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Biomedical subjects

T Akabane

Publications and source records attributed to T Akabane.

At least 73 records · Page 4Linked to original sources
PubMed1985

Quantitative evaluation of monocyte differentiation by electron microscopy: impairment of differentiation ability in monocytes from children with acute lymphoblastic leukaemia.

The differentiation of monocytes was evaluated quantitatively by electron microscopy and was analyzed in relation to the clinical features of childhood acute lymphoblastic leukaemia (ALL). The monocyte cellular size increased and cell organellae became mature after a 72-h culture. Phagolysosome formation developed markedly- and the nucleus became circular--accompanied by chromatin deconcentration. The differentiation degree of the cell organellae was indexed and classified as mature by electron microscopy. The indexes of nuclear shape, chromatin deconcentration, cytoplasmonuclear ratio and vacuole formation increased with time. The total index increased linearly with time dependence. These results indicate that the ultrastructural parameters and indexes allowed a quantitative assessment of cell organellae and cellular differentiation of the monocyte. At the acute phase of ALL, the degrees of cell organnellae and cellular differentiation were significantly lower than the control. The above findings suggest that monocytes from children with ALL have impaired differentiation ability, which results in defective function of macrophages.

Cell Differentiation↗
PubMed1985

Leukaemia cell mobility in childhood acute myeloid leukaemia based on the FAB classification.

Leukaemia cell mobility was evaluated by the agarose plate method in 20 children with acute myeloid leukaemia (AML) based on the FAB classification. M1 blasts from 3 patients did not show any migration, probably reflecting their cellular immaturity. Leukaemia cells from 3 of 8 patients with M2 AML showed random migration, but those from the remaining 5 did not have this ability. The results thus demonstrated the heterogeneity of M2 AML in the function as well as the morphology. The M3 leukaemia cells failed to migrate under agarose in 2 patients studied, implying that a certain cytoskeletal defect in the cells. In all of 2 M4, 2 M5A and 3 M5B AML patients, leukaemia cells showed active mobility. The random migration value (mean +/- SD) of M5A and M5B cells was 5.7 +/- 1.7 compared with that of normal monocytes of 4.0 +/- 0.4 (p less than 0.01), indicating the enhanced random migration of leukaemia monocytes. M4 and M5B leukaemia cells had chemotactic responsiveness to zymosan-activated serum comparable to that of normal monocytes, but M5A cells were different from them in lacking apparent chemotactic responsiveness to the factor. Lymphadenopathy and leucocytosis were more prominent in the patients whose leukaemia cells were capable of migration than in those not having such cells. Mobility of leukaemia cells probably reflects their cell lineage, cellular maturity and functional distortion during leukaemic transformation, and appears to be related to clinical features.

Adolescent↗
PubMed1985

Impaired natural killer cell recycling in childhood chronic neutropenia with morphological abnormalities and defective chemotaxis of neutrophils.

Natural killer (NK) cell activity was measured by a 51Cr-release assay using K562 target cells in 12 neutropenic children. NK cell activity was depressed in four patients who had childhood chronic neutropenia with abnormal neutrophil morphology and chemotaxis. The percentage of lysis at a 40:1 effector-target ratio was 28.4% to 42.1% (P less than .001) of the normal lymphocyte value during the study period (32 to 40 months). NK cell activity was normal in the other eight children with chronic neutropenia without any of these neutrophil abnormalities: lazy leukocyte syndrome, Shwachman syndrome, or dysgammaglobulinemia type I with neutrophil defects. NK cell activity of the four patients was depressed at 5:1 to 40:1 effector-target ratios. The NK cells responded to in vitro interferon (IFN)-alpha and interleukin 2, as did normal lymphocytes, but the activated levels were still lower than those of normal lymphocytes (P less than .01). Because NK cells kill a target through recognition, binding, killing, and detaching, and they repeat this lytic sequence (ie, recycling), the localization of the NK cell defect was further analyzed in the four patients using both 51Cr-release and single cell-in-agarose assays. The patients' NK cells were normal in recognizing, binding, and killing a target but were defective in recycling; the estimated maximum recycling capacity (MRC) values in a four-hour assay were 1.8 to 2.4 (P less than .01), as compared with the normal lymphocyte value of 5.5 +/- 0.6 (mean +/- SD). The stimulation of the effector cells with 1,000 U/mL IFN-alpha did not significantly increase the estimated MRC. These results demonstrate that NK cells are defective in recycling in some type of childhood chronic neutropenia with abnormal neutrophil morphology and chemotaxis. The NK cell deficiency is of clinical interest in terms of its relationship to the recurrent infections, development of malignancy, and dysgranulopoiesis in the disorder.

Adolescent↗
PubMed1985

Single-cell origin of human mixed hemopoietic colonies expressing various combinations of cell lineages.

We have established single-cell culture for human mixed hemopoietic colonies using a micromanipulator. Mononuclear cells from human umbilical cord blood were cultured at a concentration of 1 X 10(4) cells per milliliter in methylcellulose medium containing medium conditioned by phytohemagglutinin-stimulated leukocytes and erythropoietin. It was possible to identify the single hemopoietic progenitors in situ in methylcellulose culture on the basis of unique morphology and migratory ability after 36 to 60 hours of incubation. Candidate single hemopoietic progenitors from methylcellulose medium were individually micromanipulated to secondary culture dishes and cultured for an additional ten to 14 days. The colonies derived from the single progenitors were individually picked and stained with May-Grünwald-Giemsa for analyses of the cellular composition. A total of 288 single cells were individually transferred to second dishes. Then 186 single cells produced secondary colonies consisting of cells in one to five different lineages. A total of 39 single cells produced mixed hemopoietic colonies consisting of cells in two, three, four, and five different lineages. There were eight types of colonies revealing two different lineages, ie, neutrophil (n)-erythrocyte (E), macrophage (m)-E, m-megakaryocyte (M), eosinophil (e)-basophil (b), eE, bE, bM, and EM lineages. Three types of colonies consisting of cells in three lineages were also seen, ie, nmM, nbE, and ebE. There were six types of colonies consisting of cells in four lineages, ie, nmbM, nmEM, nebE, mebM, and meEM. One type of colony consisted of cells in five different lineages (nmbEM). These results indicate the single-cell origin of human mixed hemopoietic colonies expressing various combinations of cell lineages. It also provides experimental data in support of stochastic mechanisms of stem cell differentiation.

Azure Stains↗
PubMed1984

Childhood acute lymphoblastic leukemia with natural killer activity. Clinical and cellular features of three cases.

Leukemic cells from 3 of 28 children with acute lymphoblastic leukemia (ALL) had natural killer (NK) activity against K562 and Molt-3, but not against Raji as determined by the 4-hour 51Cr release assay at a 40:1 effector:target ratio; the highest percent lysis against K562 in each patient ranged from 55.9% to 147.4% of the normal lymphocyte value and that against Molt-3 from 28.0% to 127.9%. Their leukemic cells were nonphagocytic, nonadherent, and negative for nonspecific esterase. Leukemic cells from two of them displayed similar morphologic and immunologic features. The cells had a round nucleus, and were E-receptors (E)+, Leu-5+, IgG-Fc+, Ia+, OKM1+ or OKM1-, T-cell antigens-, B markers-, and monocyte antigen-, indicating their NK cell origin. The other patient's cells were characterized by the irregularly shaped nucleus, and were E+, Leu-5+, IgG-Fc+, T+, OKT6+, Leu-2a+, and OKM1+. The presence of E which are identical to E of T-cells and a high density of T-cell antigens including OKT6 on the cells suggested their T-cell nature. Of the three patients, two without thymic enlargement had leukemic cells of NK cell origin, and the other one with the symptom leukemic cells of the T-cell lineage, the clinical feature probably reflecting the cell lineage of their leukemic cells.

Adolescent↗
PubMed1984

A monocyte disorder in siblings with chronic candidiasis. A combined abnormality of monocyte mobility and phagocytosis-killing ability.

Immunologic studies were performed on siblings (a 9-year-old boy and an 11-year-old girl) with chronic candidiasis since infancy and showed defective monocyte functions. In vivo migration and in vitro mobility of the monocytes were impaired. In addition, they had defective phagocytosis-killing ability against Candida albicans. There was no factor(s) to inhibit the monocyte functions in the patients' serum, and their mononuclear cells (75% to 80% lymphocytes) did not secrete such an inhibitory factor(s) in vitro. The serum IgG, IgA, IgM, and C3 levels were normal. Delayed hypersensitivity responses to five antigens, including Candida antigen, were absent in the two patients. In vitro T-lymphocyte functions, such as Candida antigen- or mitogen-induced blastogenesis and lymphokine (leukocyte migration inhibitory factor and leukocyte-derived chemotactic factor) production, were normal. The clinical features of our patients were similar to those with chronic mucocutaneous candidiasis (CMC); however, their primary immunologic defect was, unlike that of CMC, in monocytes, but not in T lymphocytes. These results demonstrated a monocyte disorder with defective mobility and phagocytosis-killing ability that contributed to chronic candidiasis.

Blood Bactericidal Activity↗
PubMed1984

Production of high levels of interleukin 1-like activity by the SPI-802 human leukemia cell line with E receptors.

The SPI-802 human leukemia cell line, which possesses E receptors and used to have natural killer activity, has been demonstrated to produce high levels of interleukin 1 (IL-1)-like activity. SPI-802 supernatants prepared in 1% serum-containing cultures with lipopolysaccharide stimulation, like similarly prepared adherent-cell-derived IL-1, enhanced phytohemagglutinin-induced mouse thymocyte proliferation. When adherent-cell IL-1 gave 50% maximum activity at a reciprocal dilution of 20, SPI-802 supernatant gave it at 200, indicating the production of high levels of IL-1-like activity by the cell line. SPI-802 supernatant promoted the production of interleukin 2 (IL-2) by the Jurkat-F1884 T-cell line: Levels of IL-2 activity obtained with 15% SPI-802 supernatant were almost equivalent to those obtained with 50% adherent-cell IL-1 as estimated by the maximum proliferation of IL-2-dependent cytotoxic T cells. SPI-802 supernatant by itself exhibited no IL-2 activity. Major IL-1-like activity of SPI-802 supernatant was present in fractions from AcA54 columns corresponding to Mr 12,000-20,000 and 60,000-70,000 and resolved on isoelectrofocusing into two distinct species with pI values of 5.0 and 7.0, being consistent with the results of adherent-cell IL-1. The SPI-802 cell line having E receptors is an ideal source of a soluble factor with the biological and biochemical characteristics of human IL-1.

Cell Line↗
PubMed1984

Neurologic deterioration with progressive CT changes in a child with Kearns-Shy syndrome.

A case of the rare juvenile form of Kearns-Shy syndrome with progressive external ophthalmoplegia and lid ptosis, carditis, skeletal muscle weakness, seizures, mental subnormality, short stature, EEG abnormality and deafness is presented. Electromyography revealed a myopathic pattern. Histochemical studies on quadriceps biopsy specimens showed atrophy of type II fibers and "ragged-red fibers." On electron microscopy these muscle cells were seen to contain an increased amount of glycogen particles and abnormal mitochondria were increased in number and size. It is of interest that abrupt deterioration of neurological findings such as seizures, mental subnormality, speech disturbance and deafness was present in our case. Computed tomographic scanning showed progressive changes of cerebral atrophy, low density of cerebral white matter and basal ganglia calcification, which were well associated with the clinical deterioration. A review of the literature also indicated that some patients with this syndrome showed abrupt neurological deterioration in childhood. Involvement of the central nervous system in this syndrome has to be considered as the cause of sudden deterioration and death in childhood.

Atrophy↗
PubMed1984

Impaired monocyte differentiation in children with acute lymphoblastic leukaemia: its evaluation by peroxidase activity and ultrastructure.

The ability of monocyte differentiation in childhood acute lymphoblastic leukaemia (ALL) was evaluated on the basis of the ultrastructure and peroxidase (PO) activity which could show the differentiation of cultured monocytes. In the control, PO activity limited to the granules decreased time-dependently during culture for 4 d, and was closely associated with the morphological development to macrophages. In childhood ALL, monocytes showed poor changes in both PO activity and morphological features during culture for 4 d compared to the control. Therefore, we conclude that monocyte to macrophage differentiation is impaired in childhood ALL.

Adolescent↗