Spin/orbital and magnetic quantum number selective magnetization measurements for CoFeB/MgO multilayer films.

Spin selective magnetic hysteresis (SSMH) curves, orbital selective magnetic hysteresis (OSMH) curves and magnetic quantum number selective SSMH curves are obtained for CoFeB/MgO multilayer films by combining magnetic Compton profile measurements and superconducting quantum interference device (SQUID) magnetometer measurements. Although the SQUID magnetometer measurements do not show perpendicular magnetic anisotropy (PMA) in the CoFeB/MgO multilayer film, PMA behavior is observed in the OSMH and SSMH curves for the |m| = 2 magnetic quantum number states. These facts indicate that magnetization switching behavior is dominated by the orbital magnetization of the |m| = 2 magnetic quantum number states.

Integration of woodchuck hepatitis virus (WHV) DNA at two chromosomal sites (Vk and gag-like) in a hepatocellular carcinoma.

Integration of woodchuck hepatitis virus (WHV) DNA into the liver DNA of a woodchuck infected by the virus was investigated. Clonal viral integration was not detected three months before the appearance of four hepatocellular carcinomas (HCC). Integration of the viral DNA was detected in all four HCCs, of which one was chosen to determine the structure of the viral integration completely in a single tumor. The integration occurred in two sites. One part contains the viral DNA from the middle of the gene encoding surface antigen to two-thirds of the way through the gene encoding X protein (X) with no structural changes. The coding frame of the truncated X gene continues into the chromosomal sequence to make a possible fusion protein. The integration seems to have occurred by recombination within two direct repeats of the viral genome in one junction and by homologous recombination between viral DNA and chromosomal DNA in the other junction. The viral DNA is integrated into a spacer of the immunoglobulin L-chain Vk (IgVk) region without any chromosomal rearrangement accompanying the integration. The viral DNA at the second site has a complex structural rearrangement: part of the preS gene is duplicated and attached to the terminus of the gene encoding core antigen in a head-to-tail fashion, followed by three small fragments derived from other parts of the viral DNA. The integrated preS gene has its own 5' regulatory element and a coding frame consisting of the truncated preS gene, the other parts of viral DNA and the chromosomal sequence.(ABSTRACT TRUNCATED AT 250 WORDS)

The primary structure of human gamma-glutamyl transpeptidase.

A cDNA hybridizable to that of rat gamma-glutamyl transpeptidase (GGT) was cloned from a cDNA library of human fetal liver. The insert of the cDNA clone contained 1866 bp consisting of an open reading frame (ORF) of 1709 bp (569 amino acids (aa), N-terminal portion truncated) and a 135-bp 3'-untranslated region followed by a polyadenylated tail. In parallel, amino acid sequences of N-terminal portions of heavy and light chains of a purified human GGT were determined. Two stretches of amino acid sequences identical to the N-terminal sequences of heavy and light chains were found in the ORF. We therefore concluded that the clone is a cDNA for human GGT. From the amino acid sequence deduced from cDNA, the heavy and the light chains of the purified enzyme are estimated to be composed of 351 aa (Mr 38,336) and of 189 aa (Mr 20,000), respectively. The heavy chain is preceded by a signal peptide of at least 29 aa presumed to be cleaved by bromelain treatment. Six putative N-glycosylation sites are present in the heavy subunit region and one in the light subunit region. Primary structure and hydrophobicity profile are closely similar to those of rat GGT.

Synthesis of human gamma-glutamyl transpeptidase (GGT) during the fetal development of liver.

We have determined expression of human GGT gene encoding gamma-glutamyl transpeptidase (GGT) during fetal development of liver using the Northern-blot analysis with a cloned human GGT cDNA and immunohistochemistry with a monoclonal antibody. GGT mRNA could be detected as early as the 12th week of gestation. It then increased gradually to a peak of approx. threefold the amount at week 12, at week 40, just before birth. The size of the mRNA in the fetal liver was 2.7 kb and mRNA of the same size was detected both in the human fetal kidney and human hepatocellular carcinoma as well as normal adult liver. Immunohistochemical analyses show that GGT increased as the fetal liver developed in parallel with the increase in mRNA. Histochemically, GGT was shown to be located in the wall of bile canaliculi when synthesis was low in early development, but to be distributed, in addition, all over the cell membrane of the fetal hepatocytes when synthesis was high at the later stage of development.

Distribution of six neuropeptides in the nucleus tractus solitarii of the rat: an immunohistochemical analysis.

Distribution of substance P-, [Leu]enkephalin-, cholecystokinin-8-, neurotensin-, avian pancreatic polypeptide- and gamma-melanocyte stimulating hormone-like immunoreactive structures were investigated in the nucleus tractus solitarii of the rat by means of the indirect immunofluorescence method. The density of the immunoreactive structures varied markedly according to neuropeptides or subnuclei, with the medial and commissural nuclei containing the highest density. This suggests that the peptides examined play a role in cardiovascular function. However, as seen in the substance P- and [Leu]enkephalin-like immunoreactive structures, these peptides were widely distributed in the nucleus tractus solitarii in addition to the commissural and medial nuclei; a high density of immunoreactive fibers in the ventral, dorsolateral and intermediate subnuclei. In addition to the immunoreactive fiber plexus, a group of immunoreactive cells was also identified in the subnuclei mentioned above. These findings strongly suggest that substance P- and [Leu]enkephalin-like immunoreactive structures are involved not only in cardiovascular function but also in other functions such as respiration, at least in the rat. Finally, the present study demonstrated that the area postrema, particularly its lateral portion, contains various neuropeptide-like structures, both neurons and fibers, substance P-, [Leu]enkephalin-, cholecystokinin-8- and neurotensin-like immunoreactive neurons and fibers, and avian pancreatic polypeptide- and gamma-melanocyte stimulating hormone-like immunoreactive fibers.

Prediction of preserved flow to the infarct area based on admission electrocardiogram in anterior wall acute myocardial infarction.

To determine whether preserved flow to the infarct area could be predicted from the admission electrocardiogram and to define the effect of preserved flow on the late results after reperfusion, 20 anterior myocardial infarction patients who were successfully reperfused were studied. Patients were divided into 3 groups: (1) no-flow group (8 patients), with an occluded infarct-related artery and no easily visible collaterals; (2) intact collateral group (6 patients); and (3) subtotal obstruction group (6 patients). From the admission electrocardiogram, the sum of ST-segment elevation (sigma ST), the sum of R-wave amplitude (sigma R) in leads V1 through V6 and the ratio of these (sigma R/sigma ST) were measured. There was no significant difference in sigma R among the 3 groups. The no-flow group had significantly lower sigma R/sigma ST and higher sigma ST than the intact collateral group or subtotal obstruction group. All patients (6 of 6) with subtotal obstruction and all except 1 patient (5 of 6) with intact collateral showed sigma R/sigma ST greater than 2.5 or sigma ST less than 2.0 mV. All patients (8 of 8) with no flow showed sigma R/sigma ST less than or equal to 2.5 and all except 1 patient with no flow (7 of 8) showed sigma ST greater than or equal to 2.0 mV. The regional wall motion was assessed by the radial method at 4 weeks. The mean percentage systolic shortening in the anterior and apical regions was significantly correlated with sigma R/sigma ST (r = 0.75, p less than 0.001) and sigma ST (r = -0.65, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Possible role of coronary artery spasm in unexplained syncope.

Coronary spasm provocation by intracoronary methylergonovine was performed in 14 patients (8 men and 6 women, mean age 56 +/- 6 years) with syncope that remained unexplained despite neurologic and noninvasive cardiac evaluations. Electrophysiologic testing was also performed in 6 of 14 patients. No patient had structural heart disease or significant fixed stenosis of greater than or equal to 75% in the coronary arteries. Six patients had no history of chest pain even when they developed syncope. Serious arrhythmia was documented in 2 patients, cardiac standstill in 1 and complete atrioventricular block in the other. Coronary spasm was induced in 9 patients using the methylergonovine provocation test. Multivessel spasms were found in 3 patients. Coronary spasm was induced in the artery supplying the inferior wall in 7 of 9 patients with positive results. In 4 of 9 patients who had a positive result, there was no prior history of chest pain. In 1 patient, whose electrocardiogram was recorded during syncope, cardiac standstill was documented and cardiac standstill and syncope also occurred during the provocation test. Monomorphic ventricular tachycardia was not induced by the electrophysiologic study. These results suggest that coronary spasm is involved in unexplained syncope.

Immediate effects of percutaneous transvenous mitral commissurotomy on pulmonary hemodynamics at rest and during exercise in mitral stenosis.

Hemodynamics were evaluated during exercise in 33 patients with mitral stenosis who underwent percutaneous transvenous mitral commissurotomy (PTMC). PTMC was performed using an Inoue balloon. Each patient underwent a supine ergometer exercise test before and on the day after PTMC. Ergometer work load was started at 20 W and increased in increments of 20 W at 3-minute intervals until terminated by the patient's fatigue or shortness of breath. Mitral valve area increased by 0.8 +/- 0.4 cm2 (1.1 +/- 0.3 to 1.9 +/- 0.4 cm2, p less than 0.001). Mean mitral pressure gradient decreased (12 +/- 5 to 6 +/- 2 mm Hg, p less than 0.001). Pulmonary arterial pressure significantly decreased and the cardiac index significantly increased both at rest and during exercise after PTMC. Before PTMC, the increases in pulmonary arterial pressure, total pulmonary resistance and pulmonary arteriolar resistance during exercise were greater in patients with a mitral valve area less than 1.0 cm2 than in patients with an area greater than or equal to 1.0 cm2. After PTMC, total pulmonary resistance still increased during exercise. However, pulmonary arteriolar resistance did not change during exercise in patients with a mitral valve area greater than or equal to 1.5 cm2, whereas it increased in patients with an area less than 1.5 cm2. An enlarged mitral valve area greater than or equal to 1.5 cm2, which may prevent pulmonary vasoconstriction and permits a greater increase in pulmonary blood flow during exercise, is considered a good result immediately after PTMC.

Cross-reaction of synthetic alpha-(1----3)-branched glucans with rabbit anti-N4 dextran.

Cross-reactions of four synthetic branched glucans (3-O-alpha-D-glucopyranosyl-(1----6)-alpha-D-glucopyranans: V39, V17, V37, and V32, each containing one unit glucose branches amounting to 11-12%, 33-43%, 50-54%, and 71-100%, respectively) with rabbit anti-N4 dextran were examined. All four samples precipitated antibodies raised in rabbits by injecting N4 dextran-concanavalin A conjugate. The ability of glucans to precipitate antibody depended on the quantity of branches, samples with more branches precipitating less antibody nitrogen under the same conditions. This may indicate an inhibitory effect of the branches on precipitation. Oligosaccharide inhibition assay showed that the precipitation reactions were specific for (1----6)-alpha-D-glucopyranosyl linkages, and the maximum size of the alpha-(1----6)-specific antibody combining site corresponded to isomaltopentaose. Determination of antibody nitrogen and glucan in the precipitates indicated that the ratios of one combining site of antibody to numbers of glucose residues were 1:9 (V39), 1:11 (V17), and 1:16 (V37) in the extreme antibody excess region. A synthetic sample of manno-glucan ((1----6)-alpha-D-glucopyranan containing about 27% of randomly linked 3-O-alpha-D-mannopyranosyl side chains) also reacted with the same antibody.

The distribution of alpha-melanocyte stimulating hormone (alpha-MSH) in the central nervous system of the rat: an immunohistochemical study. II. Lower brain stem.

The distribution of immunoreactive alpha-melanocyte stimulating hormone (alpha-MSHI) in the rat lower brain stem was examined by indirect immunofluorescence or peroxidase- anti-peroxidase immunohistochemical method using an antiserum against synthetic alpha-MSH. The results confirmed the presence of alpha-MSHI fibers in the midbrain central gray matter and parabrachial area, and demonstrated a much more extensive distribution of these fibers in various parts of the lower brain stem areas previously thought not contain alpha-MSHI fibers. In addition, the commissural nucleus was identified as a new alpha-MSHI neurons-containing site. No alpha-MSHI neurons were seen in other regions of the rat lower brain stem.

Carboxyl terminal region of the MukB protein in Escherichia coli is essential for DNA binding activity.

The purified MukB protein of Escherichia coli has DNA binding activity and nucleotide binding activity. We have isolated a mutation, mukB1013, causing a substitution of valine at position 1379 to leucine. This mutant MukB protein was defective for DNA binding, while the ATP binding activity remained unaffected. A truncated MukB protein that is short of 109 amino acids from the C-terminus failed to bind DNA.

Distribution of neuropeptide Y in the lower brainstem: an immunohistochemical analysis.

The distribution of neuropeptide Y (NPY)-like immunoreactive (NPYI) structures in the rat lower brainstem was examined by means of indirect immunofluorescence or peroxidase-antiperoxidase methods. In addition to the well known immunoreactive NPYI containing cell groups, the present study demonstrated a much wider distribution of immunoreactive NPYI cells in the lower brainstem, i.e. substantia nigra pars lateralis, interpeduncular nucleus, inferior colliculus, nucleus cuneiformis, dorsal tegmental nucleus of Gudden, nucleus laterodorsalis tegmenti, nucleus vestibularis medialis, nucleus vestibularis inferioris, in the fasciculus longitudinalis medialis and nucleus parvocellularis compacta. We also demonstrated an extensive network of NPYI fibers in various areas of the lower brainstem including the auditory system, viscerosensory system, visceromotor system, raphe nuclei, reticular formation, parabrachial area, locus coeruleus and interpeduncular nucleus, etc. The possible importance of NPY is briefly discussed.

Negative NO3- difference in human coronary circulation with severe atherosclerotic stenosis.

To examine whether or not the levels of NOx (nitrite; NO2- and nitrate; NO3-) in coronary circulating blood reflect endothelial dysfunction due to coronary atherosclerosis, NOx levels in plasma obtained from ostium of left coronary artery and coronary sinus of patients who complained of chest pain were evaluated in relation to their coronary angiographic findings. Prior to the study, a HPLC-Griess system for NOx measurement was critically evaluated. This system has a detection limit of 0.1 microM of NO2- and NO3- by 10 microl of loading and was able to distinguish a difference of 0.1-0.2 microM of these substances. Heparin (1 U/10 microl) did not affect the detective and discriminative abilities. NO3- difference, calculated from sino-arterial difference of NO3-, was almost zero (-0.2 +/- 0.2 microM) in patients with either normal coronary arteries or mild organic coronary stenosis (< or = 20% narrowing), while a significant negative value (-5.9 +/- 1.7 microM) was obtained from patients with significant stenosis (> or = 70% narrowing) in the left coronary arteries. These results demonstrate reliable ability on the HPLC-Griess system in evaluating NO2- and NO3- in biological samples, and that the negative NO3- difference through coronary circulation may reflect endothelial dysfunction in the patients with coronary atherosclerosis with severe organic stenosis.

Angina-linked syncope and lack of calcium antagonist therapy predict cardiac arrest before definitive diagnosis of vasospastic angina.

BACKGROUND: Several prognostic factors have been identified in patients with vasospastic angina; however, factors that would predict potentially fatal cardiac arrest during the period between the onset of angina and its definitive diagnosis remain unknown. We investigated the predictive value of the clinical findings that are available when a patient is hospitalized after a cardiac arrest but before a definitive diagnosis of vasospastic angina is made. METHODS: We compared the clinical findings in 11 patients who experienced cardiac arrest before vasospastic angina was definitively diagnosed (group I) with 81 patients with vasospastic angina without cardiac arrest (group II). The definitive diagnosis of vasospastic angina was made on the basis of results of coronary spasm provocation test or ECGs during spontaneous attacks, or both. RESULTS: The incidence of angina-linked syncope was significantly higher in group I than in group II (six out of 11 versus nine out of 81, P < 0.005). Significantly fewer group I patients were receiving calcium antagonists than group II patients (three out of 11 versus 63 out of 81, P < 0.005). Serious arrhythmias were significantly more common in group 1 than in group II (seven out of 11 versus 12 out of 81, P < 0.005). Logistic regression analysis of the eight clinical variables available when first seen in the hospital indicated that angina-linked syncope and the lack of calcium antagonist therapy were independently related to risk of cardiac arrest. CONCLUSIONS: From the clinical findings available, a history of angina-linked syncope and lack of calcium antagonist therapy were found to be independent predictors of cardiac arrest before a definitive diagnosis had been made. Patients who have suspected vasospastic angina may benefit from early treatment with calcium antagonists if they have a history of angina-linked syncope.

Coronary artery spasm is a major cause of sudden cardiac arrest in survivors without underlying heart disease.

BACKGROUND: The role of coronary spasm in underlying disease-free patients who were resuscitated from sudden cardiac arrest remained uncertain. This study investigated the cause of cardiac arrest, and the etiologic and prognostic differences were compared between patients with underlying heart disease (group I) and those patients without underlying heart disease (group II). METHODS: Twenty-five survivors of sudden cardiac arrest were classified into two groups according to the presence or absence of underlying heart disease. To investigate the cause of cardiac arrest, we performed ergonovine testing and electrophysiologic study. Fifteen of the patients had underlying heart disease, while 10 did not. RESULTS: Electrophysiologic abnormalities were found in 13 of the 15 patients in group I. In group II, spontaneous attack of coronary spasm occurred in four patients during the observation period, and coronary spasm was induced in three of the remaining six period of 32 +/- 23 months, whereas no patients in group II had recurrence of sudden cardiac arrest at a median follow-up of 32 months (range, 10 to 72 months). CONCLUSIONS: Electrophysiologic study identified a potential cause in 13 of 15 patients with underlying heart disease. Coronary spasm was involved in the pathogenesis of sudden cardiac arrest in survivors without identifiable underlying heart disease.

Increasing vasoconstrictor response to ergonovine with oxidative injury in canine coronary artery.

BACKGROUND: The effects of oxygen free radicals on coronary vasoreactivity remain unknown. OBJECTIVE: To examine whether oxygen free radicals increase coronary arterial tone and sensitivity to vasoconstrictor stimulation in closed-chest dogs. METHODS: Oxygen radicals were generated by the reaction of xanthine plus xanthine oxidase (XXO) and effects of these substances on the left coronary artery (the percentage diameter change) and on the constrictor effect of ergonovine were examined in vivo in 19 anesthetized, closed-chest dogs by selective coronary angiography. The effects of XXO solution and ergonovine were assessed in a cumulative fashion using 100, 200, and 300 ml XXO and 50, 100, 150, and 200 micrograms ergonovine, in 5 (group I) and 6 dogs (group II), respectively. The effects of XXO on the constrictor responses elicited by 50 micrograms ergonovine were examined in eight dogs (group III). Changes in the vascular endothelium were examined by postmortem electron microscopic examination. RESULTS: Oxidative injury alone produced slight constriction of the coronary artery, but the change was not significant. However, ergonovine-induced vasoconstriction was enhanced after administration of 100 and 200 ml (cumulative amount) XXO solution (P < 0.05, group II versus group III). The enhancement was no longer observed after administration of 300 ml (cumulative amount) XXO solution. Scanning and transmission electron microscopies revealed the formation of blebs and ulceration in the coronary endothelium after administration of XXO solution. CONCLUSION: These results suggest that oxygen radicals can enhance the ergonovine-induced coronary vasoconstriction in a concentration-dependent manner. There seems to be a critical level of oxygen radicals for the production of the effect.

Correlation between arteriographic and electrocardiographic features during spasm in the left anterior descending coronary artery.

BACKGROUND: The clinical role of collateral vessels, which are transiently augmented during coronary artery spasm, remains controversial. OBJECTIVE: To examine the correlation between coronary arteriographic and electrocardiographic features during spasm in the left anterior descending artery (LAD). METHODS: We studied 45 patients in whom LAD spasms were induced by administration of acetylcholine or ergonovine maleate into the left coronary artery, or in whom spontaneous LAD spasms were documented during diagnostic cardiac catheterization. RESULTS: During spasm, only three patients had transient appearance or augmentation of collateral flow opacifying the LAD. In these three patients, electrocardiograms obtained from anterior precordial chest leads during LAD spasm showed ST-segment depression, ST-segment elevation followed by ST-segment depression, and only T-wave change, respectively. Except for these three patients, ST-segment elevations were observed in all other patients (31 of 34) with main-branch spasm of the LAD. However, ST-segment elevation was observed in only two of 11 patients in whom spasm of the diagonal branch alone was induced. CONCLUSIONS: Our observations suggest that the electrocardiographic changes during spasm are not always a sensitive indicator of LAD side branch spasm or LAD main-branch spasm associated with collateral circulation. From consideration of the angiographic features of the collaterals in the three patients with LAD main-branch spasm, we speculate that the balance of tonus of both the recipient and donor arteries, and the degree of organic stenosis of the recipient artery, may have important roles in the mechanism responsible for the change in the appearance of collaterals in patients with coronary spasm.

[A case of dual origin of the left anterior descending coronary artery from the left and right coronary arteries with variant angina].

We present a case of a 68-year-old male inflicted with a rare anomaly of the coronary artery. He had been suspected to have worsening effort angina and underwent urgent cardiac catheterization. The coronary angiography revealed 75% stenosis in the first diagonal branch. The left anterior descending artery was terminated in the mid portion and did not reach the apex. Instead, an anomalous coronary artery from the portion just proximal to the right coronary artery reached the apex. After cardiac catheterization, nocturnal chest pain at rest started to occur frequently. We suspected that vasospasm may have occurred because ST segment elevations in leads II, III, aVF were recorded on the electrocardiogram. Administration of diltiazem (120 mg per day) suppressed angina. Exercise stress electrocardiogram and thallium-201 myocardial scintigram did not show apparent ischemia. This case suggests that we must consider the presence of coronary vasospasm even in patients with clinically-supposed effort angina, to be possibly due to vasospasm occurring in anomalous coronary arteries.

Response of the left ventricle in idiopathic dilated cardiomyopathy to postextrasystolic potentiation.

The effectiveness of postextrasystolic potentiation (PESP) was assessed to detect residual function of the left ventricle in seven patients with idiopathic dilated cardiomyopathy (IDC). The postextrasystolic changes in the aortic pressure pulse, global left ventricular function, and quantitative regional left ventricular wall motion were investigated. PESP caused an increase in the peak systolic aortic pressure (116 +/- 17 to 130 +/- 25 mm Hg, p less than 0.01), a decrease in the peak diastolic aortic pressure (74 +/- 12 to 61 +/- 11 mm Hg, p less than 0.001), a decrease in preejection period/left ventricular ejection time (PEP/LVET) ratio (0.637 +/- 0.136 to 0.457 +/- 0.097, p less than 0.001), and an increase in the global left ventricular ejection fraction (LVEF) (0.26 +/- 0.09 to 0.40 +/- 0.12, p less than 0.01). Postextrasystolic changes in LVEF were inversely related to changes in PEP/LVET (r = -0.76, p less than 0.05). The postextrasystolic patterns of the regional wall motion of the left ventricle were different in each patient. The results of this study suggest that residual left ventricular function can be detected in patients with IDC by their response to PESP.

Different localization of SeqA-bound nascent DNA clusters and MukF-MukE-MukB complex in Escherichia coli cells.

MukF, MukE and MukB proteins form a complex that may participate in the organization of folded sister chromosomes in Escherichia coli. We have found that a MukB-GFPuv4 fusion protein is observed as discrete fluorescent foci, which are localized within cellular spaces occupied by nucleoids, but not at the constriction site of cell division in living cells. In contrast, MukB-GFPuv4 is distributed throughout the whole cell when either MukF or MukE is absent. Statistical analysis revealed that most newborn cells have two foci of mukB-gfpUV4 at one-quarter and three-quarter positions in the cell length and one focus of SeqA-bound nascent DNA at or near the middle of the cell. Subsequently, the single SeqA focus divides into two foci, and then these migrate to the one-quarter and three-quarter positions. Before cell division, most long cells have two SeqA foci and four MukB-GFPuv4 foci. In early stationary phase, SeqA foci disappear, but one or two foci of MukB-GFPuv4 remain. We discuss the reorganization and proper arrangement of folded sister chromosome in the cell quarter positions, which are performed after release from the long-time cohesion of sister chromosomes.