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Biomedical subjects

T Akabane

Publications and source records attributed to T Akabane.

At least 19 recordsLinked to original sources
PubMed1992

[Clinical evaluation of effects of KRN8601 (rhG-CSF) on neutropenia].

Clinical effects of KRN8601 (recombinant human granulocyte colony-stimulating factor:rhG-CSF) were studied in 26 patients with chronic neutropenia including 4 Kostmann's disease, 1 Shwachman's syndrome, 1 Lonsdale's syndrome, 1 glycogen storage disease Ib-associated, 6 chronic benign, 5 chronic hypoplastic, 2 cyclic, 4 autoimmune and 2 miscellaneous neutropenia. The patients were given rhG-CSF intravenously at doses of 20-540 micrograms/m2 or subcutaneously at doses 20-400 micrograms/m2, over the periods of 2-32 weeks. Increases in neutrophil counts occurred after rhG-CSF administration in 23 of the 26 patients. Patients with Kostmann's disease, Shwachman's syndrome and chronic hypoplastic neutropenia responded poorly compared to patients with other types of neutropenia. There were no serious side effects which caused interruption of the study. These results indicated a beneficial effect of KRN8601 in various types of chronic neutropenia.

Adolescent↗
PubMed1979

Abnormal neutrophil maturation in a neutrophil defect with morphologic abnormality and impaired function.

Neutrophils from a patient with recurrent pyogenic infections since infancy were found to have morphologic abnormalities and impaired functions. The neutrophils had an abnormal nuclear shape, no or few secondary granules, and no alkaline phosphatase activity. Primary granules were normal in number and structure, and were positive for peroxidase. Immature granulocytes were structurally normal. The neutrophils were impaired in chemotaxis and bactericidal capacity. The patient's marrow cells formed increased numbers of granulocytic colonies of small size in culture. Her peripheral leukocytes produced elevated levels of CSA and adherent marrow cells did not inhibit colony formation. These data indicate an intrinsic neutrophil defect which allows normal proliferation of precursor cells, but results in abnormal morphogenesis and impaired function as the cells mature.

Bone Marrow↗
PubMed1978

In vitro assay for responsiveness of lymphocytes to transfer factor by a new leukocyte migration inhibitory test.

Transfer factor (TF) causes nonimmune lymphocytes to produce leukocyte migration inhibitory factor (LMIF) in the presence of purified protein derivative (PPD). The activity of TF was measured by leukocyte migration inhibitory test (LMIT). The LMIT was a modification of the conventional agarose droplet method. To express the activity of LMIF quantitatively and simply, LMIF titer was introduced. The LMIF titer was obtained from the combination of two factors, LMIF dilution and cell migration diameter, and therefore this made the LMIT much more sensitive as compared to the conventional LMIT. The responsiveness of lymphocytes from acute lymphoblastic leukemia (ALL) and from cell-mediated immunodeficiency in children to TF was assayed by LMIT. In ALL, the lymphocyte responsiveness was poor in relapse but improved with remission. The responsiveness was remarkably well in 3 patients with cell-mediated immunodeficiency. This method appears useful for the in vitro evaluation of responsiveness of lymphocytes to TF.

Cell Migration Inhibition↗
PubMed1978

Measurement of Donath-Landsteiner antibody-producing cells in idiopathic nonsyphilitic paroxysmal cold hemoglobinuria (PCH) in children.

A 2-yr-old girl with a nonsyphilitic type of paroxysmal cold hemoglobinuria (PCH) is reported. We applied the plaque-forming cell (PFC) assay to the measurement of Donath-Landsteiner (DL) antibody-producing cells in the patient. Some of the circulating B lymphocytes formed plaques in our assay system. Initially the number of PFC was 1442 +/- 225/10(6) lymphocytes and DL titer was 1:16. Thereafter the PFC decreased in number as the DL titer decreased. Eight weeks later circulating PFC were not found but the DL titer was still 1:1 positive. The PFC assay appears to be useful as a new method for obtaining rapid imformation as to the disease status of PCH.

Antibody-Producing Cells↗