Biomedical subjects
Publications and source records attributed to S Abe.
The taxonomic description of Streptomyces spadicogriseus, a new species belonging to the Gray Series of streptomycetes as classified by Pridham and Tresner, is presented. This new species is distinguishable from the known members of the Gray Series. Streptomyces spadicogriseus produces anthramycin but bears no taxonomic relation to the known producer of the antibiotic: S. refuineus var. thermotolerans.
On the basis of a bromodeoxyuridine chromosome-labeling method, we have studied the sister chromatid exchange (SCE) incidence and growth pattern in cultured leukemic marrow cells from 12 acute nonlymphocytic leukemia patients, 10 with acute myeloblastic leukemia. 1 with acute erythroleukemia, and 1 with acute promyelocytic leukemia with various karyotypic abnormalities. The leukemia cells in these patients were readily identified on the basis of the chromosome anomalies. There was no clear karyotypic relevance to the SCE incidence and growth pattern among the aneuploid leukemic cells. In most of the cases examined, however, the aneuploid leukemic cells were characterized by a low SCE incidence and considerably prolonged cell cycle time, as compared with those in the normal diploid cells which appeared during remission or coexisted with the leukemic cells at the early stages or during relapse of the disease. In most cases, this situation did not change in the aneuploid leukemic cells even after chemotherpeutic treatment, while the normal diploid cells exhibited an increased SCE frequency and, in some cases, alteration of growth pattern after chemotherapy. Possible differences in the susceptibility to the chemotherapy of the leukemic and normal cells in relation to the different growth capacity of these cells are discussed.
An in vitro BrDU chromosome labelling technique has been used for analysing the growth pattern and incidence of sister chromatid exchanges (SCE) in the bone marrow cells of twelve patients with acute lymphoblastic leukaemia (ALL): six with only diploid cells and six with aneuploid cells, containing various numerical and structural chromosome abnormalities, with or without concurrent diploid cells. There was no clear-cut karyotypic relevance to the growth pattern or SCE incidence in such cells. An increased SCE incidence was observed during or immediately after treatment with certain chemotherapeutic regimens. Serial analyses of the growth pattern of cells at diagnosis, at the active stage of the ALL, and during induction of remission, revealed a distinct difference in cell cycle time between leukaemic cells and non-leukaemic ones, the former having a considerably longer cell cycle time than the latter. However, no clear change in the growth pattern of such cells was observed as a function of chemotherapy. Our data also suggest that the growth pattern and SCE incidence in ALL cells are not related to the age of patients and the type of cells involved, as defined by cell surface marker studies.
The incidence of sister chromatid exchange (SCE) and growth pattern were studied in vitro with a bromodeoxyuridine (BrdU) chromosome labelling technique in the Ph1-positive leukaemic marrow and/or blood cells from 20 patients with chronic myelocytic leukaemia (CML) at various stages of the disease. Additional chromosome abnormalities, besides the Ph1 or unusual Ph2-translocations, were found in three out of twelve cases in the chronic phase (CP), in two of four cases entering the blastic phase (BP), and in all four cases in the BP during the study. The growth pattern and SCE incidence in these cases were similar to those in cases in the BP during the study. The growth pattern and SCE incidence in these cases were similar to those in cases with a Ph1 as the sole abnormality. Ph1-positive CML cells undergoing second or more generations predominated in the marrow in the CP, whereas in the active stage of the CP and in the BP the CML marrow cells tended to go through only one generation. There were no clear correlations between the SCE incidence and the state of the CML. However, a marked increase in the SCE frequency was observed in some cases after chemotherapy, irrespective of the state of the disease. The results indicate that the type of Ph1-translocation and/or the presence of additional karyotypic abnormalities hardly affect the growth pattern and SCE incidence in the Ph1-positive CML cells, and that the in vitro BrdU-labelling methods may have a potential for detecting chemotherapeutic effects in CML patients and in the 'staging' of the clinical course of such patients.
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We have investigated the ability of ARL-6 cells, a cell line derived from rat liver, to synthesize various collagens and two glycoproteins of the extracellular matrix, fibronectin, and laminin. Using immunofluorescence, we detected types I, II, and IV collagen plus laminin and fibronectin. Antibodies to types I and III collagen and to fibronectin were associated with most cells and showed a similar distribution. Type IV collagen and laminin were found in thin filaments associated with a small proportion of the cells. Chemical studies showed that ARL-6 cells synthesize predominantly types I and III collagens. The level of collagen synthesis was greatly affected by the presence of exogenous fibronectin added to the cells in the media. Cells maintained in fibronectin-free serum synthesized much less collagen. These studies indicate that liver-derived cells can synthesize a variety of connective tissue proteins and that collagen synthesis by these cells is enhanced by the presence of fibronectin.
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We found rod-like shadows suggesting bronchial involvement in bronchial atresia, allergic bronchopulmonary aspergillosis, bronchiectasis, bronchial stenosis, bronchogenic carcinoma and mucoviscidosis. Typical cases are presented. Various nomenclatures of bronchial involvement based on radiological features or pathological states, such as gloved-finger, tooth-paste shadow, bronchial mucocele and mucoid impaction, are clinically used. We propose "bronchial cast shadow" as an unified term for the roentgenologic diagnosis of these various conditions. The purpose of this paper is; 1) From the radiologic diagnostic stand of view, mucoid impaction of bronchial mucocele is inappropriate, because the same radiologic appearance is not necessarily caused by impacted mucus. In some disorders, the contents of the bronchial lumen might be pus, blood or cells. Initially the abnormal shadow should be described according to the radiologic features, then the pathology of the shadow should be considered. 2) Several different terms are currently used for the same condition. The use of an unified terminology would be convenient for roentgen diagnosis. 3) The recognition of bronchial cast shadow is useful for differential diagnosis of abnormal shadows in the lungs and understanding of abnormal findings. When the bronchial cast shadow is recognized, the underlying cause of it must be determined.
This study describes the establishment of three non-Burkitt B-lymphoma cell lines (BALM-3, BALM-4 and BALM-5) originating from the pleural effusion of a patient with a poorly differentiated diffuse lymphocytic lymphoma. The cells of BALM-3, -4 and -5 exhibited a number of properties which distinguish them from the usual B-cell type lymphoblastoid cell lines. Thus, they lacked the Epstein-Barr virus genome and had abnormal chromosome constitutions including a 14q+ marker. The presence of the identical surface immunoglobulin isotypes (gamma and chi chain determinants), and Ia-like B-cell-associated antigen in the cultured cells and in the "fresh" lymphoma cells in vivo was demonstrated. These findings strongly suggested that these cell lines have B-cell characteristics and were derived from the original tumor cell population. BALM-5 cells, however, showed somewhat different growth, cell surface marker profile and functional characteristics compared to those of BALM-3, and -4 cells. These variations suggest that the BALM-5 cells were probably at different stages of B-cell maturation than those of BALM-3 and -4, even though all three cell lines (established in three separate flasks) originated from the cells of the same pleural effusion of a lymphoma with monoclonal B-cell characteristics.
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HUMAN fibroblasts in culture synthesise both type I and type III collagen(1), with type I accounting for 70-90% of the total(2). In culture, the rates at which these proteins are synthesised is constant and apparently rather rigidly controlled(3). However, the proportions of these collagens differs in cells cultured with increased amounts of serum (increased type III/I)(4) as well as in cells obtained from patients with certain diseases. Cells from patients with the Ehlers-Danlos type IV syndrome make little or no type III collagen(5,6), whereas cells from patients with osteogenesis imperfecta have an increased type III/I (refs 7, 8). We have found that cells from some patients with systemic sclerosis (scleroderma), have a reduced type III/I ratio. However, as previously reported, these cells grew to a lower density than control cells(9). We report here that normal fibroblasts from human and guinea pig skin produce proportionally more type III collagen at high cell density, probably because of a reduction in the synthesis of type I collagen.
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A p-nitrophenyl-alpha-D-glucopyranoside-hydrolyzing alpha-glucosidase of a thermophile, Bacillus thermoglucosidius KP 1006, was purified to an electrophoretically-homogeneous state. Its molecular weight was estimated as 60 000 by gel electrophoresis. The molecular activity (ko) and the Km value at 60 degrees C and pH 6.8 for p-nitrophenyl-alpha-D-glucopyranoside were 233 s-1 and 0.24 mM, respectively. The enzyme cleft the non-reducing terminal alpha-1,6-glucosidic bonds of isomaltose, panose, isomaltotriose, isomaltotetraose, and isomaltopentaose. The ko values were 72.4, 194, 208, 233 and 167 s-1, and the Km values were 3.3, 9.5, 11, 13 and 21 mM, respectively. Each isomaltosaccharide was hydrolyzed to glucose by the cleavage of single glucose units from its nonreducing end. The present study suggests that the enzyme is an oligo-1,6-glucosidase (dextrin 6-alpha-glucanohydrolase, EC 3.2.1.10) and an exo-glucosidase.
Five cases of Ph1-positive AML were studied. In all cases a Ph1-chromosome was shown with banding techniques to be due to a translocation between chromosomes No. 9 and No. 22. Cases 1 and 4 were found to have more than one Ph1 with evidence of only on Ph1-translocation accompanying other chromosome abnormalities. Two cases represented an unusual pattern of appearance and disappearance of the Ph1-positive clone during their clinical courses: Case No. 2 was originally Ph1-positive (46,XY,Ph1) but two months before his expiration the Ph1-positive clone was completely replaced by a newly developed Ph1-negative clone with an abnormal chromosome No. 21 (46,XY,21q+), whereas case No. 3, primarily Ph1-negative, developed a Ph1-positive clone among the previously karyotypically normal cells one month before death. The Ph1-positive AML cases presented have been discussed in relation to: 1) the genesis and significance of the Ph1-positive clone, 2) differentiation from the blastic phase of CML and 31 the general experience with Ph1-positive acute non-lymphocytic leukemia (ANLL), the world literature of which have been tabulated.
The case of a 4-year-old boy with ALL, possibly developing subsequent to a lymphoma involving the thoracic cavity, which was shown to be of the T-cell type, is presented. The leukemic cells had a 5q-- anomaly, which had previously been described only in cases of refractory anemia and/or AML. The 5q-- abnormality was invariably accompanied by a 9p-- chromosome in the leukemic cells. The interstitial deletion leading to the 5q-- chromosome was shown with banding techniques to be similar to that described previously in myeloproliferative disorders. Some aspects of the 5q-- anomaly in ALL and its relation to previous experience with this karyotypic change are discussed.
Among 300 patients with chronic myelocytic leukemia (CML) followed at our institute during the last ten years, 36 (12%) were thought to have Ph1-negative CML. In eight of these patients, chromosomal abnormalities were found in the leukemic cells; in four, the karyotypic abnormalities were established with banding techniques. The data of the present study and a review of the literature regarding chromosomal changes in Ph1-negative CML indicate that: 1) no characteristic or consistent karyotypic change is present in Ph1-negative CML and that diploidy is more common in this than any other leukemia; 2) the most common changes involve group C chromosomes (particularly +8); and 3) a missing Y is less common in Ph1-negative CML than in its Ph1-positive counterpart. The karyotypic changes in Ph1-negative CML resemble more those encountered in Ph1-positive CML than in acute myeloblastic leukemia (AML). The much shorter survival of the Ph1-negative CML patients vs that of the Ph1-positive group was again substantiated, and some of the previously reported clinical and laboratory findings unique to Ph1-negative CML were confirmed. On the basis of the cytogenetic findings it is concluded that Ph1-negative CML appears to be an entity unto itself.