[Liver disease and DIC].
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Blood Coagulation Factors↗
Biomedical subjects
K Ando
Publications and source records attributed to K Ando.
[AIDS and neurological manifestations].
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Acquired Immunodeficiency Syndrome↗
[Combination therapy of local administration of OK-432 and radiation on a murine fibrosarcoma (NFSa)--combination effect and histological examination].
The combined effect of radiation with local administration of OK-432 was studied using natural fibrosarcoma (NFSa) of C3H mice that are less immunogenic and resistant to radiation (TCD 50, 83, 15 Gy). When 2KE of OK-432 was administered together with 1 X 10(6) tumor cells, tumor survival was inhibited in 7/8 (87.5%) of mice. Single local administration of OK-432 (2KE, 4KE, 8KE) showed hardly any effect on tumor survival. Combined treatment of 2KE of OK-432 and 4-Gy radiation, however, not only controlled tumor growth but also eradicated 1/5 (20%) of them, compared with single application of 45-Gy radiation. OK-432 worked most effectively when administered just before or after the application of X-rays. The optimum dose of OK-432 was studied by administering 2KE, 4KE and 8KE of the agent together with the application of 55-Gy radiation. 8KE groups showed the best eradication rate but 4KE groups showed the best cure rate. Therefore, the optimum dose was considered to be between 4KE and 8KE. With regard to histological effects, both the single radiation treatment and its combined treatment with OK-432 were most effective on the 6th day. The degree of degeneration and necrosis of tumor cells together with lymphocyte exudation were much higher in the combined treatment than in single radiation application.
Animals↗
A case of neurilemmoma originated from intercostal nerve.
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Adult↗
Depression of afferent arc of the in vivo cytotoxic T-cell immunity by bacterial lipopolysaccharides.
The afferent arc of the in vivo cytotoxic T-cell immunity assessed by second set rejection of ascitic allogeneic tumors was shown to be depressed by bacterial lipopolysaccharide (LPS) that was administered simultaneously with or 1 day before injection of allogeneic spleen cells as stimulators. Two different LPSs from Escherichia coli O55 and Klebsiella O3 displayed similar activities whereas dextran sulfate, concanavalin A, or poly A:U was not effective. Stimulator activities of allogeneic cells was not directly modified by LPS. Any definite suppressor activity on afferent or efferent arc of the T-cell response was not demonstrable in mice receiving LPS and allogeneic cells. Further, the LPS effect for immune depression was not diminished by whole body X-ray irradiation to the recipient at 300 R, which ablated the B-cell reactivity to LPS for polyclonal activation, or by treatment of the recipient with carrageenan, a known toxic agent to macrophages. It was suggested from these results that LPS suppresses the cytotoxic T-cell immunity by modulating responder T cells to be temporarily refractory to the allogeneic stimulus rather than by activating suppressor cells such as radiation-sensitive lymphocytes and carrageenan-sensitive macrophages.
Animals↗
Cellular vitamin A-binding proteins in liver tumors and adjacent tissues.
The levels of cellular retinol-binding protein (CRBP) and retinoic acid-binding protein (CRABP) were assessed in surgically resected ten human liver tumors and their adjacent tissues by sucrose density gradient centrifugation and Scatchard analysis. The tissues adjacent to hepatocellular carcinomas usually showed portal cirrhosis or hepatitis. There was no significant difference in the dissociation constant (Kd) values of binding proteins of CRBP or CRABP between tumors and adjacent tissues. Five of the ten liver tumors showed similar levels of CRBP as in their adjacent tissues whereas three of the ten liver tumors showed about 40% or less contents of CRBP in comparison with their adjacent tissues and two others had no CRBP activity. By contrast, CRABP activities were found in five liver tumors and in adjacent tissues of one case, whereas there were no detectable CRABP activities in the adjacent tissues except in one case.
Adult↗
Modification of fatty acid composition in adipocyte plasma membranes by an oral treatment with a new antidiabetic agent, AS-6, in genetically obese diabetic mice, db/db.
Male 12-week-old C57BL/KsJ db/db mice were treated for 1 week with a dietary admixture of an experimental antidiabetic agent, AS-6 (4-O-carboxymethylascochlorin, 0.1%). The fatty acid composition of the adipose tissue and its plasma membranes in the treated mice was compared with that in untreated db/db mice and their lean littermates. The results indicate that, when compared with the lean, the db/db adipose tissue and its plasma membrane are extremely rich in nonessential fatty acids, and AS-6 treatment modifies the fatty acyl composition only in the membranes in which 16:1 and 18:1 increase and C18 decreases.
Adipose Tissue↗
[Relative biological effectiveness of the therapeutic proton beams at NIRS and Tsukuba University].
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Animals↗
Treatment with an ascochlorin derivative, AS-6 increases 45Ca2+ binding on the plasma membrane of adipocytes in db/db mice.
Genetically obese diabetic mice (db/db) have greatly diminished 45Ca2+ binding on the plasma membranes of the adipocytes (45-55%) compared with their lean littermates. Treatment for 1 week with a diet admixture of AS-6 (0.1% in the diet) significantly restored the binding to a level comparable to the lean littermates. The addition of AS-6 in vitro had no effect on the binding, which eliminates the possibility that AS-6 is a Ca2+ ionophore. The results suggest that AS-6 treatment enhances the Ca2+ binding by causing structural alteration(s) in the membranes.
Adipose Tissue↗
Effect of oral treatment with a new hypoglycemic agent, AS-6, on the metabolic activities of adipocytes in db/db mice: a comparative study.
The mechanism of a new hypoglycemic agent, AS-6, was comparatively studied using the adipocytes from AS-6 treated and untreated genetically obese diabetic mice, db/db. the db/db mice were treated for 1 week with a diet admixture of AS-6 (0.1%). The treatment resulted in the following alterations in metabolic activities; AS-6 treatment increased 125I-insulin binding by 1.4-3.3 fold over the insulin range of 1-1000 microU/ml, the treatment increased the basal activities in 2-deoxyglucose uptake, and in CO2 generation and lipogenesis from U-(14C)-glucose compared with the db/db controls, the treatment partially restored insulin responsiveness in 2-DG uptake and CO2 generation, and 1 mU/ml of insulin greatly stimulated lipogenesis by 5.6 fold above the basal in the control adipocytes while AS-6 treatment changed the lipogenic response less stimulative to the insulin. The results suggest that AS-6 treatment significantly increases insulin binding to the adipocytes associating with an enhancement in glucose metabolism under basal and physiological concentrations of insulin.
Adipose Tissue↗
Idiopathic dystonia-parkinsonism with marked diurnal fluctuation of symptoms.
Studies were performed on 5 patients with idiopathic dystonia-parkinsonism, each of whom had minor dystonic movements and parkinsonian symptoms with marked diurnal fluctuation. Levels of homovanillic acid and 5-hydroxyindoleacetic acid were not different from those in controls. Considerable improvement in dystonic movements and parkinsonian symptoms was obtained with a small dose of L-dopa, trihexyphenidyl hydrochloride, amantadine, or bromocriptine hydrochloride. Electrophysiological investigation confirmed that the dystonic movements, which became remarkably worsened on attempted movement, contributed importantly to the diurnal fluctuation of symptoms.
Adult↗
Genetic and stimulatory cell type requirements for inducing class I major histocompatibility complex alloantigen-specific in vivo cytotoxic T cell immunity.
Current interpretation based on analytical in vitro works that actions of Ia antigens and accessory cells such as macrophages and dendritic cells are crucial for inducing cytotoxic T cell responses to class I major histocompatibility complex (MHC) alloantigens has been challenged by experiments performed in a newly developed system handling in vivo cytotoxic T cell immunity. We first characterized the transplantation immunity for second-set rejection of ascitic tumor allografts as principally induced by allogeneic stimulator cells via direct pathway, and as exclusively mediated by class I MHC alloantigen-specific in vivo cytotoxic T cell activity. By comparison of activities of limiting effective doses (10(4)-10(5) cells per mouse) of various stimulator cells in this defined system, we could demonstrate that genetic disparity at the D region of H-2 to the recipient is just enough for inducing the immunity, and presence of allogeneic or syngeneic Ia antigens in addition to H-2D alloantigens on stimulator cells does not give any premium effect. Further study revealed that allogeneic peritoneal cells rich in macrophages or glass-adherent spleen cells enriched for dendritic cells are not stronger stimulators than allogeneic adherent cell-depleted spleen cells and semi-allogeneic thymocytes. These results fit with the alternative concept that the physiological pathway inducing in vivo cytotoxic T cell immunity for graft rejection entirely depends on class I MHC antigens on live lymphocytes as self-supported stimulators, and does not crucially involve additional stimulator activities of Ia antigens and special accessory cell types, which must be in vivo concerned with induction of other types of transplantation immunity.
Animals↗
Concentrations of immunoreactive thyrotropin-releasing hormone in the brain of patients with olivoponto-cerebellar atrophy.
The concentrations of immunoreactive thyrotropin-releasing hormone (ir-TRH) in the brain of patients with olivoponto-cerebellar atrophy (OPCA) were studied. Three patients with OPCA and 8 non-central nervous system degenerative diseases were subjects in this study. Ir-TRH concentration in the brain was measured by radioimmunoassay. Ir-TRH was present in all parts of the dissected brain tissues (hypothalamus, frontal lobe, cerebellar cortex, olivary n., dentate n. and caudate n.) of patients with OPCA and non-central nervous system degenerative diseases. Ir-TRH concentration in the brain of case 1 and 2 was lower in the cerebellar cortex and olivary n., in contrast, ir-TRH concentration in case 3 was higher in the dentate n. The regions and the severity of pathological changes were different in each case of OPCA and changes in ir-TRH concentration in the brain did not always correlate with the severity of pathological changes. These findings suggest that changes in ir-TRH concentration in the brain of patients with OPCA may differ in each case, and may play some pathophysiological role in OPCA.
Adult↗
Sensitivity changes to dopaminergic agents in fine motor control of rhesus monkeys after repeated methamphetamine administration.
Long-term behavioral and neurochemical effects of repeated methamphetamine (MA) administration were investigated in rhesus monkeys trained to perform a fine motor task requiring control of exerted force for a specified time. Rhesus monkeys were trained to extend their arms into a tube to press a lever with a force between 25 and 40 g for 5 sec in order to receive 1.5 ml of water. The effects of intramuscular administration of MA, apomorphine (APO) and haloperidol (HAL) on responding were compared before and after a 2-week period of repeated MA administration. During this period, MA was given in 4 divided doses starting at a total daily dose of 4 mg/kg/day and increasing to 40 mg/kg/day. Tolerance to MA, increased sensitivity to HAL and no consistent sensitivity change to APO were observed when dose-response functions were redetermined starting 1 month after the repeated MA administration. One month after these determinations were completed, the brains of the monkeys were analyzed for changes in monoamines. Significant depletions of dopamine in the caudate nucleus and serotonin in the frontal cortex were seen. It is hypothesized that the sensitivity changes to the drugs on performance were related to the dopamine depletion.
Animals↗
Ontogeny of the transplantation immunity of mice for rejecting ascitic allogeneic tumors.
Ontogeny of the murine transplantation immunity for rejecting ascitic allogeneic tumors (chemically-induced RG lymphoma and L1210 leukemia) as a model of in vivo cytotoxic T cell immunity was studied. Challenge by 10(6) to 10(7) allogeneic tumor cells per 20 g body weight (b.w.) of the mouse was fatal to 1-3 day-old mice, whereas 7-30 day-old mice rejected the tumor. In newborn mice however some yet undetermined mechanism worked to temporally depress the initial tumor growth. Injection of low (10(6) cells per 20 g b.w.) to moderate (10(7)) doses of semiallogeneic spleen cells into newborn mice prepared for second set rejection of the tumor carrying the same alloantigens as the spleen cells, although injection of high dose (3 X 10(8)) cells reduced the tumor rejecting immunity. This second set rejection occurred even against the allogeneic tumor inoculated as early as 3 days old, if the mice had been primed with the alloantigens at birth. It appears therefore that newborn and early suckling mice are protected from tumor invasion by cytotoxic immunity more powerfully than expected from earlier in vitro works.
Age Factors↗
Direct activation of Sendai virus (HVJ)-specific cell-mediated immunity of mice for second set rejection of the virus-infected syngeneic tumor by noninfectious virus-sensitized spleen cells.
Syngeneic spleen cells (SPC) sensitized in vitro with noninfectious NVJ were shown to effectively stimulate mice to generate the HVJ-specific cell-mediated immunity for second set rejection (SSR) of virus-infected syngeneic leukemia cells. As few as 10(4) live but not disrupted SPC either infected with a temperature-sensitive mutant of HVJ (HVJts) or sensitized passively with ultraviolet (UV)-inactivated HVJts were active as immunogen. Syngeneic SPC as the carrier of virus could be replaced by allogeneic SPC or L cells, a fibroblast cell line, without reduction of the immunogenicity. Further study demonstrated that a special density of antigen on the surface of HVJts-sensitized SPC is required for high immunogenicity. It was suggested that live cells appropriately sensitized with noninfectious virus would serve as an excellent vaccine for virus-specific cell-mediated immunity.
Animals↗
The relationship between lung colony and in situ assays.
The relationship between three different assays: tumor control, tumor growth delay and lung colony formation, was examined after fast neutron and gamma ray irradiations. Fibrosarcomas (NFSa) in syngeneic C3Hf mice were irradiated locally with 60Co gamma rays, fast neutrons or mixed beams (gamma rays and fast neutrons). A comparison between the lung colony assay and the TRT50 (50% tumor growth delay time) assay when cells were exposed to single doses of fast neutrons or gamma rays, resulted in identical growth delay times. The fraction of cells surviving a single dose of fast neutrons, was 10 times higher than the surviving fraction of cells after a single dose of gamma rays. Both doses resulted in the same tumor control probability (TCD50 assay). Neither repair of potentially lethal damage nor tumor bed effect was sufficient to explain the difference between cell survival and tumor control probability. The surviving fraction of cells following fractionated irradiations of gamma rays and fast neutrons were identical at 50% tumor control probabilities.
Animals↗
A new beta-naphthylamide substrate of p-guanidino-L-phenylalanine for trypsin and related enzymes.
N alpha-Benzyloxycarbonyl-p-guanidino-L-phenylalanine beta-naphthylamide (Z-GPA-beta NA) was synthesized and the susceptibility of this compound to trypsin and related enzymes was compared with that of N alpha-benzyloxycarbonyl-L-arginine beta-naphthylamide (Z-Arg-beta NA). Both Z-GPA-beta NA and Z-Arg-beta NA were rapidly and almost completely hydrolyzed by trypsin and pronase. Z-Arg-beta NA was hydrolyzed slowly by thrombin, while Z-GPA-beta NA was not susceptible to this enzyme at all. The rate of hydrolysis of Z-GPA-beta NA by papain was slower than that of Z-Arg-beta NA. Neither beta-naphthylamide substrate was hydrolyzed by alpha-chymotrypsin. The specificity constant (kcat/Km) for the hydrolysis of Z-GPA-beta NA by trypsin was somewhat larger than that for the hydrolysis of Z-Arg-beta NA. Contributions of the benzene ring in the side chain of Z-GPA-beta NA to good binding of this substrate to the specificity site of this enzyme and to the poor fit of the scissile bond in the substrate molecule to the active serine residue are presumed from comparison of the individual kinetic parameters (Km and kcat) for the two beta-naphthylamide substrates. Z-GPA-beta NA was ascertained to be a useful substrate in the study of the binding and catalytic specificities of various trypsin-like enzymes.
Benzoylarginine-2-Naphthylamide↗