CP asymmetries in B0 decays in the presence of flavor-changing neutral currents.
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Biomedical subjects
Publications and source records attributed to T Morozumi.
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The epidemiological studies of S. suis infections in Japan were carried out between 1987 to 1991. A total of 380 S. suis strains isolated from pigs, cattle and a horse were serotyped by using antisera against S. suis types 1 to 22. A total of 318 (83.7%) of S. suis isolates were serologically typable. Serotype 2 was the most prevalent with 28.2%, followed by type 7 (10.8%), 1/2 (8.4%), 3 (7.4%) and 4 (5.5%). Of twenty S. suis strains isolated from cattle, eight were type 9, one was type 10, five were type 18, one was type 20 and five were untypable. One out of all the strains was also isolated from a racing horse with pneumonia. The majority of the isolates were originated from meningitis (38.2%), followed by from pneumonia (33.4%) and endocarditis (9.2%). Of all of the S. suis isolates, 333 isolates (87.6%) were identified correctly by API STREP 20 system.
To assess whether regionally depressed myocardial uptake of beta-methyl-p-(123I)-iodophenyl-pentadecanoic acid (123I-BMIPP), is related to regional ventricular diastolic dysfunction in patients (pts) with hypertrophic cardiomyopathy (HCM), we carried out 123I-BMIPP myocardial SPECT and radionuclide ventriculography (RNV) at rest in 9 HCM pts (eight pts with asymmetric septal hypertrophy (ASH), and one patient with apical hypertrophy). The defects of 123I-BMIPP were semiquantitatively estimated by segmental analysis. Regional LV function was determined by sector analysis in RNV: regional peak filling rate (rPFR), regional time to peak filling rate (rTPFR), and early 1/3 filling rate (1/3 fil) were estimated in the LV septal and posterior sectors. Wall thickness was evaluated with M-mode echocardiography. As results, the defects of 123I-BMIPP myocardial SPECT, were found frequently in septal wall, but any defect was not recognized in all septum with significant hypertrophy. Also, the degree of septal hypertrophy was not significantly related to BMIPP defect score. However, the regional diastolic function (rPFR, rTPFR, 1/3 fil) in the septal lesions with 123I-BMIPP defects was decreased more than those without 123I-BMIPP defect in HCM. Furthermore, the relative regional diastolic dysfunction (the differences between rTPFR and 1/3 fil in the septum and in the posterior wall) was significantly related to BMIPP defect score. In conclusion, this results suggest that the decreased uptake of 123I-BMIPP is related to regional diastolic dysfunction more than wall hypertrophy.
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We studied the significance of I-123 MIBG (metaiodobenzylguanidine) myocardial scintigraphy for evaluating the severity of congestive heart failure. I-123 MIBG scintigraphy was performed in 7 patients with congestive heart failure (CHF) of NYHA class I-III (6 with dilated cardiomyopathy and 1 with Adriamycine cardiomyopathy) and in 2 normals. The SPECT and anterior planar myocardial images were obtained 15 minutes after (initial images) and 4 hours after (delayed images) an injection of I-123 MIBG (111 MBq). Compared with normals, patients with CHF demonstrated (1) low myocardial uptake and (2) rapid myocardial washout of I-123 MIBG, indicating myocardial sympathetic disarrangement. Then, quantitating these abnormalities with the heart to upper mediastinum uptake ratio (H/B) and the percent washout rate (%WR) during 4 hours, respectively, we compared these two indices with LV ejection fraction (EF) at rest measured by echocardiography and exercise capacity (max VO2 and VO2 at anaerobic threshold (AT] determined with respiratory gas exchange analysis during maximal bicycle exercise. H/B was lower and %WR was greater in patients with CHF than in normals. H/B correlated with EF (r = 0.77, p less than 0.05) and AT (r = 0.74, p less than 0.05). On the other hand, %WR significantly correlated with EF (r = 0.79, p less than 0.05), max VO2 (r = -0.74, p less than 0.05) and AT (r = -0.81, p less than 0.05). Thus, H/B and %WR were closely related to the severity of CHF. These results suggest that I-123 MIBG myocardial scintigraphy and the quantitative analysis of I-123 MIBG myocardial uptake provide useful information about the severity of CHF.
Regional denervation of adrenergic nerves has been clinically demonstrated in patients with myocardial infarction using I-123 metaiodobenzylguanidine (MIBG) scintigraphy. However, it is not clarified whether adrenergic denervation can be induced by prolonged myocardial ischemia as well as by myocardial infarction. This case with effort angina had 99% stenosis of right coronary artery and showed perfusion defects at inferior myocardial regions in the exercise thallium-201 study. However, inferior wall motion estimated by echocardiography and left ventriculography was normal indicating the absence of myocardial infarction. After percutaneous transluminal coronary angioplasty for the stenosis, I-123 metaiodobenzylguanidine (MIBG) and thallium-201 (Tl-201) myocardial scintigraphies were done to estimate the therapeutic effect of PTCA. Although the Tl-201 study during exercise showed normal findings indicating the success of PTCA, marked defects was detected at inferior myocardial regions in the I-123 MIBG studies just after and 4 hours after an intravenous injection of I-123 MIBG. These results suggest that adrenergic derangement may be induced by prolonged myocardial ischemia and may persist for periods even though myocardial perfusion is normalized.
To detect Adriamycin cardiomyopathy, radionuclide myocardial imagings with Tl-201, Tc-99m pyrophosphate, I-123 metaiodobenzylguanidine and Ga-67 were performed in a 49 year-old-woman receiving Adriamycin (a total dose of 230 mg/m2) for the treatment of breast cancer. This patient demonstrated symptoms of congestive heart failure 2 months after the last intravenous administration. At the period of performing the radionuclide studies, echocardiographic LV ejection fraction (EF) was 22%. Despite severe deterioration of cardiac function, Tl-201 SPECT demonstrated no defect and Tc-99m pyrophosphate (PYP) SPECT demonstrated no positive finding. I-123 metaiodobenzylguanidine (MIBG) scintigraphy demonstrated no regional defect. However, I-123 MIBG washout rate during 4 hours was markedly enhanced, probably reflecting abnormalities of norepinephrine kinetics due to the progression of heart failure. Compared to these pharmaceuticals, Ga-67 was diffusely accumulated in the heart. Then, 5 months after the first study, when LV EF improved to 30% and congestive symptoms disappeared probably owing to beta-blockade therapy, myocardial accumulation of Ga-67 markedly reduced. It has been reported that Ga-67 accumulates in malignant tumor cells and leukocytes. Since, in Adriamycin cardiomyopathy, myocardial accumulation of leukocytes with myocardial fibrotic changes have been histologically demonstrated, the results of Ga-67 scintigraphy may reflect the accumulation of leukocytes. Thus, this case indicates that Ga-67 scintigraphy is advantageous for detecting Adriamycin cardiomyopathy and may be more useful than Tl-201 and Tc-99m PYP scintigraphies.
To validate the significance of technetium-99m-pyrophosphate (Tc-99m PYP) myocardial scintigraphy in diagnosing cardiac amyloidosis, 2 patients with familial amyloid polyneuropathy (FAP) and 1 patient with amyloidosis secondary to chronic rheumatic arthritis were studied. All three patients had echocardiographic abnormalities, which were increased wall thickness of the interventricular septum and the left ventricular posterior wall, and granular sparkling appearance in the septum. In 2 patients with FAP, abnormal myocardial uptake of Tc-99m PYP was diffusely detected in Tc-99m PYP SPECT. In the remaining 1 patient with secondary amyloidosis, however, Tc-99m PYP SPECT showed no abnormality, although we had confirmed the presence of myocardial amyloid deposits (type AA amyloid protein) with high amount in the histological examination. Thus, these results indicate that Tc-99m PYP scintigraphy may have a limitation in detecting cardiac involvement in secondary amyloidosis although it is useful in FAP.
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The extracellular proteases of Staphylococcus hyicus subsp. hyicus were assayed by a zymogram showing caseinolysis and gelatinolysis. Four bands were associated with caseinolysis or with gelatinolysis. The patterns shown by strains isolated from pigs, chickens and cows were compared; isolates from pigs differed from those isolated from chickens or cows but strains isolated from diseased and healthy pigs could not be differentiated.
Haemophilus parasuis strains isolated from the noses of apparently healthy animals and from animals with pathological conditions were examined for the presence of a capsule, for their ability to agglutinate in acriflavine or after boiling, and for their peptide profile after polyacrylamide gel electrophoresis (PAGE). The capsule was identified by precipitation against hexadecyl trimethylammonium bromide (Cetavlon), by demonstration of iridescence, and by means of a capsule-staining method. We found a group of capsulated strains showing a rather coccobacillary morphology compared with the morphology with polymorphism, varying from rod-like to filamentous, in strains without detectable capsules. The strains of the latter group were agglutinated by acriflavine or by boiling. Soluble antigens of capsulated strains reacting with Cetavlon were thermostable and resisted proteolytic enzymes, thus suggesting the presence of an acidic polysaccharide. A few of the capsulated strains did not precipitate with Cetavlon, which indicated that their chemical composition was different. Acriflavine-positive strains belonging to a definite PAGE pattern (type II) seemed to be associated with pathological conditions more frequently than were capsulated strains which were mostly isolated from nasal cavities of apparently healthy pigs. We put forward the hypothesis that the agglutinability in acriflavine, together with the PAGE profile type II, may be associated with particular structures responsible for virulence.
We propose a serological classification of Haemophilus parasuis into at least five serovars, using an agar-gel-precipitation test with extracts from autoclaved cells. Thirty-two strains were examined, and it was possible to classify 26 of them. The specific antigens were thermostable and soluble and were not affected by pronase treatment but could be extracted by phenol, suggesting a polysaccharide. This polysaccharide seemed to be identical with the capsular substance of serovars 1, 2, and 3. In the presumably uncapsulated strains of serovars 4 and 5, the specific antigen was probably located in the outer membrane. The diversity of the specific substance within the different serotypes was shown by the differences in their electrophoretic migration patterns. Other extraction procedures showed that the washing supernatant and extracts at 60 and 100 degrees C were identical with the 121 degrees C extracts for serovars 1, 2, and 3. In serovars 4 and 5, washing antigens, if present, were different from 100 and 121 degrees C extracts. Other common antigens, presumably proteinaceous antigens, were detected after extraction at 60 and 100 degrees C. The slide and tube agglutination tests allowed classification only for the capsulated strains of serovars 1, 2, and 3. The specific agglutinogens were very sensitive to incubation temperature, and the absorption test showed them to be identical with the 121 degrees C precipitinogens.
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