The magnetocardiogram in right ventricular overloading.
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Biomedical subjects
Publications and source records attributed to M Sumi.
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We have isolated a tyrosine-specific protein kinase from the acetylcholine receptor (AChR)-rich membranes of the electric ray Narke japonica. The enzyme is immunologically related to p60v-src, the product of the transforming gene of Rous sarcoma virus. A substantial phosphatidylinositol (PI) kinase activity was associated with this enzyme when it was purified through tyrosine-agarose affinity chromatography used previously for the purification of p60v-src. However, by subsequent chromatography on casein-agarose, most of the associated PI kinase activity was separated from the tyrosine kinase activity. The results suggest that the tyrosine-specific protein kinase in the AChR-rich membranes of N. japonica has no intrinsic PI kinase activity.
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The P wave of the magnetocardiogram (MCG) was investigated in normal subjects and patients with mitral stenosis to determine its characteristics in normal conditions and left atrial overloading (LAO) and to analyze atrial activation by a magnetic field. In normal subjects, the MCG P wave was negative in left parasternal sites and positive in right lower sternal sites. The current source deduced from the MCG pattern and isomagnetic map was directed inferiorly and to the left through the entire phase of atrial activation, suggesting that in most normal cases the P wave reflects right atrial activity. In patients with mitral stenosis, a negative-positive biphasic P wave was seen more frequently than in normal subjects in left parasternal sites (p less than 0.005). In the late phase of atrial activation, the current source deduced from the isomagnetic map was shifted superiorly and to the left, suggesting an increased leftward force due to LAO. The MCG was similar in sensitivity to the ECG, for diagnosis of LAO, but in a few cases LAO could be detected from the MCG but not the ECG. These findings suggest that the MCG is clinically useful for diagnosis of LAO.
The observations of immune complex (IC) deposition in the surface of rheumatoid arthritis (RA) cartilage, in conjunction with degradative changes in superficial and midzone chondrocytes, raised the question of causal relationships. In antigen-induced arthritis in rabbits, cartilage degradation occurred in association with IC deposition and is accompanied by chondrocyte damage. Superficial and midzone chondrocytes in rabbit tibial cartilage of arthritic joints, induced by bovine serum albumin (BSA) or ferritin (Fn), were examined by electron microscopy during the evolution of the arthus response. The first cell changes were noted at six hours, by which time superficially formed IC had begun to extend into the matrix. Elongated cytoplasmic footlets, numerous lysosomes, and lipid droplets occurred initially. By 24 hours, concomitant with the deeper extension of surface IC, prominent changes in chondrocytes of both superficial, and midzones progressed to ultrastructural evidence of cell death. The pinocytosis of electron-dense amorphous materials, which included IC, preceded degradation. These data suggest that the observed cytopathology is a manifestation of locally deposited IC.
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Immune complexes were detected by plain and immunoelectron microscopy amongst electron-dense material that rapidly formed and extended over and into the cartilaginous surfaces of immune arthritic rabbits' knees. The sinuous extension of electron-dense material into the surface matrix was associated with fragmentation and detachment, resulting in erosions. The findings implicate the formation of immune complexes in the destructive process of the matrix. Since the eroded pannus-free matrix of rheumatoid cartilage surfaces contains extensive concentrations of immune complexes, the data of this immune arthritis model suggest a causative relation between immune complexes and matrix loss in rheumatoid arthritis.
Magnetocardiograms (MCGs) were recorded by means of a second-derivative SQUID (superconducting quantum interference device) magnetometer in 60 normal subjects and 95 patients with left ventricular overloading to determine the clinical value of the MCG. In patients with left ventricular overloading, the Q or S wave was increased in the upper anterior part of the thorax, and the R wave was increased in the left lower part of the thorax, indicating increased leftward force due to left ventricular overloading. For detection of left ventricular hypertrophy or dilatation from echocardiographic measurements, the sensitivity and specificity of the MCG were similar to those of the standard ECG, or slightly better. In patients with left ventricular systolic overloading, the Q wave was decreased in the lower anterior part of the thorax, indicating a decreased septal vector. Inversion of the T wave was seen more frequently in the MCGs than in the ECGs of patients with left ventricular overloading, suggesting that the MCG is useful for detecting early abnormalities of repolarization. These results suggest that the MCG may provide information that is difficult to obtain from the standard 12-lead ECG.
The U loops of vectorcardiograms (VCG) were recorded in 100 normal subjects and 123 subjects with hypertension, using a direct-writing vectorcardiograph with memory function. These U loops were examined qualitatively and quantitatively. Subjects with hypertension were classified into four groups on the basis of electrocardiographic findings, and the correlation between findings on the U loop and the severity of hypertension was studied. The U loop of normal subjects was directed similarly to the T loop, showing either an arc or semilunar shape in the horizontal plane. In hypertensive subjects the U loop tended to be displaced anteroinferiorly and to the right with an increase in severity of hypertension. In these subjects the U loop was of slightly greater amplitude than in normal subjects, and was long and slender in shape. Anterior and rightward displacement of the U loop was also observed in hypertensive cases who showed no abnormality in the T wave of standard lead ECGs or in the T loop of the VCG. These findings seem useful as clinical parameters of the hemodynamic state in the early stage of hypertension. Based on these results, it was hypothesized that mechanical factors, such as stretch of the ventricular muscles induced by pressure loading of the left ventricle, may contribute greatly to genesis of the U loop.
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Vector arrow maps and isomagnetic maps were constructed with a second derivative SQUID (superconducting quantum interference device) gradiometer in normal subjects and in various pathological conditions to study the inverse problem of electromotive forces and to determine whether the magnetocardiogram (MCG) provides different information from the electrocardiogram (ECG). The current sources deduced from these maps corresponded well with the activation sequences in normal and pathologic conditions reported previously. As second derivative gradiometer measures of the spatial differentiation of the magnetic field, these maps reflected well the current sources close to the anterior chest, namely the right ventricle and right atrium. In addition, it was possible to better localize the sources with this detector than with the ECG or first order gradiometer, suggesting that the isomagnetic and vector arrow maps obtained with the second derivative gradiometer were useful for solving the inverse problem. The MCG also provided different information from the ECG, so use of the MCG in addition to the ECG might be helpful in determining current sources more accurately.
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The purpose of this study is to investigate effects of calcitonin (CT) on bone tissues in fracture healing. Rats were fractured at middle of the femur and given [ASU1,7] eel CT. Following biochemical changes in the serum and histological findings of bone tissue were demonstrated. At the early stage of fracture healing process, CT activated the periostal ossification and elevated serum level of alkaline phosphatase activity. At the stage of cartilagenous callus, the number of chondroclasts were decreased and the development of cartilagenous tissue to primary cancellous bone was inhibited. After this, number of osteoclasts was decreased and bone resorption due to osteoclasts was decreased and bone resorption due to osteoclasts were suppressed. By these process, remodelling at the fractured site was suppressed and serum alkaline phosphatase activity was maintained at a low level. But as for each osteocyte in this stage, CT gave rise to periosteocytic osteoplasis. It is clear that CT accelerates the fracture healing by activating the periostal ossification in the early stage, whereas the fracture healing is suppressed after the stage of cartilagenous callus formation.
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Symmetrical polyneuropathy developed in two patients after they had been in contact with acrylamide and methyl n-butyl ketone, respectively. In sural nerve biopsy material from both patients, electron microscopy showed frequent focal axonal swellings containing masses of neurofilaments. Some axons undergoing axonal degeneration also were seen. These morphologic features are identical to those produced in experimental animals after exposure to these chemicals and are similar to those found in n-hexane neuropathy and in the three reported cases of giant axonal neuropathy. Sural nerve biopsy is an important diagnostic test in identifying cases of peripheral neuropathy caused by these chemicals.