[Use of an automatic cutoff valve for the heart-lung machine].
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Adult↗
Biomedical subjects
S Amano
Publications and source records attributed to S Amano.
General pathology of Kawasaki disease. On the morphological alterations corresponding to the clinical manifestations.
Systemic pathological alterations were studied in thirty-seven autopsied patients with Kawasaki disease. Systemic vasculitis was the most characteristic pathological finding and was present in all the patients. In addition to the vasculitis, there was a high incidence of inflammatory lesions in various organs and tissues: in the heart, endocarditis, myocarditis, and pericarditis; in the digestive system, stomatitis, sialoduct-adenitis, catarrhal enteritis, hepatitis, cholangitis, pancreatitis, and pancreas ductitis; in the respiratory system, bronchitis and segmental interstitial pneumonia; in the urinary system, focal interstitial nephritis, cystitis, and prostatitis; in the nervous system, aseptic leptomeningitis, choriomeningitis, gangliontis, and neuritis; in the hematopoietic system, lymphadenitis, splenitis, and thymitis. Dermatitis, panniculitis or myositis were also observed in some patients. Therefore, Kawasaki disease is a systemic inflammatory disease which mainly affects the cardiovascular system. These systemic inflammatory lesions are considered to correspond to the variegated clinical manifestaitions. The relationship between Kawasaki disease and infantile polyarteritis nodosa (IPN) were discussed, based on the clinicopathological characteristics.
Child↗
Acid phosphatase activity of the brain in SHR-- the first report of enzyme histochemical studies of spontaneously hypertensive rat brain.
Changes in acid phosphatase activity in the cerebrovascular system and brain parenchyma in SHR were investigated histochemically. An increased activity of the enzyme was demonstrated in the SHR endothelial and medial smooth muscle cells of the cerebral arterial system as compared to the control. The pericytes of intraparenchymal blood vessels also showed an intensified enzyme activity. The enzyme activity increased with advancing age. In SHR brain parenchyma, the enzyme activity was decreased in the cortical nerve cells. Glial cells with the enzyme activity were increased in number and showed an intensified activity. Causative factors of changes in acid phosphatase activity in SHR cerebral arteries and parenchyma were discussed.
Acid Phosphatase↗
Pathology of Kawasaki disease: I. Pathology and morphogenesis of the vascular changes.
Histopathological investigation of the vascular changes in Kawasaki disease was carried out on thirty-seven autopsied Japanese patients. Arterial lesions could be classified into following five stages from the view point of morphogenesis of arteritis; 1) endothelial degeneration and increased vascular permeability, 2) edema and degeneration of the media, 3) necrotizing panarteritis, 4) granulation formation, and 5) scarformation. Aneurysm with thrombus was observed mainly in the coronary artery in most patients. It is considered that the initial changes begins in the endothelial cells with increased vascular permeability. Platelet aggregation in the damaged endothelial cells seems to play an important role in the further development of the arteritic changes. Vascular lesions were observed not only in the arterial system but also in the venous system, therefore Kawasaki disease is a systemic vasculitis rather than a systemic arteritis.
Aneurysm↗
Pathology of Kawasaki disease: II. Distribution and incidence of the vascular lesions.
Histopathology, distribution and incidence of vascular changes were studied in tissues obtained at autopsy on thirty-seven children. Elastic and musculoelastic arteries showed a high incidence of arteritic changes, however the degree of the lesions was in general mild to moderate with the exception of the iliac artery, which revealed severe changes and a necrotizing panarteritis which was often accompanied with an aneurysm formation. A high incidence of arteritic changes, of which main histological feature was necrotizing panarteritis, was seen in extravisceral middle sized arteries. The coronary artery in particular was involved in each case and most had an accompanying aneurysm, some of which had ruptured. Intravisceral small sized arteries showed a relatively low incidence of arteritic changes and the degree of inflamation was in general mild. Phlebitis was present in over half the number of patients. The degree of lesions was mild in the small veins and mild to moderate in the large veins. Vascular lesions in Kawasaki disease should be termed systemic vasculitis rather than a systemic arteritis. There was a correlation between the caliber of involved vessels and the degree of vascular lesions. According to the histopathology, distribution and incidence of angitis, Kawasaki disease does resemble infantile periarteritis nodosa with the exception of the different manner of the coronary and iliac involvement.
Aorta↗
Studies on antibiotics BN-227 and BN-227-F, new antibiotics. I. Taxonomy, isolation and characterization.
The two new antibiotics, BN-227 and BN-227-F, were isolated from the fermentation broth of Pseudomonas sp. BN-227. BN-227 has a molecular formula C7H9NO3, and melts at 115 degrees C. BN-227-F has a molecular formula C21H24N3O9Fe, and melts at 156 degrees C. BN-227-F is a chelate compound consisting of three similar ligands (antibiotic BN-227) and ferric ion. The two antibiotics have antimicrobial activity against Gram-positive and Gram-negative bacteria.
Animals↗
Studies on Actinomycetales producing antibiotics only on agar culture. I. Screening, taxonomy and morphology-productivity relationship of Streptomyces halstedii, strain SF-1993.
Soil Actinomycetales that produce antibiotics during growth on agar but not in submerged culture were searched for and about 25 strains were obtained. One of these, Streptomyces halstedii, strain SF-1993, which produces an antibiotic designated SF-1993 was studied taxonomically and morphologically. The antibiotic-productivity of strain SF-1993 was correlated with mycelial morphology. The vegetative mycelium was filamentous in antibiotic-producing agar cultures, but fragmented in non-producing submerged cultures. By maintaining submerged cells filamentous, production of antibiotic in the submerged fermentations was accomplished. Filamentation was maintained by the use of diluted media or non-fragmented mutant substrains.
Agar↗
Genetic mapping of the locus controlling structural variations of murine C3 in the chromosome 17.
Backcross progeny, (NC X TF/GnLe)F1 X TF/GnLe, was tested for C3 allotype controlled by C3-1 and the expression of mutant gene tf, repeated loss and regrowth of hair. The recombination frequency between these two loci both located in chromosome 17 of the mouse was 24%. Taken together with our previous linkage data, C3-1 is now localized to a position 11 cm more distal than H-2 on chromosome 17.
Animals↗
A novel aminoglycoside antibiotic, substance SF-2052.
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Aminoglycosides↗
The expression of the allelic gene of murine C3 in fetal and neonatal mice.
A single co-dominant gene locus linked to H-2, tentatively designated C3-1 locus by us, controls allotypic variation of murine complement (C) C3 as previously described. We used this genetically determined variation of murine C3 as a marker in the probe for the synthesis of this C component in fetal and neonatal mice. Phenotypes of murine C3 were determined by a combined use of analytical isoelectric focusing and immunofixation and by antigenic analysis with alloantiserum directed to the gene product of one of the alleles at the C3-1 locus. Fetuses and neonates of inbred mice (BALB/c and NC strains), F1 hybrids, and backcross progeny express the same C3 phenotype as the one observed in adult mice of the corresponding C3 genotype. No evidence for the occurrence of "fetal C3" in fetal mice was obtained. Furthermore, allotypic differences of C3 between mother and fetus or neonates provide evidence that murine C3 is synthesized by fetus or neonate and is not transferred from mother transplacentally nor via colostrum. In summary, mice synthesize C3 according to the allelic structural gene(s) at the C3-1 locus even during their early developmental life.
Alleles↗
Allotypes of C3 in laboratory and wild mouse distinguished by alloantisera.
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Animals↗
Ectopic ACTH-MSH producing carcinoid tumor with multiple endocrine hyperplasia in a child.
An autopsy case of a 9-year-old Japanese girl revealed a carcinoid tumor originating in the duodenum and hyperplasia of the multiple endocrine organs as manifested by ectopic ACTH syndrome, carcinoid syndrome and giantism. The tumor cells were positive for histochemical argyrophile reaction and two types of secretory granules were identified by electron microscopy. Biochemical assay revealed the production of ACTH and beta-MSH by the tumor cells. Other changes of multiple endocrine organs included acidophil dominant hyperplasia of the pituitary, diffuse hyperplasia of the thyroid, chief cell hyperplasia of the parathyroid, hyperplasia of the islets of Langerhans and the adrenal cortex. This case was considered to be a type of multiple endocrine adenomatosis including carcinoid tumor. The relationship between the carcinoid tumor and multiple endocrine adenomatosis was discussed.
Adenoma↗
Enzymatic histo and cytochemical investigation on the cardiovascular system in spontaneously hypertensive rats.
The functional abnormalities of the cells in the cardiovascular system in SHR were revealed by enzyme histo-cytochemical study. The enzymatic activity was usually increased in the area where the arteries branched and in proliferating cells in the thickened wall. Such was more remarkable in the distorted arteries with aging. Functional roles of these 4 enzymes were discussed.
Acid Phosphatase↗
Preparation of an alloantiserum to murine C3 and demonstration of multiple alleles.
An antiserum was produced in C3H/He mice that can recognize the antigenic variations of murine C3. The alloantiserum is directed to the gene product of one of the alleles (C3-1a allele) of the C3-1 locus that controls genetic variations of murine C3 and is linked to H-2. The antiserum formed a single precipitin line in the Ouchterlony test with sera obtained from mice that carry the C3-1a/a or C3-1a/b genotype, but it did not react with sera from mice that do not have C3 coded for by the C3-1a allele. By the use of the alloantiserum, we detected a new C3 allotype (C3-1 CC) in SWR/J mice. The C3-1 CC is distinct from the other two allotypes on the basis of antigenicity and isoelectric point (pI). Therefore, at least three alleles have been identified for the C3-1 locus.
Alleles↗
Pathological changes of cerebral vessel endothelial cells in spontaneously hypertensive rats, with special reference to the role of these cells in the development of hypertensive cerebrovascular lesions.
Changes of endothelial cells of the cerebral arterial system in spontaneously hypertensive rats were investigated using scanning electron and transmission electron microscopes. The endothelial cells revealed on the one hand, progressive changes such as enlargement, increased plasmalemmal pits, numerous microvilli and well-developed marginal folds. On the other hand, regressive changes such as balloon-like protusions and craterlike concavities were also noted. Platelet adhesion was often encountered on the injured endothelial surface of the cerebral arteries in SHR. The significance of these findings in the development of hypertensive cerebral vascular changes was discussed.
Animals↗
Autoradiographic investigation of cell proliferation in the brain of spontaneously hypertensive rats.
Cell proliferation in the brain of spontaneously hypertensive rats (SHR) and control Wistar rats of various ages was autoradiographically investigated using [3H]thymidine. The brain of SHR showed an increase in labeled cells. The increase of labeled cells was seen in the early stage of the development of hypertension when there were still no definite morphological changes in the cerebral vessel walls or brain parenchyma. The labeled cells tended to increase in number with the age of the animals. The distribution of these cells corresponded with areas of increased vascular permeability and cerebrovascular lesions, that is, water-shed regions. The labeled cells consisted of endothelial and adventitial cells of the intracerebral arterioles and pial arteries as well as glial cells. Arachnoid cells, subarachnoid cells, medial smooth muscle cells of the pial arteries were also labeled, though less intensely. The significance of labeled endothelial cells in the development of cerebrovascular changes and sequential parenchymal changes is discussed.
Animals↗
Vascular changes in the brain of spontaneously hypertensive rats: hyaline and fibrinoid degeneration.
The arterial changes designated as "hyalinosis" in the vessels of spontaneously hypertensive rats were studied using light- and electron-microscopy. Such changes were classified into three types, hyaline, fibrinoid and atypical fibrinoid degeneration. Hyaline material consisted mainly of excessive lamellar thickening of the basement membrane synthesised by endothelial and smooth muscle cells and associated with cellular debris and electron-dense particles. Acid mucopolysaccharides were found to be one of the components of the hyaline material. The nature of fibrinoid material was primarily fibrin derived from polymerised fibrinogen which has permeated through the injured endothelial cell layer. Atypical fibrinoid material consisted of granular and fibrillar substances derived from blood plasma. In some cases, all three changes were encountered in the same artery.
Animals↗
Investigation of the endothelial cell changes in the brain of SHR using horseradish peroxidase technique and enzyme histochemistry [proceedings].
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Adenosine Triphosphatases↗