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Biomedical subjects

A Ohsaka

Publications and source records attributed to A Ohsaka.

At least 55 records · Page 3Linked to original sources
PubMed1989

In vivo activation of human neutrophil functions by administration of recombinant human granulocyte colony-stimulating factor in patients with malignant lymphoma.

Recombinant human granulocyte colony-stimulating factor (rhG-CSF) was administered (50 to 800 micrograms/m2) once daily as a half-hour intravenous (IV) infusion for 14 days to seven patients with malignant lymphoma. In all patients, administration of rhG-CSF not only ameliorated the decrease in absolute neutrophil count after the cytotoxic chemotherapy but also enhanced superoxide (O2-) release in neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP). The priming effect of rhG-CSF on neutrophil O2- release was rapid (evident within 6.5 hours) and sustained at least for 24 hours after a single IV administration of rhG-CSF. The responsiveness to further in vitro challenge of rhG-CSF was lost or reduced in neutrophils isolated after rhG-CSF treatment, indicating that neutrophils already primed in vivo by rhG-CSF are desensitized to this factor. In contrast to the results obtained with FMLP, when phorbol myristate acetate (PMA) was used as stimulus, no consistent enhancement of O2- release was observed, suggesting that rhG-CSF modulates the signal transduction pathways linked to FMLP receptors rather than increases the components of the O2- producing enzyme complexes. Administration of rhG-CSF also rapidly (evident within 15 minutes) caused an increase in expression of neutrophil C3bi-receptors that was sustained for at least 24 hours after a single IV administration of rhG-CSF. Pharmacokinetic study of rhG-CSF showed a half-life (t1/2) of 114 min. These findings show that rhG-CSF is a potent activator for neutrophil functions both in vivo and in vitro.

Aged↗
PubMed1989

[Germ-line configuration of the immunoglobulin heavy chain gene in a case of B cell precursor acute lymphoblastic leukemia].

A 20-year-old man was admitted to our hospital because of fever and knee joint pain on March 20, 1986. Physical examination revealed generalized lymphadenopathy and hepatomegaly. White blood cell count was 32,800 microliters with 74.4% blast cells. Bone marrow was hypercellular with 93.6% blast cells. Blast cells were weakly positive for acid phosphatase and PAS stainings but were negative for peroxidase, sudan black B and esterase stainings. Cell surface marker analysis of blast cells disclosed that they were positive for anti-HLA-DR, CD19, CD24, CD33 and CD38, but were negative for CD10 and CD20. Cytoplasmic immunoglobulin of blast cells was negative and TdT activity by immunofluorescent method was positive. Chromosomal analysis of bone marrow samples revealed normal karyotype. Therefore, this case was diagnosed as having acute lymphoblastic leukemia (L2) and achieved complete remission with LVP therapy consisting of 1-asparaginase, vincristine and prednisolone. Gene analysis of blast cells disclosed germ-line configuration of both the immunoglobulin heavy chain gene and T cell receptor beta chain gene. We speculated that the phenotype of leukemic cells might precede the genotype in some cases of acute leukemia.

Acute Disease↗
PubMed1989

13C-NMR spectroscopic studies on the glucose metabolism of Angiostrongylus cantonesis' eggs with special reference to the end-products and metabolic pathway.

13C-nuclear magnetic resonance (NMR) spectroscopy was used to identify metabolites excreted by Angiostrongylus cantonensis eggs which had been maintained aerobically in the presence of D-[13C6] glucose. Using 13C-NMR we proved that lactate, acetate and alanine originated from glucose present in the medium via glycolysis. Aminooxyacetate, an inhibitor of alanine transferase, inhibited simultaneously alanine production and the ability to take up glutamate, aspartate and valine from the medium. In addition, we demonstrated that these amino acids can serve as amino group donors of the pyruvate to alanine transamination system in the eggs.

Amino Acids↗
PubMed1989

Glucose metabolism of adult Schistosoma japonicum as revealed by nuclear magnetic resonance spectroscopy with D-[13C6]glucose.

Excretory end-products of adult Schistosoma japonicum, fed D-[13C6]glucose in vitro under aerobic and anaerobic conditions, were studied using 1H- and 13C-nuclear magnetic resonance (NMR) spectroscopy. The glucose in the medium is degraded to produce lactate and alanine aerobically and succinate and acetate as well as lactate and alanine anaerobically. Succinate and acetate have not been previously recorded as excretory products resulting from the metabolism of glucose for schistosomes. The presence of [13C3] and [2,3-13C2]lactate, and [1,2,2'-13C3] and [2,2'-13C2]succinate as end-products suggests that a partial reversed tricarboxylic acid (TCA) cycle is active in adult Schistosoma japonicum under anaerobic conditions. The physiological role of this pathway in adult schistosomes remains obscure.

Acetates↗
PubMed1989

A transient hemolytic reaction and stomatocytosis following vinca alkaloid administration.

We analyzed hemolytic reaction following vinca alkaloid administration in patients with acute lymphoblastic leukemia, blast crisis of chronic myelogenous leukemia and malignant lymphoma in the leukemic phase. During the course of chemotherapy in which vinca alkaloids were included, indirect-form dominant hyperbilirubinemia was observed in 21 of the 31 evaluable patients. In 8 patients with hyperbilirubinemia, reticulocytosis coincided with vinca alkaloid administration. Peripheral blood films showed prominent anisocytosis in 4 patients and increased stomatocytes in 10 patients. Red cell membrane studies in patients with hemolysis revealed increased sodium transport and increased activity of Na+, K+-ATPase. These findings were considered to represent the abnormal membrane "leakiness". Thus, vinca alkaloids might induce erythrocytotoxicity, which leads to acquired stomatocytosis with hemolysis in some patients.

Adult↗
PubMed1989

Transformed malignant lymphoma from Lennert's lesion is a CD4+ T cell lymphoma: an immunohistochemical study.

We describe a case of Lennert's lesion terminating in T cell non-Hodgkin's lymphoma (NHL). A 53-year-old woman showed inguinal lymphadenopathy. This was histologically interpreted as toxoplasmic lymphadenitis. However, Lennert's lesion was diagnosed in subsequent biopsies. Because additional lymphadenopathy and constitutional symptoms were absent, anti-neoplastic therapy was not given. During the five and a half years after the initial biopsy, generalized lymphadenopathy and constitutional symptoms developed. Histological examination of the cervical lymph node disclosed NHL, diffuse, large cell type. Transformed lymphoma cells were confirmed to be of peripheral T cell origin with a helper/inducer phenotype. We speculate that some cases of Lennert's lesion have a potentiality of spontaneous transformation into high grade malignant lymphoma associated with disappearance of epithelioid histiocytes.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1988

Phorbol myristate acetate potentiates superoxide release and membrane depolarization without affecting an increase in cytoplasmic free calcium in human granulocytes stimulated by the chemotactic peptide, lectins and the calcium ionophore.

We investigated the inter-relationships of superoxide (O2-) release, membrane depolarization and an increase in cytoplasmic free Ca2+, [Ca2+]i, in human granulocytes stimulated by various agonists. When concanavalin A or the Ca2+ ionophore ionomycin was used as stimulus, an increase in [Ca2+]i clearly preceded the onset of membrane depolarization, which was followed by O2- release. On the other hand, when N-formylmethionylleucylphenylalanine or wheat-germ agglutinin was used as stimulus, no demonstrable lag was seen in any of the responses. O2- release and membrane depolarization stimulated by all these agonists were markedly potentiated in parallel by pretreatment of cells with a low concentration of phorbol myristate acetate (0.25 ng/ml), whereas an increase in [Ca2+]i was not affected or minimally potentiated. The lag time between addition of the stimulus (concanavalin A or ionomycin) and onset of membrane depolarization or O2- release was significantly reduced by pretreatment of cells with phorbol myristate acetate, whereas the lag time between addition of concanavalin A and onset of the increase in [Ca2+]i was not affected. The dose-response curves for triggering of O2- release and membrane depolarization by each of receptor-mediated agonists in phorbol myristate acetate-pretreated or control cells were identical. These findings suggest that; (a) an increase in [Ca2+]i stimulates membrane depolarization indirectly; (b) a low concentration of phorbol myristate acetate potentiates membrane depolarization and O2- release by acting primarily at the post-receptor level, in particular, at the level distal to an increase in [Ca2+]i, but not by augmenting an increase in [Ca2+]i; and (c) the system provoking membrane depolarization and the system activating NADPH oxidase share a common pathway, which may be susceptible to a low concentration of phorbol myristate acetate.

Calcium↗
PubMed1988

1H- and 13C-NMR spectroscopic study of the metabolites in young adult Angiostrongylus cantonensis maintained in vitro.

1H- and 13C-nuclear magnetic resonance (NMR) spectroscopy were used to study metabolites excreted by young adult Angiostrongylus cantonensis maintained aerobically in the presence of D-[13C6]glucose. End-products of glucose metabolism identified and quantitated by means of 1H-NMR were lactate, acetate and alanine, in the molar ratio of 1:0.13:0.05 for males and 1:0.07:0.04 for females. 13C-NMR analyses proved that all the three products originated from the glucose present in the medium.

Acetates↗
PubMed1988

The respiratory burst of granulocytes: modulation by inflammatory mediators and its mechanism.

Prior exposure of granulocytes to inflammatory mediators such as chemotactic factors, colony-stimulating factors and tumor necrosis factor primes the cells for enhanced activity of the respiratory burst, which appears not only to play an essential role in the increased host-defenses against invading microorganisms but also to be responsible for tissue damage at the inflammatory sites. The molecular basis for this priming is presently under investigation. Changes in one or more of the signal transduction events may lead to more efficient stimulation of the NADPH oxidase responsible for the respiratory burst. The mechanisms of priming appear to be different according to the priming stimuli: the chemotactic peptide and the Ca2+ ionophore may prime the cells by causing an increase in cytoplasmic free Ca2+; phorbol esters by activating protein kinase C; and colony-stimulating factors and tumor necrosis factor by activating the distinct mechanism, which is independent of an increase in cytoplasmic free Ca2+ and activation of protein kinase C.

Animals↗
PubMed1987

In vitro study of the binding of terbium to tryptophan by 1H-NMR and fluorescence spectroscopy.

Terbium (Tb), a rare earth element having an ionic radius similar to that of Ca2+, is used as an antagonist of Ca2+. Recently, we found that when giant axon membrane of a loligo treated with Tb was excited at 290 nm, where tryptophan (Trp) gives absorption mechanism, emits fluorescence of Tb at 490 nm and 545 nm in addition to that of Trp at 345 nm. The present study was undertaken to locate on the Trp molecule the interaction between Trp and Tb by carrying out in vitro binding experiments with Tb and Trp and the molecular mechanism was analyzed by 1H-NMR spectroscopy and fluorescence spectroscopy. Fluorescence spectroscopy showed that Tb and Trp are combined at a molecular ratio close to 1:1. 1H-NMR spectroscopy revealed that Tb interacts with the amino group at the alpha-position and the imido group of the indole ring of Trp. Since all amino groups of Trp are involved in peptide linkages in vivo, it seems likely that the binding of Tb to Trp is undertaken by the imido group of the indole ring.

Hydrogen↗
PubMed1987

Cerebral metabolism in brain tumor of mice studied by in vivo 31P-NMR spectroscopy.

We now report a mouse model system of brain tumor for 31P-NMR spectroscopic study of in vivo cerebral metabolism. In vivo 31P-NMR (109 MHz) spectra were taken on the 9th day by the Faraday shield method of the brain of mice (3-week-old) transplanted intracerebrally with mKS X A tumor cells. In tumor-bearing mice, the amount of creatine phosphate decreased markedly and that of inorganic phosphate plus sugar phosphate increased accordingly. Furthermore, the broadening and splitting of individual signals were also noted with tumor-bearing mice; this is interpreted as indicating a variety of changes in chemical shift occurring in the brain of the animals due to heterogeneous distribution of pH. Binding or detaching of divalent cations to and from phosphometabolites may also be responsible for these changes.

Adenosine Triphosphate↗