Biomedical subjects
Publications and source records attributed to K Machii.
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In nude mice experimentally infected with mouse hepatitis virus (MHV), the numbers of early and later plaque forming cells (PFC) to sheep red blood cells (SRBC) generated in the spleen were 7 to 20 times and 2 to 163 times, respectively, greater than those in non-infected nude mice, when SRBC were given at day 0 to day 21 postinfection. Splenic theta-positive lymphocytes in infected nude mice were shown to increase only at day 10 or more postinfection. PFC response to bacterial lipopolysaccharide, a T cell-independent antigen, was not modified in MHV-infected nude mice.
Echocardiographic evaluation of left ventricular volume change during rapid and atrial filling periods was made in patients with mital stenosis. The significant reduction of rapid filling volume was observed and the rate of rapid filling was approximately the half of normal in mitral stenosis. The rapid filling period showed a good correlation to the mitral valve area measured at operation. After surgical treatment, the rate of rapid filling was significantly increased but was still significantly smaller than normal. It was suggested that the remained structural abnormality of mitral apparatus depressed the inflow through the mitral valve in early diastole despite successful mitral valvotomy. Left ventricular filling during atrial contraction (atrial filling) was augmented twice as much as normal in patients with milder mitral stenosis, compensating the decreased early diastolic filling. In contrast, the atrial filling did not increase in severe mitral stenosis, resulting in the decreased cardiac output. Following mitral commissurotomy, the atrial filling in milder mitral stenosis was reduced but remained significantly larger than normal. There was no change of atrial filling in severe mitral stenosis postoperatively. This fact suggested the existence of impaired contraction of left atrium in cases with severe mitral stenosis. Our results show that the altered left atrial transport function plays an important role in the left ventricular filling in mitral stenosis.
Major and minor axes of the left ventricle were measured by single beam echocardiography in ten cardiac patients and the measurements and calculated volumes by formula V=pi/6 D2 were compared with the angiocardiographic estimates. There was a favorable correlation between echocardiographic and angiocardiographic major axis dimention (r=0.79), left end-diastolic volume (r=0.96), and ejection fraction (r=0.81). On the contrary, left end-diastolic volume calculated by formula V=D3 was less correlated with angiocardiographic estimates (r=0.93) and the former had a tendency to overestimate the volumes where D exceeded 6.5 cm. These data indicate that in cases with markedly enlarged left ventricle, the use of formula V=pi/6 D2L is a more accurate predictor of volumes than formula V=D3.
Nude (nu/nu) mice fail to resist to challenge infection of Tyzzer's disease after pretreatment with formalin-killed organisms that was effective for protecting heterozygous haired (nu/ł) mice from challenge. Resistance was induced nu/nu mice after the transfer of spleen cells from immunized nu/ł and concomitant formalin vaccine treatment.
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Tyzzer's organisms from a hamster case were administered perorally to 6- to 8-week-old APG hamsters and the growth of organisms and lesions produced in the intestine and the liver were studied. When cortisone was given after oral infection with 2 X 10(5) or more organisms, most animals died in 4 to 7 days showing severe necrotic lesions in the liver but no diarrhea was observed. Without cortisone, watery diarrhea was seen between 2 and 7 days after infection and some animals died in 7 to 13 days. Dead and surviving animals showed liver lesions to a lesser degree as compared to those with cortisone treatment. Two days after inoculation either with or without cortisone, a number of organisms were found within mucosal epithelial cells of the cecum and colon, and 1 or 2 days later when focal necrosis occurred in the liver, they were also found in the duodenum, jejunum and ileum. Inoculated into a ligated cecal sac, organisms were shown to multiply in epithelial cells and the lamina propria of the ligated sac, then producing hepatic lesions in 3 to 4 days when bacterial growth was not detected at any other parts of intestines, suggesting that organisms might gain access to the liver from the cecum via the portal circulation or lacteals.
Nude (nu/nu) mice failed to resist to virulent mouse hepatitis virus (MHV) infection after vaccination with inactivated virus. Resistance was induced in nu/nu mice by the transfer of spleen cells from heterozygous haired (nu/ +) mice concomitantly with the vaccination, and the effect was more remarkable with spleen cells from immunized nu/ + mice. Antibody was demonstrable in nu/nu mice having received nu/ + cells and survived challenge infection.
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