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Biomedical subjects

K Iida

Publications and source records attributed to K Iida.

At least 307 records · Page 17Linked to original sources
PubMed1988

Sudden death in hypertrophic cardiomyopathy, a guideline to prevention in daily life.

To establish guidelines for individuals with hypertrophic cardiomyopathy (HCM) to follow in their daily lives and minimize the chance of sudden death (SD), circumstances of SD in 24 autopsied definite HCM cases were compared with those with 905 autopsied cases of other heart diseases. Circumstances of symptoms experienced in daily activities of 35 age-matched surviving HCM cases were also studied. In the autopsied HCM cases, SD occurred during exertion more frequently (79.2%) than in the other autopsied cardiac patients (22.7%). Sudden changes in pace or movement accompanied by mental excitement, such as hurrying to board a train, were more frequent causes of SD in HCM (47.4%) than in other cardiac patients (8.3%). In the surviving HCM cases, symptoms of distress occurred frequently during very hard work or with sudden rapid movement. Thus, one probable daily guideline for HCM sufferers would appear to be not only to eliminate very hard work but also to lead mentally and physically quiet and relaxed life.

Adolescent↗
PubMed1988

[Evaluation of secondary tricuspid regurgitation by intraoperative epicardial pulsed Doppler echocardiography].

Since 1985, we have evaluated secondary tricuspid regurgitation associated with acquired mitral valve disease in patients undergoing open mitral surgery by intraoperative epicardial two-dimensional and pulsed Doppler echocardiography. We found intraoperative pulsed Doppler echocardiography to be a sensitive, safe technique allowing surgeons to evaluate the severity of tricuspid regurgitation intraoperatively, even in critically ill patients who cannot afford preoperative cardiac catheterization. To assess the severity of tricuspid regurgitation intraoperatively, the transducer was placed directly on the right atrium. The ultrasound beam was transmitted into the right atrium at right angles to the tricuspid valve orifice to record intraoperative four-chamber two-dimensional echocardiograms, which were used to detect the sites of eight sample volumes, one in the right ventricle and seven in the right atrium, for pulsed Doppler echocardiography. The pulsed Doppler signals were recorded in each sample volume before and after cardiac procedures. The pansystolic abnormal signals lasting from tricuspid valve closure to the subsequent opening and consisting of components moving away from the tricuspid valve were interpreted as tricuspid regurgitant flows. Without operative correction of the tricuspid valve, secondary tricuspid regurgitation can resolve following mitral valve surgery alone. However, to our knowledge, there are no published reports of objective findings of intraoperative changes of secondary tricuspid regurgitation. Here we present the unique intraoperative pulsed Doppler echocardiographic features of tricuspid regurgitation before and after cardiac procedures. A 30-year-old woman with preoperative diagnosis of aortic regurgitation, mitral stenosis and severe tricuspid regurgitation underwent aortic and mitral valve replacement. The intraoperative pulsed Doppler echocardiograms recorded after pericardiotomy and before cannulation of the heart showed tricuspid regurgitant flow signal in all of the seven sample volumes in the right atrium, which was interpreted as severe tricuspid regurgitation. After surgical procedures, no regurgitant flow from the tricuspid orifice to the right atrium was detected in the eight sample volumes. This suggested that preoperative secondary tricuspid regurgitation improves without operative procedures for the tricuspid valve. All intraoperative echocardiographic procedures were performed within 5 min, and no arrhythmias or other complications related to this technique were noted. Epicardial pulsed Doppler echocardiography is helpful in assessing tricuspid valve function of patients undergoing mitral valve surgery bef

Adult↗
PubMed1987

The mechanism of action of decay-accelerating factor (DAF). DAF inhibits the assembly of C3 convertases by dissociating C2a and Bb.

DAF is a 70,000-Mr membrane protein that inhibits the amplification of the complement cascade on the cell surface, and protects cells from damage by complement. The precise mechanism of action of DAF is not entirely clear. Purified DAF was incorporated into the membrane of EAC4b cells. EAC4b2 and EDAF AC4b2 cells were prepared with radiolabeled C2. The same amount of labeled C2 bound to both cells, showing that DAF does not prevent the binding of C2 zymogen to C4b. After adding Cl, the radioactivity of bound C2 dissociated more rapidly from EDAF AC4b cells than from EAC4b cells. In EAC4b cells, bound C2 was converted to C2a, which gradually dissociated into the supernatants. In the DAF-treated cells, on the other hand, a large amount of C2a rapidly appeared in the supernatants and only a small amount of C2a remained on the cells. In a similar experiment using EhuAC4b, DAF on human erythrocyte membrane also dissociated the C2a from the cells. These results were confirmed by hemolytic assay and the accelerated decay of C2a caused the rapid depletion of C2 from the fluid phase. In addition, we found that DAF functions on the alternative pathway C3 convertase, C3bBb in the same manner. Thus, DAF, which associates with C4b and C3b in the membrane, acts on C2a and Bb, but not on intact C2 and B, and dissociates them rapidly from the binding sites, thereby preventing the assembly of the classical and alternative pathways C3 convertases.

Animals↗
PubMed1987

Polyphosphoinositide micelles and polyphosphoinositide-containing vesicles dissociate endogenous gelsolin-actin complexes and promote actin assembly from the fast-growing end of actin filaments blocked by gelsolin.

The Ca2+-activated actin-binding protein gelsolin regulates actin filament length by severing preformed filaments and by binding actin monomers, stabilizing nuclei for their assembly into filaments. Gelsolin binds to phosphatidylinositol 4,5-bisphosphate (PIP2), with consequent inhibition of its filament severing activity and dissociation of EGTA-resistant complexes made with rabbit macrophage or human plasma gelsolin and rabbit muscle actin. This study provides evidence for an interaction of gelsolin with phosphatidylinositol monophosphate (PIP) as well as PIP2 and further describes their effects on gelsolin's function. Both phosphoinositides completely dissociate EGTA-insensitive rabbit macrophage cytoplasmic gelsolin-actin complexes and inhibit gelsolin's severing activity. The magnitude of inhibition depends strongly on the physical state of the phosphoinositides, being maximal in preparations that contain small micelles of either purified PIP or PIP2. Aggregation of PIP or PIP2 micelles by divalent cations or insufficient sonication or their incorporation into vesicles containing other phospholipids decreases but does not eliminate the inhibitory properties of the polyphosphoinositides. The presence of gelsolin partly inhibits the divalent cation-induced aggregation of PIP2 micelles. PIP2 in combination with EGTA inactivates gelsolin molecules that block the fast-growing end of actin filaments, thereby accelerating actin polymerization. Regulation of gelsolin by the intracellular messengers Ca2+ and polyphosphoinositides allows for the formation of several different gelsolin-actin intermediates with distinct functional properties that may be involved in changes in the state of cytoplasmic actin following cell stimulation.

Actins↗
PubMed1987

Functional and antigenic properties of complement receptor type 2, CR2.

This is the first report demonstrating that C3d receptor (CR2) has functional activity in regulating complement cascade. Purified CR2 was examined for its cofactor activity in factor I-mediated cleavage of membrane-bound iC3b. CR2 plus C3b inactivator (I) released C3c from EA 125I-iC3b, and the release was inhibited when CR2 was preincubated with OKB7 monoclonal anti-CR2. Furthermore, immunoelectroblotting analysis showed crossreactivity of CR2 with 57H anti-CR1. These results indicate that CR2 has functional and antigenic similarity to CR1, thus providing a supporting evidence for placement of CR2 as a member of the recently defined gene family of C3- and C4-regulatory proteins composed of CR1, C4-binding protein, and factor H.

Collodion↗
PubMed1987

A solid-phase anti-C3 assay for detection of immune complexes in six distinguished forms.

A solid-phase anti-C3 assay detecting immune complexes associated with C3 fragments is described. Two monoclonal antibodies against C3 fragments are used; one recognizes an epitope expressed on C3b, C3c and C3i, the other recognizes an epitope expressed on C3dg and iC3b. Combining these monoclonal anti-C3s with antibodies against class-specific immunoglobulins in enzyme-linked immunosorbent assay (ELISA), immune complexes (ICs) are detected in six distinguished forms; C3b-IgG-IC, iC3b/C3dg-IgG-IC, C3b-IgA-IC, iC3b/C3dg-IgA-IC, C3b-IgM-IC and iC3b/C3dg-IgM-IC. About three-fourths of the plasma samples from patients with active SLE or IgA-nephritis were found positive in one or more types of ICs. IgA-type ICs were found very frequently in patients with autoimmune or renal diseases.

Antibodies, Monoclonal↗
PubMed1987

Variable neurohumoral and hemodynamic responses to exercise in patients with exertional angina: influence of the severity of coronary artery disease.

To assess neurohumoral and hemodynamic responses to exercise in patients with exertional angina, we measured plasma norepinephrine (NE) concentrations in 23 patients with exertional angina (with no heart failure) and compared the results with their coronary arteriographic findings. The 23 patients were divided into two groups: 14 cases with multiple vessel disease (MVD) and 9 cases with one-vessel disease. At resting state there were no significant differences between the two groups in levels of NE. At maximal exercise there were no significant differences between the groups in increases of heart rate, blood pressure, and rate-pressure product, but exercise-induced increase of plasma NE (%) was significantly larger in MVD (131.6 +/- 95.4%) (mean +/- SD) than in one-vessel disease (69.0 +/- 45.3%) (p less than 0.01). In conclusion, plasma NE responses to exercise differ between patients with multiple vessel disease and patients with one-vessel disease.

Angina Pectoris↗
PubMed1987

Impaired left ventricular rapid filling during exercise in patients with hypertrophic cardiomyopathy.

The influence of exercise on left ventricular diastolic filling was evaluated in 14 patients with hypertrophic cardiomyopathy (HCM) and 14 normal controls (NC) by dynamic exercise echocardiography. Using X-Y digitizer and computer, normalized peak rate of change of the left ventricular dimension during systole (pVs) and the rapid filling phase (pVd) were determined from the left ventricular echocardiograms at rest and during exercise when heart rate reached 100 beats/min. At rest and during exercise, pVs was significantly higher in HCM (3.2 +/- 0.4/s at rest, 4.3 +/- 1.4/s during exercise) than in NC (2.4 +/- 0.5/s at rest, 3.0 +/- 0.4s during exercise) (p less than 0.001, p less than 0.001, respectively), but pVd in HCM (4.2 +/- 1.0/s at rest, 5.8 +/- 1.0/s during exercise) was not significantly different from that in NC (4.1 +/- 1.0/s at rest, 6.0 +/- 0.7/s during exercise). The ratio of pVd to pVs (pVd/pVs) in HCM did not show significant increment during exercise (1.35 +/- 0.38 to 1.43 +/- 0.35), though that ratio in NC was significantly increased by exercise (1.67 +/- 0.22/s to 1.97 +/- 0.19/s, p less than 0.001). There was no correlation between pVd and the degree of left ventricular hypertrophy. These results suggest that diastolic reserve to exercise is depressed in HCM and that other factors besides left ventricular hypertrophy may account for diastolic abnormality.

Adult↗
PubMed1987

Malignant histiocytosis in infants: surface marker analysis of malignant cells in two cases.

Two infants with malignant histiocytosis, as diagnosed by morphological and cytochemical examinations of malignant cells infiltrating pleural effusion, skin, and bone marrow, are described. Surface marker analysis of the malignant cells with monoclonal antibodies showed these cells to express markers of T-lymphocytes and HLA-DR antigen, but not those of B-lymphocytes, granulocytes, or monocytes. These immunological findings demonstrated that the neoplastic cells in malignant histiocytosis of infancy may be of T-cell origin, rather than histiocytic or monocytic origin.

Antibodies, Monoclonal↗
PubMed1987

Cofilin is a component of intranuclear and cytoplasmic actin rods induced in cultured cells.

Incubation of cultured cells under specific conditions induces a dramatic change in the actin organization: induction of intranuclear and/or cytoplasmic actin rods (actin paracrystal-like intracellular structures). We have found that cofilin, a 21-kDa actin-binding protein, is a component of these rods. Antibodies directed against cofilin labeled intranuclear actin rods induced in cells treated with dimethyl sulfoxide or exposed to heat shock and also labeled cytoplasmic actin rods induced in cells incubated in specific salt buffers. Moreover, we found that these actin rods are not stained with fluorescent phalloidin derivatives at all and appear to be right-handed helices, different from straight bundles of F-actin such as stress fibers. In vitro experiments revealed that cofilin and phalloidin compete with each other for binding to F-actin. Since cofilin and phalloidin have the ability to stoichiometrically bind actin molecule in the filament in vitro, the above results seem to suggest that cofilin directly binds to actin molecule in nearly an equimolar ratio in these rods. We call these rods "actin/cofilin rods."

Actin Depolymerizing Factors↗
PubMed1987

Effects of nifedipine on left ventricular systolic and diastolic function in patients with ischemic heart disease. Radionuclide angiocardiographic studies at rest and during exercise.

The purpose of this study was to evaluate the acute effects of sublingual nifedipine (10 mg) on left ventricular systolic function (ejection fraction, peak ejection rate, time to peak ejection rate) and diastolic function (peak filling rate, time to peak filling rate, filling fraction during rapid filling) at rest and during exercise using radionuclide angiography in 17 patients with ischemic heart disease. The results of the study were as follows. Diastolic indexes in the patient group were significantly different from the values in the control group at rest and during exercise. Peak filling rate and filling fraction improved significantly after nifedipine administration. These values did not show significant differences from the values in normal subjects which were obtained before nifedipine administration. The peak filling rate during exercise after nifedipine administration increased significantly, although the value was lower than that in the control group. At rest, systolic indexes in the patient group showed abnormal values, although the differences from the control values were not significant. Ejection fraction and peak ejection rate were significantly lower than those in the control group during exercise. After nifedipine administration, peak ejection rate at rest and during exercise, and ejection fraction at rest in the patient group improved significantly. Seven of 17 achieved the same exercise workloads as control conditions without symptoms or ECG changes. These data suggest that nifedipine improved left ventricular systolic and diastolic dysfunction, as well as exercise tolerance in patients with ischemic heart disease.

Coronary Disease↗
PubMed1987

Characterization of three monoclonal antibodies against C3 with selective specificities.

We raised 15 mouse monoclonal antibodies against human C3 from two separate fusions. Mouse plasmacytoma cells were fused with spleen cells from mice immunized either with a mixture of C3, C3b and C3c, or with a mixture of C3dg and C3d. Three of the 15 monoclonals were characterized in detail. N-7A reacted with native C3 as well as C3b and C3c. Two other monoclonals, C-5G and G-3E, recognized neoantigenic determinants on C3c and C3dg, respectively. In ELISA, C-5G reacted with C3b and C3c but not with native C3 nor with C3dg; and on the other hand G-3E reacted only with C3dg. The selective specificities of these monoclonals were further confirmed in a binding assay to C3 fragments formed on cellular intermediates. C-5G bound exclusively to EC3b, and G-3E bound to EiC3b, EC3dg and EC3d. N-7A bound only very poorly to EC3b. C-5G inhibited both the haemolytic activity of C5 convertase and also the CR1-mediated rosette formation of B-enriched peripheral mononuclear cells with EC3b. G-3E inhibited the CR2-mediated EC3dg-rosette formation of Raji cells. These monoclonals, with selective specificities, can distinguish the state of activation and degradation of the C3 molecule.

Antibodies, Monoclonal↗