Biomedical subjects
Publications and source records attributed to Y Masuda.
Three cases of persistent bilateral sensorineural hearing loss following Mycoplasma pneumoniae (MP) infection are reported. These cases were characterized by highly elevated MP complement fixation titer and cold hemagglutinin titer. All the patients had bilateral acute otitis media with a moderate to high degree of mixed hearing loss in the early stage following primary atypical pneumonia (PAP).
The paravestibular canaliculus was studied by light microscopy in serial sections of the temporal bones from otosclerotic patients who underwent fenestration or stapes surgery. In all examined 23 specimens (13 cases), the endolymphatic duct and sac were observed to be normally developed with no pathological findings. The paravestibular canaliculus was found in 14 of the specimens (60.9%). Its course was traced from the proximal to the distal area in 12 specimens, and it appeared to merge into the distal portion of the endolymphatic sac in 7 of them. Twelve of the paravestibular canaliculi contained one vein, and 3 contained several veins. No artery was found. The paravestibular canaliculus was observed to originate from small vascular channels around the vestibule in the otic capsule, lateral to and near the internal aperture of the vestibular aqueduct.
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To assess the usefulness of X-ray computed tomography (CT) and magnetic resonance imaging (MRI) in detecting and evaluating ischemic heart disease, conventional and enhanced CT were performed for 180 patients (150 with transmural infarction, 12 with subendocardial infarction, and 18 with angina pectoris). MRI examinations were performed for 38 patients (31 with transmural infarction, three with subendocardial infarction, and four with angina pectoris). With enhanced CT, two findings in the myocardium were direct evidence of myocardial infarction: 1. filling defects on the early scans, and 2. late enhancement of the myocardium on the delayed scans. The former were observed mainly at the sites of recent anterior myocardial infarction and the latter were seen in about half of the patients with recent and remote anterior myocardial infarctions. However, these findings were inadequately imaged in patients with inferoposterior infarction and subendocardial infarction. Among 137 patients with transmural infarction, enhanced CT revealed left ventricular aneurysms in 51 (37%) and ventricular thrombi in 26 (19%). ECG-gated MRI apparatus having a superconducting magnetic operating at 0.25 Tesla was used, and data for this study were collected using the single-slice spin echo technique. In eight of nine patients with acute myocardial infarction, gated MRI demonstrated the infarcted myocardium as regions of high signal intensity relative to that of the adjacent normal myocardium. Such a difference in MRI signal intensity was scarcely recognized in the chronic stage of myocardial infarction, but the indirect findings of infarction, such as regional wall thinning, wall motion disturbances, left ventricular aneurysms, and ventricular thrombi were easily detected using MRI. No characteristic finding was obtained by CT or MRI in patients with angina pectoris.
We found recently that exogenously administered PGD2, PGE1 and PGI2 showed a protective effect against cerebral hypoxia/ischemia in mice. In the present study, to find out whether these PGs play a pathophysiological role in cerebral hypoxia/ischemia, we examined a possible role of PGs in the development of adaptive protection against cerebral hypoxia/ischemia. Mice were pretreated with a sublethal dose of KCN, hypoxic gas mixture and electroshock 10-120 min before tests. Ten to thirty min after pretreatment with a sublethal dose of KCN, mice proved to be significantly protected against cerebral hypoxia/anoxia in all models studied: KCN-induced anoxia, normobaric hypoxia and decapitation-induced gasping. Similar results were observed when hypoxic gas and electroshock were used as pretreatments. These facts indicate that the protective effect does not depend on how cerebral hypoxia/anoxia is induced but on the substances formed in the brain after hypoxia/anoxia as well as electroshock. Brain concentrations of cyclooxygenase products markedly increased subsequent to hypoxia/anoxia as well as electroshock. The increase in PGs formation as well as resistance to hypoxia was prevented by pretreatment with indomethacin. These findings suggest that endogenously formed PGs at least including the three PGs, PGD2, PGE1 and prostacyclin in mouse brain during or after hypoxia/ischemia are responsible for the increase of resistance to hypoxia/ischemia.
Typical characteristic of tumor cells is a decreased dependence on the growth factors for promotion of their growth. Growth factor independence and autonomous growth of tumor cells has been thought to be due to the ability of the cells to produce growth factors. According to an autocrine hypothesis, growth factor can be secreted by tumor cells and then binds to its receptor on the same cells to create an uncontrolled growth stimulation. Although there has been much circumstantial evidence to support this hypothesis, an autocrine mechanism is still uncertain. We purified DSF (DNA synthesis factor) from an extract of rat Rhodamine fibrosarcoma. This factor with strong affinity for heparin-Sepharose was a basic protein with molecular weight of 17,000. These properties were similar to those of basic FGF (fibroblast growth factor). We found that primary cells from the sarcoma could grow in serum-free medium supplemented with the extract of the same sarcoma tissue. The extract was fractionated to purify proteins which supported the growth of primary cells. DSF, transferrin and albumin which localized in the tissue, not due to contamination of blood, were purified. When they were added to the serum-free medium, the cells grew at a similar rate to that in medium supplemented with serum. This finding suggests that the growth of sarcoma cells is stimulated by their own growth factor and by some environmental factors.
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We studied the morphological features of defects of the interatrial septum using magnetic resonance imaging (MRI) to determine the sizes of defects and other abnormalities. MR images were obtained in 28 patients with atrial septal defect, including five cases with complicated anomalies (two with Ebstein's anomaly, one pentalogy of Fallot, and one anomalous pulmonary vein connection and azygos continuation). Images were also obtained in the control subjects including seven normal volunteers and 142 patients with various acquired heart diseases. The diagnosis of atrial septal defect was established by cardiac catheterization, angiography and two-dimensional echocardiography prior to the MRI studies, and in 14 patients, the diagnosis was confirmed by surgery. The MRI unit had a superconducting magnet and operated at 0.25 or 0.50 Tesla. A spin echo pulse sequence was used with an echo time of 40 or 60 msec. At the beginning of this study, non-gated MRI images were obtained in the 28 controls and in three patients with atrial septal defect. Nongated MRI could not image the anatomical structure of the interatrial septa of 12 of the 28 controls, or any of the three patients with atrial septal defect. Nongated MRI was, therefore, inadequate for visualizing cardiac anatomy. Gated MRI images were obtained in 141 controls and in 25 patients with atrial septal defect. Gated MRI revealed the interatrial septum, interventricular septum, atrioventricular septum, mitral valve, tricuspid valve and other intracardiac structures in most subjects. In 17 control subjects (12%), however, there was a very faint signal from the central portion of the interatrial septum. In these instances, there was a gradual fading of the signal of the interatrial septum, so that they could be distinguished from the atrial septal defect. The sudden disappearance of the signal from the interatrial septum was observed by gated MRI in all 25 patients with atrial septal defect. The sizes of the defects by MRI coincided with the findings at surgery in all 14 patients. MRI showed right atrial dilatation, right ventricular hypertrophy and dilatation, and pulmonary artery dilatation in most of the patients having atrial septal defect. Complex anomalies associated with atrial septal defect were also clearly shown by MRI, such as displacement of the tricuspid leaflets in two patients with Ebstein's anomaly, and anomalous pulmonary venous connection and persistent left superior vena cava in one patient. These results indicated that gated MRI is a valuable noninvasive method of diagnosing atrial septal defect and complicating anomalies.
Positron emission computed tomography (PET) is regarded an excellent technique for quantitative measurements. However, its accuracy is related to the spatial resolution of the system. The relation between myocardial wall thicknesses as measured by X-ray CT or MRI and the radioactivity as measured using PET was studied in 37 patients. 1. In patients with transmural infarction, the infarcted myocardium was imaged as a region of low radioactivity. However, the myocardium usually exhibited wall thinning, so that partial volume effects must be taken into account in evaluating the radioactivity. 2. In the infarcted regions, the regions of the low radioactivity tended to be larger than those of wall thinning. 3. There were cases with the regional low radioactivity without wall thinning in myocardial infarction and in hypertrophic cardiomyopathy. Because patients with myocardial infarction frequently had regional wall thinning, it seems necessary to correct partial volume effects for the infarcted regions which differ from the normal. It was concluded that, to estimate regional myocardial blood flow or metabolism using PET, it is necessary to supplement another morphological diagnostic method to evaluate myocardial wall thickness.
A major attribute of positron computed tomography (PCT) is its ability to dynamically measure physiologic processes of the heart. However, quantitative data acquisition and analysis are limited by three major problems: bidirectional activity-cross contamination between the myocardium and the blood, the partial volume effect, and the lower temporal resolution of PCT devices. In the present study, we performed serial six-second PCT scans (fast dynamic study) using 13N-ammonia, and evaluated measurements of regional myocardial blood flow. Six patients with hypertrophic cardiomyopathy (HCM) and five normal subjects were observed. 13N ammonia (4.2-13.0 mCi) was intravenously injected as a bolus, and serial six-second PCT scans were initiated at the times of the tracer injections. The results were as follows: 1. Initial passage of the tracer through the right and left sides of the heart were observed with serial six-second images. 2. In patients with HCM, Myocardial 13N activity was determined by assigning a region of interest (ROI) over the myocardium of greater than 25 mm wall thickness as measured by contrast enhanced CT. In these ROIs, corrections for the partial volume effect and spillover of radioactivity from the blood were not necessary. Arterial 13N activity was determined noninvasively by assigning a ROI over the left atrium. 3. The temporal relationships between the arterial input function and myocardial tracer concentrations were demonstrated. Arterial 13N activity was greatest in the second or third frame, and it rapidly declined thereafter. Myocardial 13N activity increased rapidly, reaching a plateau from the sixth to the ninth frame.(ABSTRACT TRUNCATED AT 250 WORDS)
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