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Biomedical subjects

H Maeda

Publications and source records attributed to H Maeda.

At least 1,153 records · Page 64Linked to original sources
PubMed1985

Recombinant gamma-interferon and lipopolysaccharide enhance 1,25-dihydroxyvitamin D3-induced cell differentiation in human promyelocytic leukemia (HL-60) cells.

The induction of cell differentiation by a combination of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], recombinant gamma-interferon (rec gamma-IFN), and a lipopolysaccharide from E. coli (LPS) was studied in a clonal population (clone-9) of human promyelocytic HL-60 leukemia cells in vitro. Treatment of clone-9 cells with 10(-9) to 10(-7)M 1,25-(OH)2D3 yielded a macrophage cell differentiation. The addition of 10 or 100 U/ml of gamma-IFN and 2 or 10 micrograms/ml LPS caused a further increase in expression of the different differentiation markers. The most pronounced effects involved increases in cell attachment to the surface of tissue-culture Petri dishes and in lysozyme, nonspecific esterase, and cytolytic activities. The combined treatment with 1,25-(OH)2D3 and rec gamma-IFN and LPS also caused an increase in the percent of multinucleated giant cells. These results indicate the effectiveness of combining different agents in inducing cell differentiation in HL-60 cells. A similar approach may be useful in controlling myeloid leukemias in vivo.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

A monoclonal anti-human platelet antibody: a new platelet aggregating substance.

A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich plasma and with washed platelets, but not with formalin-fixed washed platelets. TP82-induced aggregation was completely inhibited by disodium ethylendiaminotetraacetate, diltiazem, W-7, PGE1, and several metabolic inhibitors. At a concentration of apyrase or CP/CPK, which inhibited adenosine 5-diphosphate-induced aggregation. TP82-induced aggregation was only partially affected. Thrombin was not required for the antibody-mediated effects, since two thrombin inhibitors failed to block the reaction. The antibody, at least at a high concentration, induced platelet aggregation by a mechanism almost independent of thromboxane A2 formation, since cyclooxygenase inhibitors had little inhibitory effect on aggregation. TP82 monoclonal antibody is a new platelet-aggregating substance that interacts with a low-molecular-weight binding site on the platelet membrane.

Adenosine Triphosphate↗
PubMed1985

[Intrauterine treatment of nonimmunologic hydrops fetalis associated with pleural effusion].

Four fetuses with nonimmunologic hydrops fetalis were treated in utero. The initial diagnosis was made between 27 and 32 weeks of gestation. All fetuses had generalized edema and pleural effusion at the time of diagnosis. In order to maintain plasma colloid osmotic pressure in the fetus, fetal transfusion of albumin was carried out. Because pleural effusion may inhibit fetal lung development, serial in utero thoracocentesis guided by ultrasonic tomography was carried out. In three of four fetuses, cord blood albumin concentration were within normal range. Urine volume in fetuses significantly increased after fetal transfusion of albumin. These results suggested that this procedure was useful in maintaining plasma colloid osmotic pressure in the fetus. Although pleural effusion was removed completely by in utero thoracocentesis, pleural effusion appeared within 1 hour after the procedure and rapidly increased thereafter until the 24th hour. There were no fatal trauma from the procedure. In all infants, generalized edema, ascites and pleural effusion were presented at birth, and Apgar scores at one minute were less than 7. All died of pulmonary insufficiency within 16 hours after delivery. At autopsy, their lungs were smaller than those of the other infants.

Albumins↗
PubMed1984

Selective targeting of anti-cancer drug and simultaneous image enhancement in solid tumors by arterially administered lipid contrast medium.

Twenty-four patients with various solid tumors including metastatic liver cancer and cancer of the lung, gallbladder, and pancreas were treated with a lipophilic macromolecular drug, copoly(styrene-maleic acid) conjugated neocarzinostatin (SMANCS). The drug was dissolved in a lipid contrast medium Lipiodol and administered by catheterizing the respective feeding arteries under x-ray monitoring. The advantages of this therapy include: (1) selective deposition of Lipiodol with the anti-cancer drug in the target tumor, (2) a pronounced and long-lasting anti-cancer effect, (3) enhanced visualization of the tumor on x-ray examinations for a prolonged period which also facilitated the long-term follow-up, (4) semiquantitative evaluation of the dosage regimen by x-ray examination before further administration, (5) general applicability due to procedural simplicity, and (6) little side effect. Since the amount of Lipiodol and SMANCS used per administration for a patient (1.0-5.0 ml; 1.0-5.0 mg) was far less than the anticipated toxicity (LD50 of Lipiodol = 95 ml/60 kg, dog, intravenously; and that of SMANCS = 3.4 mg/kg, mouse, IV), no deleterious effects to such critical organs as the brain, heart, lung, liver, or kidneys were observed upon radiologic and general clinical examination.

Adenocarcinoma↗
PubMed1984

A revised primary structure for neocarzinostatin based on fast atom bombardment and gas chromatographic-mass spectrometry.

The amino acid sequence of the antitumor protein neocarzinostatin was revised on the basis of mass spectrometric studies. Gas chromatographic mass spectrometry on the O-trimethylsilyl polyaminoalcohol derivatives of peptide mixtures derived from tetra S-carboxymethyl-neocarzinostatin were used to partially sequence neocarzinostatin. In addition, fast atom bombardment-mass spectrometric experiments on neocarzinostatin and its tryptic fragments gave the molecular weights of various peptides and, in some cases, partial sequence information. The revised sequence involved reordering of two chymotryptic peptides, the identification of a new di- and tripeptide sequence (Ala-Asp and Ala-Ser-Thr), the repositioning of Trp at position 39, and the assignment of the remaining Asx residues. The revised structure for neocarzinostatin (Mr = 11,105) now shows considerable homology with the other antitumor antibiotic proteins macromomycin and actinoxanthin.

Amino Acid Sequence↗