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H Sawada

Publications and source records attributed to H Sawada.

At least 361 records · Page 20Linked to original sources
PubMed1989

[Identification and characterization of effector lymphocytes lysing autologous tumor cells].

Effector lymphocytes cytotoxic to autologous tumor cells consist of heterogeneous populations. In this communication, we have presented the results of experiments, in which these heterogeneous effector cells were classified based on their surface markers and modes of differentiation depending upon culture conditions. NK cells with a typical phenotype of CD2+ 3-16+ were one of major populations, which could respond to IL-2 and be differentiated into lymphokine activated killer (LAK) cells. LAK cells were also induced from a CD3+4-8- T cell subset by IL-2 stimulation. Effector cells with a phenotype of CD2+ 3-4-8-16-, which may belong to the T cells at early stages of differentiation, could also be induced by stimulation of immunoadjuvants. Finally, it was shown that the effector cells with a typical phenotype of cytotoxic T lymphocytes, CD3+4-8+16-, and a non-MHC-restricted cytotoxicity were induced by IL-2 in the tumor infiltrating lymphocytes.

Adjuvants, Immunologic↗
PubMed1989

Quick-freeze, deep-etch visualization of the nuclear pore complex.

We have visualized the nuclear pore complex (NPCx) three-dimensionally by quick-freeze, deep etching and suggest that NPCx is composed of four rings and associated filaments. The rings were located at the cytoplasmic side, at the nucleoplasmic side, and at the pore waist as well. Some of the filaments emanated toward the cytoplasm, some sprawled over the cytoplasmic face of the nuclear membrane, and some intervened the rings. The emanating filaments were considered to be vimentin filaments judging from the replica and thin-sectioned image.

Freeze Etching↗
PubMed1989

[A case of venous dural sinus thrombosis presenting dementia syndrome. An autopsy case].

We report clinical and pathological features of a case of dementia syndrome due to dural sinus thrombosis. In three years before admission, the patient, a 64-year old man, had had four convulsive attacks; scattered calcification shadows were disclosed by plain CT. Ten months before the admission, he complained of progressive memory disturbance and dyscalculia. General physical examination showed no remarkable abnormalities except for bruit at the left mastoid process. Although his time orientation was poor, he was otherwise fully awake. Neurologically, memory disturbance, finger agnosia, and dyscalculia were observed. Right Barré's sign, and exaggerated right patellar tendon reflex were observed. Plain X-ray CT revealed calcification-like, scattered high-density areas in the floor of the cerebral cortical sulci. Enhanced CT showed abnormal vessel high-density areas in both the cerebrum and brainstem. Cerebral angiography showed thrombosis of bilateral transverse sinuses, arterio-venous fistula in the left transverse sinus, and remarkably dilated cortical veins over both cerebral hemispheres. Positron emission tomography revealed misery perfusion areas in bilateral cerebral hemispheres. We presume that the mass effect of venous engorgement and chronic ischemia due to the arterio-venous fistula caused the dementia syndrome. These clinical manifestations were improved by amantadine and the patient was discharged. During follow-up, he died of subarachnoid hemorrhage, and an autopsy was performed. Pathological findings were as follows: 1) cortical and subcortical multiple-infarction in the cerebrum, 2) hematoma in the subarachnoid space, 3) venous dilatation of the cortical veins and pseudocalcification of their walls, and 4) thrombus in the transverse dural sinus.

Amantadine↗
PubMed1988

Subcellular distribution and properties of carbonyl reductase in guinea pig lung.

On subcellular fractionation, carbonyl reductase (EC 1.1.1.184) activity in guinea pig lung was found in the mitochondrial, microsomal, and cytosolic fractions; the specific activity in the mitochondrial fraction was more than five times higher than those in the microsomal and cytosolic fractions. Further separation of the mitochondrial fraction on a sucrose gradient revealed that about half of the reductase activity is localized in mitochondria and one-third in a peroxidase-rich fraction. Although carbonyl reductase in both the mitochondrial and microsomal fractions was solubilized effectively by mixing with 1% Triton X-100 and 1 M KCl, the enzyme activity in the mitochondrial fraction was more highly enhanced by the solubilization than was that in the microsomal fraction. Carbonyl reductases were purified to homogeneity from the mitochondrial, microsomal, and cytosolic fractions. The three enzymes were almost identical in catalytic, structural, and immunological properties. Carbonyl reductase, synthesized in a rabbit reticulocyte lysate cell-free system, was apparently the same in molecular size as the subunit of the mature enzyme purified from cytosol. These results indicate that the same enzyme species is localized in the three different subcellular compartments of lung.

Alcohol Oxidoreductases↗
PubMed1988

Kinetic mechanism of pulmonary carbonyl reductase.

The kinetic mechanism of guinea-pig lung carbonyl reductase was studied at pH 7 in the forward reaction with five carbonyl substrates and NAD(P)H and in the reverse reaction with propan-2-ol and NAD(P)+. In each case the enzyme mechanism was sequential, and product-inhibition studies were consistent with a di-iso ordered bi bi mechanism, in which NAD(P)H binds to the enzyme first and NAD(P)+ leaves last and the binding of cofactor induces isomerization. The kinetic and binding studies of the cofactors and several inhibitors such as pyrazole, benzoic acid, Cibacron Blue and benzamide indicate that the cofactor and Cibacron Blue bind to the free enzyme whereas the other inhibitors bind to the binary and/or ternary complexes.

1-Propanol↗
PubMed1988

Prerequisite for the induction of lymphokine-activated killer cells from T lymphocytes.

Human blood mononuclear cells were separated into Leu-11+7-NK, Leu-11-7+, and Leu-11-7-T cells by means of a combination of the Percoll gradient method and C-mediated cytolysis using mAb. When purified Leu-11+7-NK, Leu-11-7+, and Leu-11-7-T cells were cultured with rIL 2 (500 U/ml) for 6 days in a medium supplemented with 10% FCS, Leu-11+7-NK cells responded at the maximum level and Leu-11-7+ cells responded moderately as shown by both cell-proliferation response and cytotoxic activity generated. On the other hand, Leu-11-7-T cells did not respond at all to rIL-2. However, when Leu-11-7-T cells were cultured with rIL-2 in a medium supplemented with 10% autologous serum, they showed considerable responsiveness to rIL-2. In addition, much greater response to Leu-11-7-T cells were produced by the addition of monocytes. Monocyte cytokines, neither IL 1, IFN-gamma, TNF, nor their combination were able to substitute for monocytes in the induction culture. In contrast, the response level of Leu-11+7- NK cells remained unchanged irrespective of supplementation with autologous serum to medium or the addition of monocytes to the culture. These results indicated that culture conditions in the experiments significantly affected the results as to determination of lymphokine-activated killer cell precursors, especially the result pertaining to the conversion of T lymphocytes to lymphokine-activated killer cells. Under appropriate conditions, not only NK cells but also T cells are important precursors of lymphokine-activated killer cells.

Adult↗
PubMed1988

Mouse liver dihydrodiol dehydrogenases. Identity of the predominant and a minor form with 17 beta-hydroxysteroid dehydrogenase and aldehyde reductase.

A major and a minor form of dihydrodiol dehydrogenase were co-purified with 17 beta-hydroxysteroid dehydrogenase and aldehyde reductase, respectively, to apparent homogeneity from liver cytosol of male ddY mice. The activities of dihydrodiol dehydrogenase and testosterone dehydrogenase or aldehyde reductase of the two enzyme forms comigrated electrophoretically. The major form of the enzyme oxidized 17 beta-hydroxysteroids and nonsteroidal alicyclic alcohols and reduced 17-ketosteroids and various synthetic carbonyl compounds, showing higher affinity for steroids than for xenobiotics. The activity of this enzyme form toward benzene dihydrodiol and testosterone exhibited identical thermostability and susceptibility to inhibition by quercitrin, SH-reagents, nonsteroidal estrogens and anti-inflammatory agents. On the other hand, the minor form of the enzyme, which oxidized benzene dihydrodiol but not 17 beta-hydroxysteroids, also reduced various aldehydes well and was specifically inhibited by barbiturates and sorbinil. These results indicate that the major form of dihydrodiol dehydrogenase is identical to 17 beta-hydroxysteroid dehydrogenase and the minor enzyme form to aldehyde reductase.

Alcohol Dehydrogenase↗
PubMed1988

Evidence of intracellular and trans-acting differentiation-inducing activity in human promyelocytic leukemia HL-60 cells: its possible involvement in process of cell differentiation from a commitment step to a phenotype-expression step.

We previously reported that human promyelocytic leukemia HL-60 cells, when treated with various inducers in magnesium-deficient medium, became committed to differentiate but did not express the differentiation-related phenotypes (Okazaki et al., J. Cell. Physiol., 131:50-57, 1987). In the present study we demonstrated the existence of an intracellular differentiation-inducing activity (int-DIA) in differentiation-committed phenotype-nonexpressing HL-60 cells by using cybrid formation between untreated HL-60 cells and cytoplasts from HL-60 cells treated in magnesium-deficient medium with 100 nM 1 alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3). Cell extracts from similarly treated HL-60 cells also showed int-DIA, which when added (10 mg total protein/ml) to culture of untreated HL-60 cells, could increase the percentages of nitroblue tetrazolium (NBT)- and nonspecific esterase (NSE)-positive cells from 1% to 53%, and from 0 to 32%, respectively. They also induced differentiation of human monoblastic leukemia U-937 cells and of human myeloblastic leukemia KG-1 cells but not of erythroleukemia K-562 cells. These results suggested that the int-DIA had a common effect on differentiation induction in several human myeloid cell lines and may be involved in inducing cells to proceed from a commitment to a phenotype-expression step during human myeloid cell differentiation.

Calcitriol↗
PubMed1988

MR imaging of syringobulbia with giant syrinx.

Syringobulbia with a large syrinx was revealed by MR imaging. The syrinx extended from the medulla to vertebral level T10. We suspect that this giant syrinx may be produced by a congenital meningioma at C7, generating pulsatile flow in the original syrinx and causing a giant syrinx.

Aged↗
PubMed1988

Establishment of a hemopoietic stimulating factor producing murine leukemia cell lines: pathogenesis of granulocytosis in L8313 bearing mice.

Thy 1.2+ cells of L8313 leukemia bearing mice were previously shown to produce granulocyte macrophage colony stimulating activity (GM-CSA) and interleukin-3 (IL-3). Cell lines with the Thy 1.2+ phenotype were established from spleen cells of the leukemic mice, and were designated STIL-3 C5 and STIL-3 D10. They produced and released GM-CSA and IL-3 activities in culture supernatant. C5 cells were phenotypically Thy 1.2+ and Lyt 2.1+ with rearrangement of the T-cell receptor beta chain gene also being identified. D10 was Thy 1.2+ and L3T4+ with T-cell receptor beta chain gene rearrangement not detectable. Since the same sized rearranged bands were observed between C5 and L8313 leukemic mouse spleen cells, it is indicated that C5 cells are derived from the leukemic cells. Inoculation of these cells into mice induced granulocytosis. These results indicated that L8313, which was thought to be a "granulocytic leukemia", is actually a T-cell leukemia, whose granulocytosis is a leukemoid reaction induced by normal hemopoietic cells responding to the hemopoietic stimulating factors, GM-CSA and IL-3, produced by the leukemic T cells. Thus, L8313 should be known as a T-cell leukemia associated with granulocytosis.

Animals↗
PubMed1988

Establishment and characterization of a transplantable erythroblastic leukemia in C3H mice.

A disease with the characteristics of an erythroblastic leukemia was induced by X-ray irradiation of 300 Rads in C3H mice. The leukemia is transplantable in syngeneic mice by i.v. injection of the spleen cells. The mice show almost pure erythroid cells of various differentiation stages in peripheral blood. The number of total nucleated cells in the peripheral blood increased, but hematocrit and platelet number decreased. Reverse transcriptase activities were measured in spleen and liver of the mice and the data suggested that the leukemia was not induced by retrovirus infection. This leukemia is distinguishable, in this respect, from diseases reported by Friend or Rauscher. The leukemia will offer a good animal model for the studies on non-viral leukemogenesis and disorders of erythropoiesis.

Animals↗
PubMed1988

Purification and characterization of NADP+-dependent 3 alpha-hydroxysteroid dehydrogenase from mouse liver cytosol.

A monomeric 3 alpha-hydroxysteroid dehydrogenase with a molecular weight of 34,000 was purified to apparent homogeneity from mouse liver cytosol. The enzyme catalyzed the reversible oxidation of the 3 alpha-hydroxy group of C19-, C21-, and C24-steroids, reduced a variety of carbonyl compounds, and was inhibited by SH-reagents, synthetic estrogens, anti-inflammatory drugs, prostaglandins, and delta 4-3-ketosteroids. Although these properties are similar to those of the enzyme from rat liver cytosol, the mouse enzyme exhibited low dehydrogenase activity toward benzene dihydrodiol and some alicyclic alcohols, it showed a strict cofactor specificity for NADP(H), and high substrate inhibition was observed in the reverse reaction. In addition, dexamethasone, deoxycorticosterone, and medroxyprogesterone acetate inhibited the mouse enzyme competitively at low concentrations and noncompetitively at high concentrations, whereas hexestrol, indomethacin, and prostaglandin A1 were competitive inhibitors. Steady-state kinetic measurements in both directions indicated that the reaction proceeds through an ordered bi bi mechanism with the cofactors binding to the free enzyme. The 3-ketosteroid substrates inhibited the enzyme uncompetitively at elevated concentrations, suggesting that the substrates bind to the enzyme.NADPH complex and to the enzyme NADP+ complex.

3-Hydroxysteroid Dehydrogenases↗
PubMed1988

Extensible and less-extensible domains of connectin filaments in stretched vertebrate skeletal muscle sarcomeres as detected by immunofluorescence and immunoelectron microscopy using monoclonal antibodies.

Two kinds of monoclonal antibodies (3B9 and SM1) against connectin, muscle elastic protein, reacted with both alpha- and beta-connectins. Immunofluorescence studies revealed that 3B9 stained both edges of the A band of chicken breast muscle myofibrils and remained as such upon stretching to a sarcomere length of 3.5 microns. On the other hand, SM1 stained the I band very close to the edges of the A band and the SM1-stained stripes moved considerably upon stretching to a sarcomere length of 3.5 microns. Immunoelectron microscopic observations with frog semitendinosus muscle revealed that three distinct stripes bound with 3B9 in the edges of the A band did not move on stretching up to 3.5 microns. On the other hand, the two stripes stained with SM1 in the I band clearly moved to the same extent as the stretching. However, when a sarcomere was stretched to 4.0 microns, all the stripes with 3B9 or SM1 disappeared and diffused deposits of the antibodies were observed. Thus it is concluded that connectin filaments in the I band region are more extensible than those at both edges of the A band.

Animals↗
PubMed1988

Genomic comparison of adenovirus type 3 isolates from patients with acute conjunctivitis in Japan, Australia, and the Philippines.

A total of 53 Ad3 isolates obtained from patients with acute conjunctivitis in Japan, Australia, and the Philippines during 1973 to 1986 were analyzed for their genome types with 4 restriction endonucleases, BamHI, BglII, HindIII, and SmaI. Two new genome types designated tentatively as Ad3f and Ad3g were identified by combination of BamHI and BglII in the isolates. The changes of restriction sites and sizes of restriction fragments in newly recognized Ad3f and Ad3g were located at the similar regions reported in other Ad3 genome types by O'Donnell et al (1986) on physical maps of the Ad3 prototype strain GB genome. In Japan, 46 Ad3 isolates obtained from 1983 to 1986 were either Ad3f or Ad3g. Yearly alternation of predominance of both genome types were observed in the northern part of Japan during the period. In Australia, two genome types Ad3p and Ad3f were found in 6 isolates, and the former was observed in the 3 isolates obtained before 1981 and the remaining 3 isolates were obtained after 1983. In the Philippines, the only isolate obtained in 1984 was Ad3p.

Adenoviridae Infections↗