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Volume 177 (1995)
- Issue 4 Pages 271-
- Issue 3 Pages 183-
- Issue 2 Pages 93-
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Volume 177, Issue 3
Displaying 1-7 of 7 articles from this issue
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HARUTO FUJIOKA, TETSURO OKABE, HIROSHI YAMAGUCHI1995 Volume 177 Issue 3 Pages 183-192
Published: 1995
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSFUJIOKA, H., OKABE, T. and YAMAGUCHI, H. Purification and Characterization of Angiotensin II Degradation Factor from Porcine Endothelial Cells. Tohoku J. Exp. Med., 1995, 177 (3), 183-192 - We investigated the degradation of angiotensin II by vascular endothelial cells and smooth muscle cells in vitro. When angiotensin II was incubated with confluent culture of endothelial cells or with serum free conditioned medium of the endothelial cells, angiotensin II was destroyed rapidly. When angiotensin II was incubated with cultured vascular smooth muscle cells or their serum free conditioned medium, degradation was not observed. To identify the angiotensin II degradation factor (ADF), we have purified ADF from the conditioned medium of endothelial cells, by column chromatographies, i.e., hydroxyapatite, ion exchange and gel filtration chromatography. The partially purified ADF had apparent molecular masses of 154kDa on gel filtration chromatography. Its pH optimum was about 7.0. ADF was inhibited by p-chloromercuribenzoic acid, iodoacetamide and high concentration of EDTA, but not by diisopropyl fluorophosphate, bestatin, amastatin or pepstatin A. Of the synthetic substrates examined, ADF degrades human angiotensin II, [Val5]-angiotensin II and [Asn1, Val5]-angiotensin II. It did not degrade angiotensin I. - angiotensinase; thiol protease; aortic endothelial cell; atherosclerosisView full abstractDownload PDF (879K) -
HIROSHI TAKAHASHI, KATSUMI HIDESHIMA, KUNIAKI KAWAZOE, NOBUO TSUDA, SH ...1995 Volume 177 Issue 3 Pages 193-211
Published: 1995
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSTAKAHASHI, H., HIDESHIMA, K., KAWAZOE, K., TSUDA, N., FUJITA, S., SHIBATA, Y., OKABE, H. and YAMABE, S. Immunophenotypes of Reed-Sternberg Cells and Their Variants: A Study of 68 Cases of Hodgkin's Disease. Tohoku J. Exp. Med., 1995, 177 (3), 193-211 - Utilizing a panel of monoclonal and polyclonal antibodies, routine paraffin sections in 68 cases of Hodgkin's disease were examined for the presence of immunoreactivity in Reed-Sternberg (R-S) and related cells by the avidin-biotin-peroxidase complex (ABC) technique. In 14 cases of lymphocyte-predominant Hodgkin's disease (LPHD), R-S cells and the polyploid lymphocytic and histiocytic (L & H) variants of R-S cells were immunoreactive for L26 and α1-antitrypsin (α1-AT) in 9 (64%) and 6 (43%), respectively, whereas the remaining antibodies were negative or rarely positive against L & H variants of R-S cells. R-S cells in 24 cases of mixed cellularity Hodgkin's disease (MCHD) were positive with α1-AT in 63% of cases, positive with LN3 in 71% of cases and positive for BerH2 in 92% of cases. The lacunar cell type of R-S cells in 19 cases of nodular sclerosing Hodgkin's disease (NSHD) were reactive for α1-AT in all cases, BerH2 in 18 cases (95%), and LN3 in 17 cases (89%). Pleomorphic variant of R-S cells in 11 cases of lymphocyte depleted Hodgkin's disease (LDHD) showed reactivity with α1-AT in 9 cases (82%), BerH2 in 6 cases (55%), and LN3 in 9 cases (82%). The incidence of L26 in R-S cells was higher in LPHD than in other three subtypes, whereas the immunohistochemical finding of α1-AT had reverse relevance to the result of L26. The incidence of BerH2 in MCHD and NSHD was higher than that of this antibody in the whole of Hodgkin's disease. R-S cells in NSHD and LDHD were highly positive to LN3, and detection rate of these two types was higher than that in the whole of Hodgkin's disease. No cases showed immunoreactivity with anti-T-cell antibodies (CD3, UCHL1 and DFT1), a marker for natural killer cell (Leu7), and a marker for interdigitating reticulum cell (S-100 protein). These results suggest that correlation between predominant staining pattern and R-S cells and variants thereof in each histological subtype of Hodgkin's disease are as follows: LPHD shows L26+, α1-AT-, BerH2-; MCHD and NSHD show L26-, α1-AT+, BerH2+; and LDHD shows L26-, α1-AT, BerH2+ or L26+, α1-AT, BerH2-. - Hodgkin's disease; Reed-Sternberg cells; immunophenotypes; paraffin sectionView full abstractDownload PDF (6004K) -
HIROSHI KUBO, TATSUO TANITA, KAORU KOIKE, SADAFUMI ONO, SIGEFUMI FUJIM ...1995 Volume 177 Issue 3 Pages 213-222
Published: 1995
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSKUBO, H., TANITA, T., KOIKE, K., ONO, S. and FUJIMURA, S. Adhesion Molecule CD18 on Polymorphonuclear Cells Correlates to the Lung Injury Caused by Continuous Infusion of Endotoxin in Sheep. Tohoku J. Exp. Med., 1995, 177 (3), 213-222 - We investigated the mechanisms of increase in the pulmonary vascular permeability, focusing on the changes in the peripheral white blood cell (WBC) counts and the surface expression of CD18 on polymorphonuclear cells (PMNs). Anesthetized sheep with chronic lung lymph fistulas were used in this study. We infused synthetic endotoxin (LPS) at a rate of 10ng/kg/min (i.v.) continuously for 24hr. We measured lung lymph flow, lymph-to-plasma protein concentration ratio and WBC counts in blood and lung lymph, and the PMNs' surface expression of CD18 before and at 2, 10 and 24hr after the start of endotoxin infusion, respectively. CD18 was analyzed by flow cytometry using monoclonal anti-CD18 antibody. We found that the pulmonary vascular permeability increased during 2-4hr after the start of endotoxin infusion, and returned to the baseline over 10hr. At time 2hr period, the number of WBCs in the lung lymph increased, the number of peripheral WBCs, mostly PMNs, decreased and the surface expression of CD18 on the peripheral PMNs was up-regulated. At time 10 and 24hr, the number of WBCs in lung lymph decreased, the number of peripheral WBCs increased and CD18 expression was down-regulated. These data indicate that up-regulation of CD18 expression promotes the PMN adherence to the pulmonary endothelium, migration into the lung and increases the pulmonary vascular permeability. We conclude that the continuous endotoxin infusion up-regulates CD18, which contributes to the PMN migration into the lung. - adhesion molecules; CD 18; continuous endotoxin infusion; sheepView full abstractDownload PDF (816K) -
SHIUN DONG HSIEH, HIDEYO YOSHINAGA1995 Volume 177 Issue 3 Pages 223-231
Published: 1995
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSHSIEH, S.D. and YOSHINAGA, H. Is There Any Difference in Coronary Heart Disease Risk Factors and Prevalence of Fatty Liver in Subjects with Normal Body Mass Index Having Different Physiques?. Tohoku J. Exp. Med., 1995, 177 (3), 223-231 - Levels of coronary heart disease (CHD) risk factors such as systolic and diastolic blood pressure, fasting blood glucose, hemoglobin A1c, triglyceride, cholesterol, HDL-cholesterol, prevalence of hypertension, abnormal glucose tolerance, hypertriglyceridemia, hypercholesterolemia, low HDL-cholesterol level, and fatty liver in normal body mass index (BMI) subjects with high or low waist/ height ratios were investigated in middle aged men (45-54 years, BMI: 22-23.2kg/ m2) undergoing a routine health examination. The subjects were divided into two groups according to whether their waist/height ratios were ≥0.5 (n=131) or <0.5 (n=121). There was no significant difference in age or BMI between the two groups, however, fasting blood glucose, hemoglobin A1c, triglyceride, cholesterol levels, the prevalence of abnormal glucose tolerance, hypercholesterolemia, fatty liver (30.5% vs. 15.7%, p<0.01), and morbidity index for CHD risk factors (sum of the five risk factors scored as one point each if present) (1.46 vs. 1.04, p<0.01) were significantly higher in the high waist/height group. In conclusion, even normal BMI subjects should pay attention to their waist/height ratio because of higher CHD risk factor levels, prevalences, morbidity index for CHD risk factors, and higher prevalence of fatty liver. - coronary risk factors; fatty liver; waist/height ratio; normal BMIView full abstractDownload PDF (866K) -
RYO KATORI, KEIZO YAMASHITA, TOSHIO MIYAZAKI, YOSHIHIDE SAKAGUCHI, TAT ...1995 Volume 177 Issue 3 Pages 233-248
Published: 1995
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSKATORI, R., YAMASHITA, K., MIYAZAKI, T., SAKAGUCHI, Y., INOKI, T., YAMAMOTO, T. and SHIBUTANI, T. Beta-Adrenergic Stimulation Induces ST-Segment Elevation in Dogs with Healing Myocardial Infarction. Tohoku J. Exp. Med., 1995, 177 (3), 233-248 - There is controversy with regard to the mechanism of the exercise-induced ST-segment elevation in myocardial infarction. The purpose of the present study was to investigate the mechanism of ST-segment elevation through pharmacologic interventions. Transmural anterior myocardial infarction was produced by gelatin sponge embolization of the left anterior descending artery in seven closed-chest dogs. One and four weeks after myocardial infarction, the dogs underwent the following three interventions: right atrial pacing, norepinephrine infusion (3.75, 7.5, and 15μg/min) with the pacing, and methoxamine injection (2.5 and 5.0mg) with the pacing. All dogs had transmural infarction with a mean infarct size of 12.0±4.2% of the left ventricular weight. Right atrial pacing did not induce significant changes in ST-segment. Norepinephrine induced a marked elevation of ST-segment at leads V1 to V4, while methoxamine did not. Norepinephrine induced a significant increase in left ventricular ejection fraction, while methoxamine produced a marked decrease in the ejection fraction and an increase in ventricular volume. The mean percent radial shortening of the non-infarct ventricular wall showed a significant increase with norepinephrine, but a decrease with methoxamine. In conclusion, myocardial ischemia and wall motion abnormality may be excluded as possible mechanisms of ST-segment elevation and an enhanced beta-adrenergic mechanism in the non-infarct myocardium is suggested to be responsible for ST-segment elevation - myocardial infarction; exercise; norepinephrine; methoxamine; ST- segment elevationView full abstractDownload PDF (3698K) -
IPPEI NAKAGAWA, MIEKO SUZUKI, TAKAHIRO YANAGIYA, NOBUMASA IMURA, AKIRA ...1995 Volume 177 Issue 3 Pages 249-262
Published: 1995
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSNAKAGAWA, I., SUZUKI, M., YANAGIYA, T., IMURA, N, and NAGANUMA, A. Effect of Glutathione Depletion on Metallothionein Synthesis Induced by Paraquat in Mice. Tohoku J. Exp. Med., 1995, 177 (3), 249-262 - The effect of Glutathione (GSH) depletion on the induction of metallothionein (MT) synthesis by paraquat (PQ) was examined in ICR mice. An increase in hepatic MT level in mice was observed after a single PQ administration. Pretreatment of mice with L-buthionine-SR-sulfoximine (BSO), an inhibitor of GSH synthesis, enhanced the induction of hepatic and renal MT synthesis by PQ depending on the decreased tissue GSH level. A similar result was obtained by pretreatment with diethyl- maleate, a GSH depleting agent. The ratio of hepatic MT-I to MT-II induced by PQ was not changed by BSO pretreatment. An increase in the hepatic MT level in GSH depleted mice was observed from 3hr to 24hr after PQ administration. An increase in the hepatic MT-I mRNA level after treatment with PQ was observed prior to hepatic MT induction in BSO pretreated mice. Pretreatment with actinomycin D, an inhibitor of mRNA synthesis, inhibits the PQ-induced increase in hepatic MT and MT-I mRNA levels in BSO pretreated mice. Pretreatment with BSO did not affect the induction of MT synthesis by zinc, cadmium or dexamethasone. Pretreatment with dexamethasone, an anti-inflammatory agent, enhanced the hepatic MT induction by PQ treatment in GSH depleted mice, while dexamethasone reduced the MT induction by turpentine oil, which is known to induce inflammation and hepatic MT synthesis. These findings suggest that GSH depletion enhances the induction of MT synthesis by PQ because of an increase in the transcription rate, and this enhancement of MT synthesis is not due to an inflammatory response caused by PQ. - glutathione depletion; metallothionein; paraquatView full abstractDownload PDF (1538K) -
ATSUSHI ISAGODA, RYUICHI NAKAMURA1995 Volume 177 Issue 3 Pages 263-269
Published: 1995
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSISAGODA, A. and NAKAMURA, R. Fitness of the Formulae of Simplified Version of Recovery Evaluating System-3 (RES-3) for Stroke Patients. Tohoku J. Exp. Med., 1995, 177 (3), 263-269 - Using the formulae for prediction of functional status at 4, 8 and 12 weeks after admission in the stroke patient (simplified version of Recovery Evaluating System-3; RES-3) and demographic data at the admission of 128 stroke patients, the estimated scores of four measures, Motor Age Score (MOA), Manual Function Score (MFS), Barthel Index (BI) and Mini-Mental State (MMS), were obtained. Fitness of the formulae was tested in terms of the agreement between the estimated and the measured scores. The results indicated that the differences between the measured and the estimated scores were statistically not significant except BI. The measured scores of BI were 3 to 5 points high compared to the estimated ones. When the confidence limits of the differences were examined at a confidence coefficient of 95%, they were within 5% of the full score for MOA, MFS and MMS, and were within 10% for BI. Accordingly, by setting the allowable limit to 5% of the full score around the means, the fitness of prediction would be more than a probability of 95%. The formulae of simplified version of RES-3 were practically useful. - stroke; medical rehabilitation; functional status; predictionView full abstractDownload PDF (638K)
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