Search PubMed⌕ Search

Biomedical subjects

Y Kanakura

Publications and source records attributed to Y Kanakura.

162 records · Page 9Linked to original sources
PubMed1986

Development of mucosal mast cells after injection of a single connective tissue-type mast cell in the stomach mucosa of genetically mast cell-deficient W/Wv mice.

Mast cells may be classified into at least two phenotypically distinct populations: connective tissue-type mast cells (CTMC) and mucosal mast cells (MMC). Mast cells in the peritoneal cavity of mice are typical CTMC, whereas mast cells in the mucosa of the stomach show morphologic characteristics of MMC. We investigated whether CTMC may change to MMC. A single peritoneal mast cell of WBB6F1-+/+ mice was identified under the phase-contrast microscope, picked up with the micromanipulator, and injected into the stomach wall of genetically mast cell-deficient WBB6F1-W/Wv mice. The cells with histochemical and electron microscopical features of MMC developed in the mucosa, and those with histochemical features of CTMC in the muscularis propria. This directly demonstrates that a certain proportion of CTMC may function as a bipotent precursor for both MMC and CTMC.

Animals↗
PubMed1986

Mitogenic response of neoplastic B cells: comparison of reactivity to Staphylococcus aureus Cowan I and anti-immunoglobulin antibodies.

Neoplastic B cells from two patients with hyperleucocytic hairy cell leukaemia (HCL) and 19 patients with chronic lymphocytic leukaemia of B cell Type (B-CLL) were investigated to examine the mitogenic responses to the F(ab')2 fraction of anti-human immunoglobulins (anti-Igs) and Staphylococcus aureus Cowan I (STA). Neoplastic cells from both HCL patients lacked surface Tac antigen. Mononuclear cells from the two HCL patients strongly responded to both anti-Igs and STA as measured by 3H-thymidine incorporation in vitro. Although the mononuclear cells from two patients with B-CLL showed high response to STA, cells from none of the patients with B-CLL responded to anti-Igs. Mononuclear cells as well as T-cell-depleted fractions from the two HCL patients showed a strong proliferative response by anti-gamma chain antibody (anti-gamma) and the mononuclear cells from one of the patients were also induced to proliferate by anti-delta, whereas those from normal subjects responded only to a high concentration of anti-mu. Based on the difference in reactivity to anti-Ig, it is suggested that the HCL cells in this study originate from a subset equivalent to 'memory' B cells, whereas the B-CLL cells originate from a subset equivalent to 'virgin' B cells.

Antibodies, Anti-Idiotypic↗
PubMed1986

[Treatment with K-18 (IgG-melphalan) in recurrent cases of hematopoietic malignancies].

K 18, an IgG-Melphalan conjugate was administered to 30 patients, who had recurrent hematopoietic malignancy. Ten out of the 30 patients received single doses of 1 to 20 enteric tablets containing 10 mg of K 18, as a phase I study. No side effects were observed. K 18 was administered every day to the remaining 20 patients in order to evaluate the side effects and therapeutic effects, as a phase II study. One patient attained partial remission. Although no remission effect was obtained in 14 of the 20 patients, antitumor effects such as a decrease in leukemia cells, were observed in 4 of 20 patients. As to side effects, neither recurrence of tumor nor cumulative toxicity were shown in one patient with NHL who received only K 18 for 14 months as maintenance therapy. Evaluation of antitumor effect was difficult in the case of the remaining 4 patients. In the 20 cases who entered the phase II study, a decrease in neutrophils was observed in 2 patients, a slight decrease in platelets in 3 patients and increased transaminase activity in one patient as side effects of K 18. In brief, compared with Melphalan, K 18 has between 1.3 and 2 times a more potent therapeutic effect, with extremely low side effects.

Administration, Oral↗
PubMed1985

[Infectious complications and infection prevention in patients with acute leukemia].

Febrile episodes in 147 patients undergoing first remission induction therapy for acute leukemia were analyzed. Febrile episodes occurred 254 times in 136 patients. The cause of fever could not be identified in 54.3% of all episodes. Antibiotic therapy was effective in 81.1% of these episodes with no cause determined. Postmortem examinations proved infections in 65.2% of patients who had fever of unknown origin before death. Sepsis and pneumonia together accounted for 53.4% of documented infections. Sepsis and pneumonia occurred most often when the patients had neutropenia (less than 500/mm3). Increase in neutrophil count and achievement of hematologic remission produced good prognosis of the infections, and the reverse was also true in some patients. Fifty percent of fetal patients died of infection. The incidence of infections, especially pneumonia and infections caused by fungi and Proteus species indicating such infections were exogenous, reduced markedly in laminar air flow rooms.

Acute Disease↗
PubMed1984

In vitro treatment of human acute lymphocytic leukemia cells in bone marrow with a cocktail of monoclonal antibodies.

Human leukemic cells which bear antigens present on the common acute lymphocytic leukemia (ALL) cell surface can be lysed with murine monoclonal antibodies and baby rabbit complement. With NALM-6 cells used as target cells, the optimal conditions for completely eliminating the cells in vitro have been defined. The antibody cocktail plus complement is more effective than any single antibody plus complement in lysing the target cells. Optimal lysis is obtained when the antibody cocktail at 10 micrograms/ml for each antibody and baby rabbit complement at a final dilution of 1:6 are used. Leukemic cells from two newly diagnosed ALL patients were also effectively killed by this treatment. Of special interest is the finding that human complement can be used in place of baby rabbit complement.

Animals↗
PubMed1984

[Phase II study of mitoxantrone for acute leukemia].

A total of seventeen patients with acute leukemia were treated with mitoxantrone for induction therapy. Nine out of 17 patients were previously untreated, while the other eight patients were previously treated. All of the previously treated cases had received chemotherapy including anthracycline derivatives. Bolus infusion of Mitoxantrone for three to ten days was employed. The daily and total doses of mitoxantrone ranged from 1.8 mg/m2 to 4.3 mg/m2 and from 7.5 mg/m2 to 40 mg/m2, respectively. CR was achieved in three (33%) previously untreated and two (25%) in previously treated cases. PR occurred in five previously untreated and in two previously treated patients. The other five failed to respond the agent. The most serious adverse effect of the drug was myelosuppression, but it was reversible in all cases. In one patient irreversible EKG change was observed. All other adverse effects such as nausea and vomiting, anorexia and diarrhea, were not serious and reversible. In conclusion, Mitoxantrone is effective in some cases with acute leukemia.

Acute Disease↗
PubMed1983

A human B lymphocyte antigen (P-76) shared by B-cell chronic lymphocytic leukemia cells and hairy cell leukemia cells.

A membrane antigen with an apparent specificity to B lymphocytes was detected with immunochemical techniques and its properties were analyzed. Anti-B-CLL serum was raised in a rabbit by immunization with B-cell chronic lymphocytic leukemia (B-CLL) cells. This anti-B-CLL serum was absorbed with erythrocytes, liver homogenate and insolubilized immunoglobulins. After further absorption with T-CLL cells, chronic myelocytic leukemia (CML) cells and acute myelocytic leukemia (AML) cells, the anti-B-CLL serum still reacted with peripheral blood B lymphocytes, B-CLL cells and hairy cell leukemia (HCL) cells. In contrast, no reactivity was seen with peripheral blood T lymphocyte or monocytes, or leukemia cells of non-B cell origin. An immunoprecipitation of radiolabeled cell surface proteins was attempted using the anti-B-CLL serum in the presence of Staphylococcus Aureus Cowan 1 (SaCl), and the precipitates were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). A membrane antigen with an apparent molecular weight of 76,000 daltons (P-76) was immunoprecipitated with the anti-B-CLL serum from the lysates of normal B lymphocyte, B-CLL cells and HCL cells. The antigen (P-76) is not composed of disulfide-linked subunits and has no structural relationship with HLA-DR (Ia-like) antigens or other known antigens. These results suggest that this antigen is B-lymphocyte specific, and favour the B-lymphocyte nature of HCL cells.

Antibody Specificity↗
PubMed1983

Heavy chain loss after treatment with Melphalan in a patient with "nonsecretory" myeloma.

A case of "nonsecretory" myeloma is described. The patient had typical osteolytic lesions and marked infiltration of myeloma cells in the bone marrow, and plasma cell leukemia. A good partial remission was obtained with Melphalan, but the patient relapsed and died one year later. Immunofluorescent and immunoelectroscopic studies on the myeloma cells demonstrated the presence of cytoplasmic gamma-and kappa-chains at the initial stage and of only kappa-chains at a relapse. The electron microscopic method for polysome analysis indicated that both L-and H-chains were synthesized on membrane-bound polysomes initially, but the ability to produce H-chain was missing at the relapse.

Female↗
PubMed1983

Ultrastructure of normal human T cell subpopulations. Parallel tubular arrays in T gamma lymphocytes and clustered dense bodies in T mu lymphocytes.

Ultrastructures of normal T-cell subpopulations, T gamma and T mu cells, were studied. T gamma cells were isolated and identified by repeating the rosetting method; firstly, by E rosette formation with neuraminidase-treated sheep red blood cells (SRBC), and next by EA gamma-rosette formation with ox red blood cells coated with IgG antibody (EAox). Before EAox rosetting, SRBC on isolated T cells were lysed by autologous plasma instead of ammonium chloride solution. Normal T gamma cells were heterogeneous with regard to their granules; the majority of T gamma cells had parallel tubular arrays (PTA) and a few had electron-dense granules. When ammonium chloride solution was employed to lyse SRBC, PTA were never observed; PTA in normal T gamma cells and in chronic lymphocytic leukemia cells with T gamma character both seemed to change into electron-dense granules after ammonium chloride treatment. In contrast to T gamma cells, T mu cells were characterized by clustered dense bodies, i.e. focal aggregates of electron-dense granules.

Ammonium Chloride↗
PubMed1983

Alteration of T cell subsets and immunoglobulin synthesis in vitro during high dose gamma-globulin therapy in patients with idiopathic thrombocytopenic purpura.

T cell subsets of peripheral lymphocytes were studied using monoclonal antibodies (OKT3, OKT4, OKT8) and immunoglobulin (IgG, IgM, IgA) synthesis in vitro by peripheral mononuclear cells stimulated with pokeweed mitogen was studied in adult patients with idiopathic thrombocytopenic purpura before and after high-dose intravenous intact gamma(gamma-)globulin therapy, at a daily dose of 0.4g/kg body weight for 5 consecutive days. A transient increase in platelet count which reached a peak on the 1st to 2nd days after the end of the therapy was observed in four of five patients. Immunoglobulin synthesis in vitro was suppressed remarkably following therapy in all cases: the mean reduction of IgG, IgM and IgA was 78, 66 and 48%, respectively. Titres of various autoantibodies, TGHA, MCHA, ANF and anti-DNA antibody, also decreased following therapy. In correspondence to this, phenotypic analysis in T cell subsets showed a decrease of OKT4+:OKT8+ ratio following therapy, without a change in the proportion of OKT3+ cells. These data indicate that the intravenous gamma-globulin preparations suppressed synthesis of antibodies non-specifically and caused a relative increase of OKT8+ suppressor T cells.

Adult↗
PubMed1983

Hairy cell leukemia: a report of 10 cases in Japan and characterization of anti-hairy cell sera.

A series of 10 cases of hairy cell leukemia (HCL) in native Japanese patients was studied. The clinicopathological features and the phenotype of the leukemic cells were compared with those of HCL in Western countries. The clinical pictures were similar to those in Western countries but some hematological findings were different. The Japanese patients had more marked leukocytosis, less granulocytopenia and thrombocytopenia, and no dry tap on bone marrow aspiration. The phenotype of hairy cells was much the same in both areas. Two kinds of anti-hairy cell sera were raised in rabbits. One (AHS 406) was obtained from rabbits immunized by injecting whole hairy cells. The other (alpha HC-G and alpha HC-M) was obtained by injection of membrane glycoproteins partially purified from hairy cells. The reactivity of the former antiserum (AHS 406) against leukemic cells from a variety of leukemias including HCL and B-cell chronic lymphocytic leukemia was studied by an immunoprecipitation technique. AHS 406 defined three cell surface antigens on HCL, P-30, P-35 and GP-135 (30,000, 35,000 and 135,000 daltons respectively). These three components are expressed only on neoplastic B lymphocytes. Quantitative differences in expression were observed in different types of leukemia, although all three antigens were most strongly expressed in HCL. alpha HC-G showed reactivity similar to that of OKIa-1. alpha HC-M reacted with hairy cells but not with other leukemic cells except mature granulocytes of chronic myelocytic leukemia. It also reacted with most granulocytes and a few mononuclear cells in normal peripheral blood. Preliminary immunochemical studies suggest that alpha HC-M reacts with a glycoprotein with a molecular weight of 26,000.

Adult↗
PubMedDate not supplied

Measurement of a newly developed thrombomodulin addition activated partial thromboplastin time assay in patients with deep venous thrombosis.

We developed a simple assay using rabbit thrombomodulin (TM) based on an activated partial thromboplastin time method, which detected the response to TM in plasma coagulation. We call it thrombomodulin addition clotting time (TACT). The anticoagulant response to TM was calculated by dividing the clotting time with TM by the clotting time with buffer solution. Results were expressed as TACT ratio, which indicates the degree of inhibition of plasma clotting by TM. Using this assay, we measured the TACT ratio in 80 patients with deep-vein thrombosis (DVT) and in 126 controls matched to the patients according to age and sex. A significant difference in the TACT ratio was observed between patients with DVT (mean 1.874) and controls (mean 1.956) (p < 0.001). Twenty- three patients (29%) had TACT ratios below the 10th percentile (1.757) of distribution of control subjects (odds ratio: 3.5; 95% confidence interval (CI): 1.7-7.2). After excluding subjects with a deficiency of protein C, protein S and antithrombin III, we found an odds ratio for DVT of 3.4 (95% CI: 1.6-7.2). These data suggest that natural anticoagulant deficiencies do not influence the TACT ratio, and our case-control study may show that the plasma of patients with DVT has a low response to TM.

Adolescent↗