricular gradient was observed. These observations by non-invasive methods present additional informations supporting the concept that conduction abnormalities per se are not responsible for abnormalities of ventricular function unless there is severe underlying heart disease.
Explore the source record for details and available documents.
In 33 patients, including 12 control subjects and 21 with eccentric LVH, LV mass determined by angiocardiogram was correlated to 26 VCG measurements (Frank system) calculated from the scalar X, Y, and Z leads. The results demonstrated that the most reliable indices of VCG in assessing the severity of eccentric LVH determined by angiocardiogram were the magnitude of the spatial mean QRS vector and the time of the spatial maximal QRS vector ("spatial VAT"), of which correlation coefficients were 0.93 and 0.93, respectively. Such high correlation coefficients have never been obtained with the usual ECG analysis. These findings strongly suggest that (1) increased QRS voltage and usual prolonged QRS duration in eccentric LVH are due to an increase in LV mass, and (2) prolonged VAT observed in eccentric LVH is closely related to an anatomic alteration, namely, the greater distance of intra-ventricular conducting pathways as the result of LV dilatation, as an increase in LV mass is usually paralleled by the grade of the chamber enlargement in this type of LVH. Regarding the T loop, correlations between the LV mass and the VCG measurements were less as compared to those of the QRS loop. In general, T changes in moderate or severe LVH may be also related to a certain altered cardiac muscle state, in addition to an increase in LV mass. Angiocardiographic and light microscopic findings of a patient with eccentric LVH in whom a widened QRS-T angle was demonstrated to an extent much more than that expected with an increase in LV mass are presented and discussed. The spatial pattern analysis by VCG is very useful and reliable in assessing the severity of eccentric LVH.
The spatial ventricular gradient (G) and the mean QRS-T angle were examined in 12 patients with angiographically determined eccentric left ventricular hypertrophy (LVH), as compared with 12 normal control subjects. In these 24 patients, a high significant correlation (r = 0.88) was obtained between the magnitude of the spatial mean QRS and LV mass. Although correlations were obtained between the magnitude of the spatial G or the spatial mean QRS-T angle and LV mass, they were lower (r = 0.56, 0.71 respectively). The magnitude of the spatial G (0.190 +/- 0.049 MVSec) in the eccentric LVH group increased significantly (p less than 0.001) in comparison with the control value (0.105 +/- 0.032 mVSec), while in the eccentric LVH group, decreased G/QRS (p less than 0.02), decreased T/QRS (p less than 0.05), and increased QRS-T angle (p less than 0.02) were observed. Furthermore, decreased G/QRS and widening of the QRS-T angle were observed in cases of LVH only. In cases of mild or moderate LVH, normal G/QRS ratios with definitely increased G magnitude and normal QRS-T angle were observed. It is concluded that the magnitude of the spatial mean QRS closely relates to an increase in LV mass. Therefore, should the magnitude of G increase proportionally to an increase in total muscle volume in ideal hypertrophy, then the widening of the QRS-T angle observed in LVH would be due not only to the large ARS complex but also to an alteration in the ventricular gradient.
In forty-one patients with various heart diseases including 29 with LVH, the vectorcardiograms of Frank system and angiocardiographic findings correlated minutely. Based on the left ventricular wall thickness in end-diastole, left ventricular end-diastolic volume, and the length of the long axis of the left ventricle obtained in angiocardiograms, typical left ventricular hypertrophy was classified into types 1a, 1b, 2a, 2b anatomically. The vectorcardiograms in these 4 types represented different patterns with regard to the QRS and T loops respectively. The QRS voltage in the left ventricular hypertrophy closely correlated to the left ventricular wall thickness in end-diastole, the left ventricular end-diastolic volume, and the left ventricular mass. Marked ST and T changes in the left ventricular concentric hypertrophy characterized by increase in wall thickness without definite chamber enlargement may be closely related to the abnormal muscle state with the increased left ventricular wall thickness, the probably due to relative hypoxia in origin. The Q loop of patients with severe left ventricular concentric hypertrophy was definitely differentiated from that of most patients with the pure left ventricular eccentric hypertrophy which was characterized by chamber enlargement with usually slight thickening of the wall. A possible mechanism regarding inconspicuous or prominent Q loops in both concentric and eccentric LVH was presented. An important factor of the delay of the time of occurrence of the spatial R vector in the left ventricular eccentric hypertrophy is the greater distance of the intraventricular conducting pathways caused by the left ventricular dilatation. By means of assessing the vectorcardiogram of the left ventricular hypertrophy, relatively exact anatomy of the left ventricular hypertrophy can be determined.
Pre- and post-operative vectorcardiograms (Frank system) and angiocardiograms in a patient with Lutembacher's syndrome, were correlated. Preoperative vectorcariogram showed the initial conduction delay, complete RBBB, increased QRS voltage, and open QRS loop, while left ventriculography and left atriography demonstrated the markedly posteriorly dislocated left ventricular major axis surrounded by the huge right ventricle and right atrium. Two months after operation, when the left ventricular major axis shifted from abnormally posteriorly directed to left and inferiorly, with the decreased right-sided heart chambers, the initial conduction delay disappeared with decreased QRS voltage. As these vectorcardiographic and angiocardiographic changes at the postoperative stage were parallel, we concluded that the initial conduction delay was a representation of "the pseudo-W-P-W syndrome" and due to the abnormally posteriorly dislocated left ventricular apex and the delayed excitation of the right ventricular free wall caused by the huge dilatation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.