Biomedical subjects
Publications and source records attributed to N Kamada.
A system useful for the collection and analysis of a large number of abnormal karyotypes and for studies on the relationship between cytogenetic abnormalities and clinical features of diseases is reported. The program is based on the disintegration and rearrangement of abnormal karyotypes recorded according to the 1978 International System for Human Cytogenetic Nomenclature (ISCN).
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A surgical experience with 530 orthotopic liver transplants in rats is reviewed with technical details. Liver transplantation in the rat can provide important data in a variety of areas, including immunology. Nevertheless, technical problems have limited the widespread use of this valuable investigative tool. Cuff techniques for microvascular anastomosis have simplified the portal venous anastomosis and have minimized the anhepatic phase in the recipient. These had previously been the most frequent causes of failure in the utilization of liver transplantation in the rat. The technique for rat liver transplantation described here was found to be reliable with a 95.3% long-term survival (longer than 100 days) in a recent group of 85 transplants where rejection was not a factor. In the early experience, most deaths were due to bleeding, infection, and biliary complications. The improvements in technique have eliminated most of these errors. We feel that the use of these technical modifications would increase the success rate of rat liver transplantation in the hands of others.
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Orthotopic liver allografts in the rat survive indefinitely without immunosuppressive agents, despite incompatibility between donor and recipient for antigens of the major histocompatibility complex. This is strain-dependent. In the DA to PVG strain combination, liver grafts are never rejected. This is not due to failure of the recipient to mount an immune response against the donor tissue, because there is unequivocal histological evidence of a rejection response during the first few weeks after grafting. This response is moderate and disappears to leave a histologically normal liver, apart from mild bile duct proliferation. Liver function tests show evidence of damage during the phase of cellular infiltration, but these test results also return to normal levels within a few weeks. In the DA to BN strain combination liver grafts are rapidly rejected, and this process is accompanied by histological signs of a violent and progressive destructive cellular response with gross alterations in liver function test results that are progressive until the death of the recipients. F1 hybrid recipients between these two strains (BN X PVG)F1 show intermediate levels of both histological damage and elevated liver function values, but they do not reject their grafts. Recovery from the rejection episode appears to be complete, as judged histologically. However, biochemical values remain slightly elevated, indicating either that the original damage was so severe that it was inconsistent with complete functional recovery or that there is continuous damage that is not visible histologically.
The prognostic value of several clinical and hematologic features, recorded at diagnosis, in chronic phase Ph1 positive chronic myelocytic leukemia (CML), was analyzed in 135 patients using life-table analysis. About one third of patients were atomic bomb survivors and they had been examined twice a year before the diagnosis of CML. In general, features representing tumor cell burden, i.e., leukocyte count, spleen sizes, and absolute differential cell counts of all granulocyte series cells except myeloblasts affected survival significantly, while sex, age, hemoglobin, platelets and features representing quality of leukemia, i.e. neutrophils alkaline phosphatase score, percent Ph1 positive cells in bone marrow, and percent differentials of all granulocyte series cells except promyelocytes and segmented neutrophils were all insignificant. Multivariate life-table analysis was also performed using age, sex, hemoglobin, platelets, and leukocyte count as predictor variables. The result was that leukocyte was the single most important factor in this analysis and annual death rates between low risk (risk ratio less than 0.8) and high risk (risk ratio greater than 1.4) differed considerably up to four years from diagnosis, indicating our formula to calculate risk ratio is valid as a grading parameter of chronic phase Ph1 positive CML within four years from diagnosis.
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Cytogenetic, morphologic, and clinical data of 33 acute nonlymphocytic leukemia (ANLL) patients with t(8q - ;21q+) and 19 patients with acute promyelocytic leukemia (APL) were collected from seven laboratories in Japan. The latter class included 18 patients with t(15q + ;17q-) and one with a normal karyotype. The t(8q - ;21q+) and t(15q + ;17q-) translocations were each shown to be associated with a specific type of ANLL, namely, AML-M2 and APL-M3, respectively. No patient with APL had the M3 variant. The t(8q - ;21q+) translocation seems to be more common as an abnormality in ANLL in Japan as compared to findings in other countries. The high incidence of t(15q + ;17q-) among Japanese patients with APL indicated in this study, however, still awaits confirmation.
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The biochemical activities of 8 lysosomal acid hydrolases in leukemic cells from 48 patients were examined. Characteristic alterations were found in alpha-mannosidase, beta-galactosidase and N-acetyl-beta-glucosaminidase activities of leukemic cells. The level of alpha-mannosidase activity was much higher in myelo(mono)genous leukemias (AML, AMoL, AMMoL, CML and CMMoL) than in lymphogenous ones (ALL, T-cell leukemia, hairy cell leukemia and CLL) without exception. The beta-galactosidase activity also differed as a result of alpha-mannosidase, except in T-cell leukemia. In T-cell leukemia it was within the range of normal lymphocytes, but in the other lymphogenous leukemias it was significantly below normal. N-acetyl-beta-glucosaminidase activity in myelo(mono)genous leukemic cells was above the range of normal granulocytes. The changes in these enzyme levels were consistent. The lymphocytic or myelocytic nature of three cases of acute undifferentiated leukemia could be determined by enzyme studies. In two cases it was lymphocytic and in one it was myelocytic. The enzymatic abnormalities were also found in morphologically mature neutrophils from patients but not only chronic types (CML, CMMoL) but also acute types (AMoL, AMMoL) of leukemias, and were similar to those of their respective leukemic cells. Analysis of lysosomal enzymes (at least three of those mentioned above), can elucidate one of the biochemical properties of leukemic cells and may be valuable in the differentiation of leukemias.
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2 children with Down's syndrome showed severe anaemia, leucocytosis with blastic cells, thrombocytopenia and hepatosplenomegaly. Bone marrow aspirations were near-dry tap and marrow biopsy revealed primary myelofibrosis with myeloid metaplasia (MMM). Their course was short with a blood picture similar to that of leukaemia. They expired 2 months and 21/2 months after diagnosis, respectively. The cases were thought to represent an acute childhood variant of MMM. Cytogenetic study of circulating white cells by 24 h culture without phytophaemagglutinin stimulation revealed aneuploidy in both cases, the first case showing marked aneuploidy with a predominant karyotype of 50,XX,+8,+19,+19,+21 and the second case a mosaic of 47,XX,+G/48,XX+G,+G. The karyotype of phytohaemagglutinin stimulated lymphocytes was 47,XX,+G in both cases. These findings suggest that the abnormal karyotypes are those of circulating blastic cells which are abnormal clones of haematopoietic cells responsible for MMM. In Down's syndrome, MMM might not be so rare as reported.
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Cytogenetic studies were made on 160 patients with acute nonlymphocytic leukemia (ANLL) between 1963 and 1979, of whom 115 had acute myelocytic leukemia with 67 patients showing aneuploidy (58.3%). Among these, 24 patients were found to have similar chromosome alterations that appeared to involve specifically chromosomes 8 and 21. Banding studies on at least 7 of these patients confirmed the presence of a translocation between these two chromosomes. Of 160 ANLL patients, 142 were scored for neutrophil alkaline phosphatase (neutrophil AP) at the time of diagnosis. Fifty-nine patients showed a low neutrophil AP score, 42 a normal value, and 41 a high value. All patients with 8;21 (or C/G) translocation had a low neutrophil AP score and leukemic cells with maturation (M2 of FAB classification) in the bone marrow. In vitro liquid culture for 2 wk of 8;21 translocated leukemic cells revealed no increase of neutrophil AP activity nor increase of mature granulocytes, whereas 9;22 translocated chronic myelocytic leukemia cells with a low neutrophil AP score did so. Neutrophil AP score at the time of diagnosis in acute myelocytic leukemia is very useful for detecting 8;21 translocation AML and for studying the pathophysiology and genetic alterations of the characteristic subgroup of AML with 8'21 translocation.
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