Prostaglandin omega-hydroxylase and related cytochrome P-450.
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Amino Acid Sequence↗
Biomedical subjects
I Kubota
Publications and source records attributed to I Kubota.
Amino acid sequence of the retinal binding site of squid visual pigment.
The retinylpeptides of visual pigments of two species of squid were identified in invertebrate visual pigments. Their primary structures were identical: H-Phe-Ala-Lys-Ala-Ser-Ala-Ile-His-Asn-pro-Hse(Met)-OH. The sequence was homologous to those of the corresponding region of other visual pigments, but the eighth amino acid, His, was found in squid visual pigments. In this experiment the retinylpeptides of eleven amino acid residues were isolated by monitoring the absorbance spectrum of the reduced retinal Schiff base without using radio-active [3H]retinal. This method is valid for the isolation and identification of retinylpeptides of other invertebrate visual pigments in which the chromophore is not exchangeable.
Amino Acid Sequence↗
Four species of cDNAs for cytochrome P450 isozymes immunorelated to P450C-M/F encode for members of P450IID subfamily, increasing the number of members within the subfamily.
A chicken antibody mono-specific to cytochrome P450C-M/F, which exists in untreated male and female rat liver and catalyses the 2- and 16 alpha-hydroxylation of estrogens (1), was used to screen a cDNA library of male Sprague-Dawley rat liver. Four cDNA clones which encoded P450 isozymes, CMF1a, CMF1b, CMF2 and CMF3, were isolated. CMF1a and CMF2 deduced consisted of 504 and 500 amino acid residues, respectively, while C-terminal 487 and 324 residues for CMF1b and CMF3, respectively, were deduced from the 5'-truncated cDNAs. The isozymes were more than 72% similar in amino acid sequences to each other and to rat P450db1, P450db2 (2), and to a mouse male specific C-P45016 alpha (3), suggesting that they belonged to a new P450 subfamily, P450IID. CMF1a and db1, and CMF2 and db2, respectively, were 99.2% and 99.0% similar in amino acid sequences, suggesting that they were virtually identical. CMF1a and CMF1b were different but 96.1% similar, and CMF3 was between 76% and 78% similar to other members of the rat P450IID family.
Amino Acid Sequence↗
Structures and actions of Mytilus inhibitory peptides.
Two congeneric peptides that inhibit contraction of the anterior byssus retractor muscle of Mytilus edulis were isolated from the pedal ganglia of the mussel. Their structures were determined to be H-Gly-Ser-Pro-Met-Phe-Val-NH2 and H-Gly-Ala-Pro-Met-Phe-Val-NH2. These hexapeptides also showed inhibitory action on contractions in several other molluscan muscles, such as the cardiac muscle of Meretrix lusoria and the penis retractor muscle of Achatina fulica.
Amino Acid Sequence↗
Cytochrome P-450C-M/F, a new constitutive form of microsomal cytochrome P-450 in male and female rat liver with estrogen 2- and 16 alpha-hydroxylase activity.
A new cytochrome P-450 isozyme, P-450C-M/F, has been purified from untreated rat liver microsomes. The purified preparation was electrophoretically homogeneous and contained 12-15 nmol of P450/mg of protein and had a minimum molecular weight of 48,500. The NH2-terminal amino acid sequence of P-450C-M/F was different from that of other P-450's. Immunoblot analysis of microsomes demonstrated that P-450C-M/F was present in the liver of untreated male as well as female rats. Treatment of rats with phenobarbital, 3-methylcholanthrene, or beta-naphthoflavone did not induce P-450C-M/F. Cytochrome P-450C-M/F exhibited little activities of 7-ethoxycoumarin and 7-ethoxyresorufin O-deethylation or hydroxylation of arylhydrocarbon, testosterone, androstenedione, and progesterone. In contrast, it was highly active in N-demethylation of ethylmorphine and benzphetamine and in 2- and 16 alpha-hydroxylation of estrogens, particularly that of estradiol. These studies establish that cytochrome P-450C-M/F is constitutively present in both male and female rats and suggest that it may be involved in the oxidative metabolism of estradiol, particularly in the formation of estriol, the uterotropic metabolite of estradiol.
Amino Acid Sequence↗
Activation sequence at the onset of arrhythmias induced by localized myocardial warming and programmed premature stimulation in dogs.
The effect of localized shortening of ventricular repolarization on arrhythmia vulnerability was studied in 10 pentobarbital anesthetized dogs. An area of the anterior right ventricle was warmed by directing a light beam through a condenser lens assembly and a rectangular aperture. Arrhythmia vulnerability was assessed with low-amplitude programmed stimulation. Activation sequence maps were constructed from electrograms recorded simultaneously from 40 epicardial sites and 24 endocardial sites in and surrounding the warmed area. Recordings were taken during regular atrial and ventricular drives and during programmed stimulation in control periods and during myocardial warming. Spontaneous activity could not be induced with low-amplitude programmed stimulation during control periods in any dog. During myocardial warming arrhythmias were induced in every dog. Most induced arrhythmias had features consistent with local reentry. However, activation sequence at the onset of some arrhythmias strongly resembled that of superventricular activation and was consistent with reentry involving the His-Purkinje system. The findings provide evidence that a localized area with short ventricular repolarization is an abnormality sufficient to increase arrhythmia vulnerability and also that even in this relatively simple setting there can be multiple mechanisms for arrhythmias.
Animals↗
Local conduction delay causes R-wave amplitude increase in patients with effort angina.
Eighty-seven unipolar electrocardiograms distributed over the entire thorax were simulataneously recorded before and after treadmill exercise in 43 patients. Exercise-induced R-wave amplitude change (delta R) and peak R time (time from the onset of QRS to the peak of R wave), were calculated for each lead. The maximal delta R of 87 leads was designated as the max delta R. After exercise, regional delay of peak R time (greater than or equal to 10 msec) on the chest was observed in 13 patients. These patients had significantly higher max delta R than those without such regional peak R time delay (0.71 +/- 0.31mV vs. 0.33 +/- 0.20mV, p less than 0.01). In each case, the site of peak R time delay was almost the same as the site of max delta R. There was no significant difference in the peak heart rate, rise of the systolic blood pressure (delta BPs) during exercise or extent of ischemic ST depression between patients with and without peak R time delay. We concluded that ventricular condition delay plays an important role in the increase of R-wave amplitude after exercise in patients with effort angina pectoris.
Adult↗
Relation of cardiac surface QRST distributions to ventricular fibrillation threshold in dogs.
The relation between ventricular fibrillation threshold (VFT) and cardiac surface QRST area distributions was studied in eight pentobarbital-anesthetized dogs. Unipolar epicardial electrograms were recorded from 64 sites evenly distributed on the right and left ventricles. Localized areas of short repolarization properties were produced by directing five intensities of light onto the surface of the anterior right ventricle through apertures of three sizes. VFT, measured at the center of the lesion, decreased during warming and had a high negative correlation to the change (warming-control) in QRST area (delta QRST1) in the electrogram recorded from the center of the lesion. This correlation was independent of lesion size. For the six experiments, the correlation coefficients for 400-, 800-, and 1,600-mm2 lesions averaged -0.95, -0.94, and -0.96, respectively. The correlation between VFT and delta QRST1 without regard to lesion size averaged -0.88. VFT also had a negative correlation to root mean square (RMS)delta QRST because of warming. RMS delta QRST was calculated from the change in QRST areas (warming-control) in all 64 electrograms. The correlation between VFT and RMS delta QRST was dependent on lesion size. For all experiments, the correlation between VFT and RMS delta QRST averaged -0.97, -0.93, and -0.93 for 400-, 800-, and 1,600-mm2 lesions, respectively. The correlation between VFT and RMS delta QRST without regard to lesion size, however, was considerably lower, -0.59. The results of this study provide the first direct evidence that VFT is correlated with cardiac surface QRST area distributions.
Animals↗
Relationship between late potentials and left ventricular function in patients with coronary artery disease.
We examined the relationship between late potentials and left ventricular function from a hemodynamic point of view in 50 patients with prior myocardial infarction. Late potentials were found in 15 (30%) of 50 patients. A left ventricular aneurysm was found in 28 patients. Late potentials were detected in 14 (50%) of 28 patients with the aneurysm but in 1 (5%) of 22 patients without it (p less than 0.01). In the 50 patients, a hemodynamic data from the late potential positive group (n = 15) were compared to those from the late potential negative group (n = 35). The late potential positive group had a significantly lower ejection fraction, cardiac index and stroke volume than the late potential negative group. We further studied the 28 patients with left ventricular aneurysm in a similar way. The cardiac index and stroke volume were also significantly lower in the late potential positive group. The ejection fraction tended to be lower in the late potential positive group. These results suggest that left ventricular function and left ventricular aneurysm are among the factors that influence the development of late potentials.
Adult↗
[A case report of a muscular ventricular septal defect confirmed by using a conduction staining method (INF type V by Goor's classification)].
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Female↗
Catch-relaxing peptide isolated from Mytilus pedal ganglia.
A peptide that relaxes catch tension of the anterior byssus retractor muscle of Mytilus edulis was purified from pedal ganglion extracts of the mussel. Its primary structure was determined to be H-Ala-Met-Pro-Met-Leu-Arg-Leu-NH2. This peptide was found to have not only catch-relaxing action on the byssus retractor muscle but also modulatory actions on contractions in various molluscan muscles.
Animals↗
ST segment changes in exercise body surface mapping after myocardial infarction in patients with isolated left anterior descending coronary artery disease.
To investigate the clinical significance of exercise-induced ST segment elevation and ST segment depression after myocardial infarction (MI), we performed 87-lead ECG mapping after previous anterior infarction in 24 patients with isolated left anterior descending coronary artery disease before and 1.5 minutes after treadmill exercise. Thirteen patients showed ST segment elevation only, seven patients showed both ST segment elevation and depression, and four patients showed ST segment depression only. ST segment elevation most frequently occurred in the left anterior chest leads corresponding to the QS area, and ST segment depression developed in the left lower chest and left lower back leads. There was good correlation between the number of lead points showing ST segment elevation (nSTe) after exercise and the number of lead points showing QS waves (nQS) before exercise (r = 0.65). nSTe was also correlated with the asynergy index (r = 0.43). These findings suggest that ST segment elevation is mainly the result of aggravation of wall motion abnormalities of the infarcted myocardium. Body surface distribution of ST segment depression was similar to that in effort angina pectoris without MI. We conclude that exercise-induced ST segment depression in MI mainly reflects the ischemia of the surviving myocardium of small infarcts or the peripheral area of large infarcts.
Adult↗
Peroxisomal acyl-coenzyme A oxidase multigene family of the yeast Candida tropicalis; nucleotide sequence of a third gene and its protein product.
We have determined the complete nucleotide sequence of gene POX2, which encodes one of the major peroxisomal polypeptides (PXPs) of Candida tropicalis. POX2 is linked to gene POX4, which codes for a subunit (PXP-4) of long-chain acyl-CoA oxidase. Southern blot analysis revealed that POX2 had a significant homology to POX4, and also to gene POX5 which encodes a subunit (PXP-5) of the isozyme of acyl-CoA oxidase. PXP-2, the protein product of POX2, was co-purified with PXP-4 from the isolated peroxisomes. PXP-2 itself was a flavoprotein and likely to form an equimolar complex with PXP-4, although its enzymatic activity was uncertain. POX2 corresponds to a single open reading frame of 724 amino acids and has no introns. The N-terminal sequence and the calculated Mr of the deduced polypeptide were consistent with those of isolated PXP-2. The primary structure was highly homologous to those of PXP-4 and PXP-5 in respect of the amino acid sequence and the hydropathy profile. We conclude that POX2 is a third gene of the peroxisomal acyl-COA oxidase multigene family.
Acyl-CoA Oxidase↗
Temporal changes in body surface peak R isochrone maps and left ventricular function in patients with myocardial infarction.
Body surface peak R isochrone mapping and radionuclide ventriculography were performed twice in 22 patients with myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously. For each lead, the time from the onset of QRS to the peak of the R wave was measured. From this data for 87 leads an isochrone map was constructed. The lead points where R waves were not observed were designated the no R-wave area (No-R area), which was postulated to correspond to the unexcited regional myocardium. Other abnormal findings, i.e., delay of peak R time near the No-R area (peri-No-R area delay), crowding of isochrone lines, and an island-like zone of delayed peak R times were postulated to indicate slow conduction in the partially excited regional myocardium. In three patients, abnormal patterns in the peak R isochrone maps during the acute phase (within a month from the onset of myocardial infarction) improved in the chronic phase with a significant increase in left ventricular ejection fraction. In two patients, the No-R area decreased after the left ventricular aneurysmectomy. In other patients, abnormal patterns of the isochrone maps and the ejection fraction remained unchanged during the chronic phase of myocardial infarction. We conclude that the comparison of peak R isochrone map patterns between the acute and chronic phase may be useful in evaluating the balance of reversible and irreversible regional damage in myocardial infarction.
Electrocardiography↗
Using body surface mapping to detect vulnerability to ventricular arrhythmias in patients with coronary artery disease.
In order to examine the clinical usefulness of the vulnerability map, body surface mapping was performed in ten normal subjects and 32 patients with CAD using dipyridamole infusion to induce ventricular arrhythmias. A vulnerability map and the vulnerability index (VI) proposed by Urie et al. were constructed from QRS and T isointegral maps in the control state and QRST isointegral map after dipyridamole infusion. Premature ventricular complexes (PVCs) did not occur in normal subjects but occurred in 13 patients after dipyridamole infusion. The vulnerability index in normal subjects was significantly lower than that in patients without PVCs (8.3 +/- 1.7 vs 10.4 +/- 1.7, P less than 0.01). Patients with PVCs showed increased density of contour lines in the vulnerability map and significantly higher VI than those without PVCs (12.6 +/- 2.1 vs 10.4 +/- 1.7, P less than 0.01). This result suggests that a higher vulnerability index indicates that the condition of the cardiac muscle is at high risk of ventricular arrhythmias. It is concluded that the vulnerability map is useful for assessing whether or not the cardiac state is at high risk of ventricular arrhythmias in CAD.
Adult↗
Reactive sulfhydryl groups of sarcoplasmic reticulum ATPase. I. Location of a group which is most reactive with N-ethylmaleimide.
Ca2+-Transporting ATPase of rabbit skeletal muscle sarcoplasmic reticulum contains several SH groups which are reactive with N-ethylmaleimide (MalNEt) at pH 7.0. The location of the one which is most reactive with MalNEt (SHN, Kawakita et al. J. Biochem. 87, 609 (1980)) was identified on the amino acid sequence of the ATPase. SHN was labeled by reacting sarcoplasmic reticulum membranes with [14C] MalNEt to a labeling density of 1 mol/mol ATPase. [14C]MalNEt-labeled membranes were digested with thermolysin and 14C-labeled SHN peptides were fractionated by Sephadex LH-20 chromatography to give two major peaks of radioactivity. [14C]-MalNEt-labeled peptides were further purified to homogeneity by C18-reversed phase HPLC. Two radioactive peptides containing modified cysteine (Cys), Leu-Gly-Cys-Thr-Ser and Val-Cys-Lys-Met, were finally obtained in roughly equal amounts and in reasonable recovery. Both of these sequences were found in the amino acid sequence of Ca2+-transporting ATPase (Brandl et al. Cell 44, 597 (1986)), and Cys344 and Cys364 were identified as the targets of MalNEt-modification. Thus, 0.5 mol/mol ATPase of each Cys residue actually reacted rapidly with MalNEt under the conditions leading to SHN-modification. Modification of either one with MalNEt may negatively affect the reactivity of the other. Both of the highly reactive SH groups are located in the neighborhood of Asp351, the phosphorylation site of ATPase.
Adenosine Triphosphatases↗
Inhibition of dipyridamole-induced myocardial ischemia by diltiazem in patients with coronary artery disease.
We investigated the effect of diltiazem on dipyridamole-induced myocardial ischemia in eight patients with coronary artery disease. Dipyridamole was infused at a rate of 0.142 mg/kg/min for 4 min, and 87-lead mapping was performed to determine the number of leads with ischemic ST-segment depression greater than or equal to 0.05 mV (nST). The range of nST was 8-24 (mean, 13.8) in the control study. Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5). It was concluded that diltiazem could suppress the myocardial ischemia following dipyridamole infusion.
Aged↗
The body surface distribution of the QT interval in patients with previous myocardial infarction and normal subjects.
In spite of the clinical importance of the QT interval, its body surface distribution is still unclear. To determine the spatial distribution of the QT interval, we studied 20 normal subjects and 45 patients with previous myocardial infarction (25, anterior; 20, infero-posterior). Unipolar electrocardiograms were recorded from 87 torso sites. The QT interval in each lead was determined semi-automatically. In normal subjects, the longer QT intervals were located on the left anterior chest and the right shoulder portion. And, the relatively shorter QT intervals were shown on the right inferior chest. In the anterior MI group, the remarkably longer QT intervals were located on the left anterior chest. In the infero-posterior MI group, the longer QT intervals were found on the left lateral and back. In both MI groups, the sites of longer QT intervals corresponded to the sites of infarcted area. In the aneurysm (+) subgroup of the anterior MI group, the remarkably longer QT intervals could be found on the left anterior chest, while in the aneurysm (-) subgroup, these characteristic patterns could not be recognized. Our data suggest that QT intervals are not equal on a torso. In patients with myocardial infarction, the sites of prolonged QT intervals corresponded to the sites of infarcted area. The QT interval was thought to have some bearing on the abnormal repolarization of the residual myocardium in the infarcted area.
Aneurysm↗