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Biomedical subjects

K Saigo

Publications and source records attributed to K Saigo.

At least 127 records · Page 7Linked to original sources
PubMed1990

Inhibitory effect of chlorpromazine on rat reproduction: a test of administration for nine weeks before breeding.

The effect of chlorpromazine (CPZ) administration prior to insemination on reproduction was studied using male and female Sprague-Dawley strain rats evaluated over three generations. CPZ in doses of 12.5, 25, 50, and 100 mg/kg was administered to both male and female rats orally every day for 9 weeks before mating with the following results: 1) The duration of the estrous cycle was prolonged in the F0 females. 2) The incidence of insemination and pregnancy of the F0 males and females as well as the number of surviving fetuses and newborns showed a tendency to decrease. 3) The body weight of the rats in F0 and F1 generations decreased depending on the dose of CPZ, but the body weight of the F2 generation increased. 4) The wet weight of the major organs of the rats in F0 and F1 generations was affected by administration of CPZ at 100 mg/kg. The weights of the liver, kidney, adrenal, pituitary, testis, and prostate glands in males and the kidney, adrenal gland, and ovary in females were increased, whereas the weights of the pituitary and the uterus were decreased in females. These results suggest that premating administration of CPZ to the parent rats exerts influence on the reproduction of the F0 and F1 generations.

Animals↗
PubMed1990

[Histidine-rich glycoprotein in blood during inflammation, surgical operation or hemodialysis].

Serum or plasma histidine-rich glycoprotein (HRGP) levels were determined in several conditions. In normal volunteers, HRGP levels did not correlate with either plasminogen contents or plasminogen activity, although HRGP has been believed to be a modulator for fibrinolysis system. In acute inflammation, HRGP levels in serum changed as a negative acute phase reactant, which was also confirmed after surgical operation. At the time of demonstrating decreased HRGP values, expression of HRGP fragment was studied using heparin-Sepharose beads. However, no new fragments were detected, suggesting that the decrease was not due to enzymatic destruction. On the other hand, in patients with rheumatoid arthritis (chronic inflammation), HRGP levels were similar to those in control subjects. As HRGP is a potent heparin antagonist, HRGP levels in plasma during hemodialysis with heparin were studied. Both levels of HRGP and albumin increased after hemodialysis in a similar degree due to concentration, indicating that turnover of HRGP was not altered in short period after heparin administration.

Acute-Phase Reaction↗
PubMed1989

Histidine-rich glycoprotein blocks T cell rosette formation and modulates both T cell activation and immunoregulation.

Histidine-rich glycoprotein (HRGP) is a plasma and platelet protein with undefined function in vivo. It has been reported to inhibit rosette formation between murine T cells and erythrocytes. We have shown that HRGP binds specifically to human T lymphocytes but not sheep erythrocytes and have demonstrated a 56-kDa HRGP-binding protein on the T cell surface which is distinct from the CD2 sheep erythrocyte receptor. We have now investigated whether HRGP can inhibit human T cell-sheep erythrocyte rosette formation and whether HRGP can modulate T cell activation. HRGP at physiologic concentrations specifically inhibited rosette formation between human T lymphocytes and sheep erythrocytes. HRGP suppressed proliferation of antigen receptor (CD3)-triggered T cells induced by interleukin 2; this suppression was specifically reversed by prior incubation of HRGP with affinity-purified anti-HRGP IgG. Addition of HRGP 12-24 h after CD3 triggering no longer suppressed T cell proliferation, suggesting HRGP suppressed T cell division by interfering with one or more early events in the process of T cell activation. Human serum (containing 100-150 micrograms/ml HRGP) was also capable of suppressing T cell proliferation; serum which had been immunodepleted of HRGP no longer inhibited T cell proliferation. Furthermore, HRGP inhibited interleukin 2 receptor expression on activated T cells, causing decreased T cell interferon-gamma release and altered T cell-dependent inhibition of erythropoiesis. HRGP is thus capable of modulating T cell activation and T cell immunoregulation; HRGP may function as a natural suppressive regulator of human T lymphocyte activation.

Animals↗
PubMed1989

Interaction of histidine-rich glycoprotein with human T lymphocytes.

Histidine-rich glycoprotein (HRGP), a human plasma and platelet protein, interacts with multiple ligands in vitro, including heparin, plasminogen, thrombospondin, and fibrinogen/fibrin. In this study, the binding of HRGP to human T lymphocytes was characterized. The binding was specific, concentration-dependent, saturable, and reversible. Scatchard plot analysis revealed two classes of binding sites: the high affinity class had an apparent dissociation constant (Kd) of 1.92 X 10(-8) M, with 0.92 X 10(4) sites/cell, and the low affinity class had a Kd of 4.97 X 10(-7) M, with 3.7 X 10(4) sites/cell. HRGP binding to T cells in the presence of HRGP-depleted serum was comparable to that observed in buffer. Dot-blot analysis showed that HRGP bound to specific T cell proteins. Using both HRGP affinity chromatography and immunoprecipitation with affinity-purified anti-HRGP IgG, a major 56-kDa HRGP-binding protein in surface labeled T cell lysates was demonstrated. The 56-kDa protein was shown not to be related to the CD2 molecule on T cells. The binding characteristics of HRGP to T lymphocytes indicate a specific ligand-receptor interaction. This is the first demonstration of HRGP binding to a cell surface, and its binding to human T cells may play an important role in T lymphocyte biology.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1989

[An aged patient with acute myelogenous leukemia complicated with liver cirrhosis: successful treatment with low-dose cytosine arabinoside].

A 76-year-old woman, who had suffered from liver cirrhosis, was referred to our hospital because of pancytopenia. Her peripheral leukocyte count was 2,500/microliters with 43% myeloblasts, hemoglobin at 9.0 g/dl and platelet count of 0.9 x 10(4)/microliters. Aspirate from bone marrow showed hypercellular marrow with 52% myeloblasts. No chromosomal abnormality was detected. She was diagnosed as acute myelogenous leukemia (AML, M2). The diagnosis of liver cirrhosis was confirmed by laboratory data and findings of abdominal sonography. Moreover, she had valvular aortic stenosis. These complications made it difficult to treat her with combined chemotherapy containing anthracycline antibiotics, so she was given a small dose of cytosine arabinoside (Ara-C, 10 mg/body/12 hr) for 18 days. After severe myelosuppression, complete remission was achieved. The highest serum concentration of Ara-C was obtained at 15 min after subcutaneous injection of Ara-C; thereafter the Ara-C concentration decreased immediately within 60 min in a pattern similar to that observed in patients without liver cirrhosis. Thus, low-dose Ara-C regimen might be a useful treatment for aged patients with AML, even complicated with liver cirrhosis.

Aged↗
PubMed1989

[Antiplasmin drugs and factor XIII concentrates in the treatment of a patient with acute promyelocytic leukemia (M3)].

A female patient what M3 was seen to incur marked hemorrhagic diathesis during therapy. Heparin infusion was performed to inhibit disseminated intravascular coagulation (DIC). However, oozing from the puncture site of the r-subclavian vein was observed. Her data on coagulation were as follows: AT-3 greater than 100%, fibrinogen 69.0 mg, XIII less than 40%, FPA 2.9 ng/ml and FDP-D dimer 256 ng/ml. The alpha-2-plasmin inhibitor (alpha 2-PI) was 44% and FDP 160 microgram/ml. These results suggested DIC with activated fibrinolysis. Thus, epsilon aminocaproic acid in conjunction with heparin, fibrinogen, and concentrated XIII was administered. The abnormal bleeding improved with an increase of alpha 2-PI and XIII. This clinical response indicated that an activated fibrinolysis and a decreased XIII might have been responsible for provoking the bleeding of the patient.

Adult↗
PubMed1989

Heparin binds to human monocytes and modulates their procoagulant activities and secretory phenotypes. Effects of histidine-rich glycoprotein.

The binding of heparin to human monocytes and the monocytoid cell line U937 was characterized. Heparin binding was rapid, specific, saturable, and reversible. There was a single class of heparin binding sites, with an apparent dissociation constant of 0.19 mumol/L and 1.9 x 10(6) sites per cell. The binding was not dependent on the anticoagulant property of heparin. Analysis of surface-iodinated cell lysates by heparin affinity chromatography revealed a major 120 Kd cell surface heparin-binding protein. Histidine-rich glycoprotein, a potent heparin antagonist found in human plasma and platelets, decreased the affinity of heparin for cell binding. Cell surface bound heparin was functionally active and markedly accelerated the inactivation of thrombin by antithrombin III. Heparin induced the release of two monocyte secretory proteins of 160 and 17 Kd. Our study supports the thesis that heparin and related glycosaminoglycans interact with monocytes and macrophages, as well as endothelial cells and smooth muscle cells, and play an important and complex role in blood vessel wall biology.

Binding Sites↗
PubMed1988

Retrovirus-like features and site specific insertions of a transposable element, tom, in Drosophila ananassae.

The tom element, putatively associated with optic morphology (Om) mutations in Drosophila ananassae, was identified as a retrovirus-like transposable element. The tom element was found to terminate with 475 (or 474) base pair direct repeats which are identical in sequence to each other. Southern blot and heteroduplex analyses showed the tom element to have high homology to 297 and 17.6, two retrotransposons found in D. melanogaster. As in the cases of 297 and 17.6, tom includes nucleotide sequences coding for a presumptive protease and reverse transcriptase, similar in amino acid sequence to those of the Moloney murine leukaemia virus. At the tom insertion site of the sn9g locus, a host DNA sequence (T)ATAT was found to be duplicated on each side of the tom insertion and all other tom elements examined were also flanked by (T)ATAT. In each of six cases, the 5' flanking host sequence was TATAT. These results indicate that the target sequence of the tom element may be TATAT and that the entire region or a part of this sequence was duplicated on insertion of the tom element.

Animals↗
PubMed1988

Alpha-interferon treatment for adult T cell leukemia: low levels of circulating alpha-interferon and it's clinical effectiveness.

We describe a patient with adult T cell Leukemia to whom alpha-interferon therapy was highly effective. Although a combination chemotherapy (ACVP) first introduced was effective in reducing total leukocyte counts, the percentage of leukemic cells relative to total leukocyte counts was decreased first after the institution of alpha-interferon therapy. The patient is now under complete remission for four years. It was noted in this patient that circulating alpha-interferon, measured by a sensitive radioimmunoassay, was consistently low as compared with the value found in the age-, sex-matched healthy control (p less than 0.001). Since adult T cell leukemia is pathogenetically related to the retrovirus infection, low levels of circulating alpha-interferon of the patient may be important from both pathogenetic and therapeutic standpoints. Alpha-interferon therapy may be an useful additive for the chemotherapy of adult T cell leukemia.

Adult↗
PubMed1987

Novel chiral stationary phases for optical resolution by ligand-exchange high-performance liquid chromatography.

Novel chiral stationary phases, (1R,2S)- and diastereomeric (1S,2S)-2-carboxymethylamino-1,2-diphenylethanol, were prepared from (1R,2S)- and (1S,2S)-2-amino-1,2-diphenylethanol, respectively, and were bound to silica gel pretreated with 3-glycidoxypropyltrimethoxysilane. The chiral stationary phases were found to be very effective for the optical resolution of amino acids, amino acid derivatives and hydroxy acids by ligand-exchange high-performance liquid chromatography.

Amino Acids↗
PubMed1987

Phagocytic myeloma cells in asymptomatic multiple myeloma.

A newly observed case of asymptomatic multiple myeloma in which phagocytic myeloma cells were observed is described. Bone marrow aspirates contained 16% myeloma cells, 2% of which engulfed red blood cells, lymphocytes, and platelets. The possibility is discussed that phagocytizing ability may be one of the markers for malignant plasma cells. Nothing is so far known of the phagocytosis by plasma cells in benign monoclonal gammopathy which is strictly defined.

Adult↗
PubMed1986

Nucleotide sequence characterization of a Drosophila retrotransposon, 412.

The nucleotide sequence of the internal region of a Drosophila retrotransposon. 412, was determined. The genome of 412 was found to consist of two long open-reading frames (ORFs 1 and 2), an unusually long putative leader region and long terminal repeats (LTRs). As with 17.6, 297 and gypsy, ORFs 1 and 2 slightly overlap each other and are out of phase by +2. ORF2 includes the nucleotide sequences coding for the putative protease, reverse transcriptase and integrase, and is similar in entire organization to the pol gene of Moloney murine leukaemia virus. In spite of the difference in insertion specificity, integrase, an enzyme presumably responsible for insertion, was found to be similar in amino acid sequence to the counterparts of 17.6, 297 and gypsy. There is no ORF in 412 which corresponds to retroviral env or ORF3s of 17.6 and 297. Analysis of 412 transcripts suggested that 412 LTR is composed of U3, R and U5. The gene for a potential primer tRNA for putative reverse transcription of 412 was also surveyed and the 3'-terminal 15 nucleotides of a putative arginine tRNA were found to be exactly complementary to the putative primer-binding site of 412.

Amino Acid Sequence↗