[Tracheobronchopathia osteochondroplastica].
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Biomedical subjects
Publications and source records attributed to K Gotoh.
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We examined the osteogenesis process in transforming growth factor beta 1 (TGF-beta 1)-treated neonatal and adult rats, aiming to investigate the age difference in the effect of TGF-beta 1 on mesenchymal cell differentiation. Recombinant human (rh) TGF-beta 1 (20 and 200 ng) was injected onto the outer periostea of the right side of the parietal bone of each rat once a day for 1-12 days starting at the age of either 1 day or 12 weeks. On the day after the final injection, the calvaria was excised and evaluated histologically. In the neonates, the 12-day treatment with rhTGF-beta 1 increased the number of osteoprogenitor cells, resulting in intramembranous ossification. In the adult rats, rhTGF-beta 1 induced differentiation of chondrocytes. Cartilage masses were surrounded by mesenchymal cells, which would differentiate into chondrocytes. The cartilage matrix was partially calcified, with chondrocytes buried therein. In the calcified matrix, marrow cavities containing some multinuclear osteoclasts were formed. These findings indicate that rhTGF-beta 1 stimulated the differentiation of mesenchymal cells into chondrocytes and produced the cartilaginous matrix. rhTGF-beta 1 induced intramembranous ossification of the parietal bone in neonatal rats, and it induced enchondral ossification in adults. This result suggests that the different responses of mesenchymal cells in the periosteum to rhTGF-beta 1 may depend on the age of the animals used: namely, they may reflect the respective osteogenic stages of modeling and remodeling.
We have investigated biological properties of an immune complex of recombinant interleukin-2 (rIL-2) and a monoclonal antibody against rIL-2 in mice for induction of killer cells and for anti-tumor activity. We have also examined the clearance of subcutaneously-injected immune complex in mice and compared it with that of rIL-2 alone. Plasma rIL-2 levels were sustained longer in mice given the immune complex than in mice given rIL-2 alone at a dose of 10 micrograms/mouse, and they were detectable even at 24 hours after the administration of the immune complex, while they fell to undetectable levels by 6 hours after the administration of rIL-2 alone. A more significant portion of rIL-2 was detected in lymph nodes after subcutaneous injection of the immune complex than that of rIL-2 alone. Splenic lymphocytes from mice given the immune complex demonstrated a higher killer cell activity against YAC-1 cells than those from mice given rIL-2 alone. The immune complex also exerted more significant anti-tumor effect in a dose-dependent manner in Meth-A fibrosarcoma-bearing mice than rIL-2 alone. Our results indicate that immunocomplexing of rIL-2 with an antibody against rIL-2 provides a useful tool as the drug delivery system for cancer therapy using rIL-2.
To test the feasibility of resting thallium-201 (201Tl) initial and delayed scintigraphy for detecting the area of viable myocardium, we performed single photon emission computed tomography (SPECT) in 57 patients with previous myocardial infarction (MI). All had received coronary arteriography (CAG) and left ventriculography (LVG). Initial and delayed myocardial imagings were carried out 10 min and 2 hours, respectively, after the injection of 201Tl at rest. Redistribution was judged by visual interpretation and/or the circumferential profile curve, and found in the infarcted or its adjacent area in 40 of the 57 cases (70.2%). A negative washout (net increase of 201Tl uptake in delayed image) was detected in 17 of these 40 cases. In 10 of the 57 patients, both exercise and rest-injected 201Tl myocardial images were obtained at exercise and rest, and compared visually. The areas of abnormal perfusion were smaller in the resting delayed images than those seen after exercise in 9 of the 10 cases, and were equal in one case. Thus, resting 201Tl delayed myocardial scintigraphy appears to reduce the underestimation of the size of the viable myocardium by the usual 201Tl images obtained after exercise or by single initial images obtained at rest in patients with previous MI.
Extravascular lung water (EVLW) was quantitatively measured in 81 patients consisting of 10 subjects with normal cardiac function and 71 patients with left-sided heart diseases, using 99mTc-RBC as a non-diffusible indicator and 99mTc-DTPA as a diffusible indicator in the equilibrium phase. EVLW averaged 3.0 +/- 1.4 (ml/kg, mean +/- SD) in subjects with normal cardiac function (n = 10), 4.3 +/- 1.7 in New York Heart Association functional class I patients (n = 30), 4.8 +/- 2.4 in NYHA functional class II patients (n = 33) and 9.4 +/- 5.4 in NYHA functional class III (n = 8) patients. EVLW was greater in NYHA class III than in normal controls or NYHA classes I or II (p < 0.01). Lung thermal volume (LTV) was also measured in 31 of the 81 patients using a double indicator dilution technique with sodium and heat. LTV averaged 6.0 +/- 1.2 (ml/kg) in normal subjects (n = 4), 8.6 +/- 2.0 in NYHA functional class I patients (n = 11), 9.7 +/- 3.0 in NYHA functional class II patients (n = 13), and 15.9 +/- 8.2 in NYHA functional class III patients (n = 3). The correlation between EVLW and LTV was significant (EVLW = 0.79 x LTV - 72.8, r = 0.80, p < 0.01). There were significant differences in EVLW/LTV ratio between NYHA class III (0.93 +/- 0.16) and NYHA class I (0.62 +/- 0.22). Thus, it was shown that EVLW was increased in left-sided heart failure and that LTV overestimated the EVLW.
In 41 patients with sarcoidosis (diagnosed according to criteria recommended by the Committee on Diffuse Pulmonary Disease, Ministry of Health and Welfare, Japan 1988), thallium-201 (201Tl) myocardial SPECT was performed to investigate: (1) the ability of 201Tl SPECT to detect cardiac involvement of sarcoidosis with images recorded at rest and 2 hours later, and (2) the relationships between 201Tl myocardial SPECT findings and the activity of sarcoidosis or endomyocardial biopsy findings. As to the abnormal findings in 201Tl myocardial SPECT, (1) a low density area was seen in 13 of 41 cases (31.7%) and non-uniform uptake was found in 17 cases (41.5%), (2) the mean washout ratio (n = 39) was 16.5 +/- 7.4%, which is significantly (p < 0.05) lower than that found in normal subjects, 23.9 +/- 7.5% (n = 10). Of the 19 patients judged visually to be normal, 5 patients had a reduced mean washout ratio less than 12%. Thus, the incidence of abnormal findings including all types of abnormality, on 201Tl myocardial SPECT in sarcoidosis was 63.4% (26/41 cases). In studying the relationship between 201Tl myocardial SPECT findings and the activity of sarcoidosis (as measured by the serum ACE (angiotensin converting enzyme) or lysozyme level, or the presence of more than 30% symphocyte fraction in BALF (broncho-alveolar lavage fluid)), 20 (80%) of 25 cases with 201Tl abnormality were judged to be active sarcoidosis, while only 6 (37.5%) of 16 cases with normal findings on 201TI SPECT were judged to be active.(ABSTRACT TRUNCATED AT 250 WORDS)
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We found that on pulmonary auscultation, fine crackles could be induced by changing the posture from sitting to supine and/or from supine to supine with passive leg elevation in patients without obvious congestive heart failure. We named these crackles "posturally induced crackles (PIC)." To investigate the relationship between PIC and long-term prognosis after myocardial infarction, we followed up 262 patients who recovered from acute myocardial infarction for a mean period of six years. Cardiac death occurred in three of 78 PIC-negative patients and in 28 of 143 PIC-positive patients. PIC-negative patients had a significantly better long-term prognosis than PIC-positive patients according to the Kaplan-Meier survival curves for cardiac death (p < 0.01). In a multilogistic model based on 70 appropriate cases, PIC was the third most important prognosticator after recovery from myocardial infarction and the number of diseased coronary vessels and the pulmonary capillary wedge pressure ranked first and second, respectively.
Lymphokine activated killer (LAK) cells can destroy not only tumor cells but also syngeneic liver cells. In this study, the effects of passive transfer of LAK cells on liver regeneration were examined by the 3H-thymidine uptake and bromodeoxyuridine (BrdU) labeling methods after resection of 70% of the volume of the liver. LAK cells were infused 12h after hepatectomy and the effects on regeneration of liver cells were examined 36 h later. The transfusion of LAK cells induced significant inhibition of liver regeneration at a dose of 5-10 x 10(7) cells. Neuraminidase treatment of lymphocytes is desirable to enhance the selective entrapment of LAK cells into the liver. When LAK cells were treated with neuraminidase (0.5 units/ml), and transfused into hepatectomized mice, more potent suppression of liver regeneration was induced in comparison with the same dose of LAK cells. The intraperitoneal injection of recombinant interleukin 2 (rIL-2) after partial hepatectomy also inhibited the regeneration of remnant liver. From these results, lymphocytes such as LAK cells appear to regulate liver regeneration.
A 44-year-old man with alcohol-induced chronic pancreatitis was referred to our institute for evaluation of severe anemia. The hemoglobin was 2.6g/dl. The results of upper gastrointestinal and colonic examination were negative. Computed tomography and ultrasound examination revealed a pseudocyst in the head of the pancreas. A pseudoaneurysm of the anterior superior pancreaticoduodenal artery shown by angiography appeared to have caused gastrointestinal bleeding by rupturing into the pancreatic cyst connected to the main pancreatic duct. A pyrorus-preserving pancreaticoduodenectomy was performed successfully.
We reported a rare case of mitral valve aneurysm. The patient was a 67-year-old woman with regurgitation of mitral and aortic valve due to infective endocarditis. Preoperative two-dimensional echocardiogram revealed a aneurysmal change and prolapsing on anterior mitral leaflet. Left ventriculogram showed mitral regurgitation of Sellers IV. She underwent mitral valve replacement with 27 mm Carbo Medicus prosthesis successfully. There was a perforated valvular aneurysm (21 x 15 x 11 mm) and inflammatory cleft on anterior mitral leaflet at histopathological findings. The pathogenesis of mitral valve aneurysm was generally infective endocarditis and rarely congenital anomaly, syphylis, Aortitis syndrome, or Marfan syndrome. Mitral valve replacement was a procedure of choice for mitral valve aneurysm, which is especially large, perforated and severely inflammatory one.
We compared the effect of hypertonic salt solution (7.2%, HS) with that of normal saline (NS) and lactated Ringer's solution (LR) for the treatment of hemorrhagic shock. We monitored hemodynamic parameters, thoracic duct lymph flow, and tissue oxygen tension over 3 hours after hemorrhage. Twenty-seven anesthetized mongrel dogs (0.5% halothane) were bled to an aortic pressure of 60 mmHg for 90 min following 40 mmHg for 30 min and then they were resuscitated with each solution. In NS group, the volume transfused was twice the bled volume, and in other two groups, each solution was transfused providing equal amounts of sodium as NS group. We found that hemodynamics were restored in HS group as well as in other two groups. On the other hand, thoracic duct lymph flow and tissue oxygen tension of renal cortex and liver increased significantly over other two groups. We conclude that small volume resuscitation with 7.2% NaCl may be effective in the initial treatment of hemorrhagic shock from the view of tissue circulation in vital organs.
We discussed the pathophysiology of left-sided heart failure with special reference to the pulmonary "venous" system and further discussed the relationship between the capacitance of the pulmonary "venous" system and the pulmonary function. The slope of the pressure-volume line (compliance) in the pulmonary "venous" system was flat in NYHA class II and III patients as compared to class I. Elevated pulmonary "venous" pressure leads to a decrease in the compliance of the pulmonary "venous" system and consequently to a decrease in the static pulmonary compliance and this causes a respiratory dysfunction and an increase in the ventilation-perfusion imbalance. These changes may finally lead to an increase in the work of breathing, resulting in clinical symptoms such as dyspnea.
The site where transcranial magnetic stimulation excites the facial nerve was studied in 6 cats. Transcranial magnetic stimulation of the facial nerve was recorded from the left mentalis muscle. A figure-of-eight shaped magnetic coil was used, and coil induction direction had more influence on the facial nerve evoked compound muscle action potentials (CMAPs) than the coil position. No change could be detected in the CMAPs before and after craniotomy, after cerebellar lobectomy and after exposure of the facial nerve in the facial canal. The facial nerve was stimulated electrically at the porus, meatal portion, geniculum and horizontal portion. The latencies of the CMAPs for each portion were measured and compared with the magnetic response, which was coincidental with that of the meatal portion. The facial nerve was then transected distally from the porus, and CMAPs following magnetic stimulation were recorded at each step. The CMAPs disappeared when the nerve was transected at the fundus. The results of both approaches in this study led to the conclusion that transcranial magnetic stimulation excites the facial nerve at the meatal portion.
In heart diseases, such as mitral stenosis and angina pectoris, the static pulmonary compliance has been reported to be decreased. By definition, the pulmonary "venous" system consists of the pulmonary veins and the left atrium. It plays an important role as the reservoir for the left ventricle. In this laboratory, the pulmonary "venous" compliance (Cp"v") has been evaluated as delta V/delta P of a short segment of the P"V" volume-pressure curve. To evaluate the influence of Cp"v" on the static pulmonary compliance and to speculate about the mechanisms of the reduction in static pulmonary compliance in left-sided heart disease, hemodynamic data and static pulmonary compliance (Cst) were measured in 27 patients with left-sided heart disease. Cst was measured with esophageal balloon technique in a sitting position. The static volume-pressure curve was fitted by a sigmoid model: V = Vm/(1 + e(A-P)/kappa), where kappa is a shape constant and an index of the lung stiffness. The pulmonary blood volume (PBV) was estimated with our own method, using radionuclide (RN) angiocardiography. The mean pulmonary artery wedge pressures (PAW) were measured using a floating catheter. Cp"v" was calculated as the delta V/delta P from the increment of pulmonary "venous" volume (delta V) and that of PAW (delta P) that occurred during passive elevation of the legs. Pulmonary arterial compliance (Cpa) was obtained from an analysis of the diastolic decline in pulmonary arterial pressure wave forms.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a 46-year-old female who presented progressive ophthalmoplegia and limb weakness. She was well until the age of 15 years when there was an onset of bilateral deafness. She became completely deaf by 20 years of age. She noted an onset of weakness in her legs when she was 27-years-old and of ptosis at 34 years of age. She was admitted to our hospital when she was 41-years-old. Neurological examination revealed near total ophthalmoplegia, bilateral ptosis, dysphagia, generalized muscle atrophy and weakness of approximately 4/5 degree, facial grimacing, athetotic movements in four limbs. Laboratory examinations revealed increase in blood lactate and pyruvate levels and diffuse low density change in the cerebral white matter in CT scans. She was thought to have a mitochondrial encephalomyopathy. She was discharged for follow-up, but her clinical course was that of a relentless deterioration. She was readmitted to our service in December 1989. She showed further progress in her weakness and muscle atrophy. Otherwise neurological examination was essentially similar to the previous one. Her cranial CT scans showed low density changes in striatum, thalamus and midbrain in addition to the white matter. Enzyme activities of the electron transport complexes revealed a moderate decrease in the succinatecytochrome c reductase activity, and the Southern blot analysis of mtDNA revealed multiple deletions in mitochondrial genomes. Two months after her admission, she developed bronchopneumonia, and expired on March 13th, 1990. Post-mortem examination revealed diffuse pallor of myeline in the cerebral white matter in K-B staining. A marked neuronal loss and gliosis were observed in putamen bilaterally. Skeletal muscles showed typical changes of mitochondrial myopathies with ragged-red fibers in Gomori-Trichrome staining, and crystalline inclusion bodies by electron microscopic observations. Some neurogenic atrophies were also seen. Oculomotor nuclei appeared intact. It was thought that she had an incomplete form of Kearns-Sayre syndrome. The patient was discussed in a neurological CPC of the departments of Neurology and Pathology of Juntendo University School of Medicine.