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M Maeda

Publications and source records attributed to M Maeda.

At least 1,045 records · Page 58Linked to original sources

The gamma-subunit of ATP synthase from spinach chloroplasts. Primary structure deduced from the cloned cDNA sequence.

cDNA clones encoding the gamma-subunit of chloroplast ATP synthase were isolated from a spinach library using synthetic oligonucleotide probes. The predicted amino acid sequence indicated that the mature chloroplast gamma-subunit consists of 323 amino acid residues and is highly homologous (55% identical residues) with the sequence of the cyanobacterial subunit. The positions of the four cysteine residues were identified. The carboxyl-terminal region of the chloroplast gamma-subunit is highly homologous with those of the gamma-subunits from six other sources (bacteria and mitochondria) sequenced thus far.

Amino Acid Sequence↗

Toxic effect of tumor necrosis factor on tumor vasculature in mice.

Stereoscopic observation via an implanted sight glass in mice bearing transplanted methylcholanthrene-induced A-cells showed tumorivascular hemorrhage at 1-2 h after tumor necrosis factor (TNF) administration, congestion at 4-6 h, and hemorrhage, congestion, and blood circulation blockage at 24 h. Histological examination after TNF administration to mice bearing similar methylcholanthrene-induced A-cell transplants showed thrombus formation in the tumor vasculature at 4 h and thereafter. Suppression of this thrombus formation with heparin had no apparent influence on the necrotic response, tumor growth inhibition or complete cure rate following TNF administration to mice bearing the methylcholanthrene-induced A-cell tumors. The results suggest that direct toxicity of TNF on tumor vasculature is a factor in the overall antitumor mechanism of TNF.

Animals↗

Modification of gastric (H+ + K+)-ATPase with pyridoxal 5'-phosphate.

Pig gastric membrane vesicles enriched in (H+ + K+)-ATPase were covalently modified with pyridoxal 5'-phosphate (PLP). The modification resulted in inhibition of K+-dependent ATP hydrolysis, formation of phosphoenzyme and ATP-driven H+-uptake catalyzed by (H+ + K+)-ATPase. ATP, ADP, and adenyl-5'-yl imidodiphosphate were protective ligands, whereas Mg2+ and K+ were not. Specific PLP-binding of about 4.5 nmol/mg membrane protein was necessary for complete inhibition of the enzyme activity, indicating that the stoichiometry of PLP-binding to the enzyme was about 1:1. Limited proteolysis of the enzyme modified with [3H]PLP by trypsin suggests that PLP specifically modifies the lysine residue located in the 16-kDa fragment of the enzyme cleaved by trypsin. These results suggested that PLP binds to a specific lysine residue in the nucleotide-binding site or a region in its vicinity and inhibits the substrate binding or phosphorylation step of (H+ + K+)-ATPase.

Adenosine Triphosphatases↗

Identification and primary structure of a calmodulin binding domain of the Ca2+ pump of human erythrocytes.

Exposure of the purified Ca2+ pump of human erythrocytes to chymotrypsin led to the rapid loss of calmodulin activation. A fragment of about 12 kDa was removed from the ATPase in 1-2 min. Blotting experiments with 125I-labeled calmodulin showed that this fragment contains the calmodulin binding region. The remainder of the ATPase molecule was degraded to a number of fragments ranging from 3 to 120 kDa; none of them bound calmodulin. To isolate the calmodulin binding domain, calmodulin which had been coupled to the Denny-Jaffe reagent (a cleavable radioactive photoaffinity cross-linker) was allowed to bind to the Ca2+ pump. After illumination to couple the cross-linker to the pump, the cleavable bond was split and the calmodulin removed, leaving the pump radioactively labeled. This pump was digested with chymotrypsin, and the products were separated by gel permeation chromatography. The only radioactive peak (migrating at about 12 kDa) was further purified on reverse-phase high pressure liquid chromatography (HPLC). Amino acid analysis showed the fragment to have a minimal molecular mass of 12.4 kDa and to contain a single methionine. After attempts to sequence the peptide directly failed. CNBr digestion was carried out on the labeled ATPase, producing both soluble and insoluble labeled material. After reverse-phase HPLC purification of the soluble material, a single radioactive peak was collected. Its sequence was (Formula: see text). A portion of this peak was passed through a microcalmodulin column; it bound in the presence of Ca2+ and was eluted by EDTA, and by a mixture of EDTA and urea. Staphylococcal V8 protease digestion of the eluted peak produced the same sequence as shown above, but starting at Leu-2 and ending at Glu-32. Structural analysis of this peptide showed that it shares features with the calmodulin binding domains of other enzymes which are regulated by calmodulin.

Amino Acid Sequence↗

Synergistic effects of recombinant human tumor necrosis factor and hyperthermia on in vitro cytotoxicity and artificial metastasis.

Synergy in cytotoxic effect between recombinant human tumor necrosis factor and hyperthermia (incubation at 38.5 degrees C or 40 degrees C) was observed to occur against L-M (mouse tumorigenic fibroblast) cells and shown to be related to an accelerated turnover rate of recombinant human tumor necrosis factor-receptor complex under elevated temperatures rather than to changes in number of cell receptors or binding strength. However, no synergy in cytotoxic effect was observed to occur against human embryonic lung (HEL) cells. A clearly synergistic inhibition of metastatic tumor growth by combined administration of recombinant human tumor necrosis factor (300 units) and whole-body hyperthermia (40 degrees C, 30 min) was also observed in BALB/c mice previously given injections of 1 x 10(6) Meth-A (MH) cells/mouse via tail vein, neither of which alone resulted in significant inhibition.

Animals↗

Synergistic cytotoxic and antitumor effects of recombinant human tumor necrosis factor and hyperthermia.

A synergistic increase in the cytotoxic effects of recombinant human tumor necrosis factor (rH-TNF) and hyperthermia was demonstrated both in vitro and in vivo. The cytotoxicity of rH-TNF against L-M cells in incubation for 12 h at 38.5 and 40 degrees C based on the concentration necessary for 50% cytotoxicity was, respectively, 125 and more than 500 times as high as in similar incubation at 37 degrees C. As observed 18 days after implantation of Meth-A fibrosarcoma cells in mice, single i.v. administration of rH-TNF at 1000 units/mouse resulted in complete cures in five mice when performed in combination with hyperthermia (40 degrees C), whereas rH-TNF alone in the same dose resulted in 27.1% inhibition of tumor growth and hyperthermia alone had no appreciable effect on tumor growth. The i.v. administration of rH-TNF three times at 100 or 300 units/mouse together with hyperthermia (40 degrees C) resulted in 41.2 and 89.0% tumor growth inhibition, respectively; similar administration without hyperthermia appeared to have little or no appreciable effect on tumor growth. The results suggest that combination therapy including rH-TNF and hyperthermia may be of value in the treatment of malignancy in human patients.

Animals↗

Ki-1+ cutaneous lymphoma. Gene rearrangement analysis of tumor cells in tissue and short-term culture of a patient.

Cutaneous malignant lymphomas developed in an 80-year-old man without any evidence of leukemic disseminations of lymphoma cells. Immunohistologic staining showed the expression of Leu-3a, Leu-4, Ki-1, Tac, and HLA-DR antigens on tumor cells in tissue and large lymphoid cells in long-term, interleukin 2-containing culture of tumor explants. DNA samples extracted from the skin tumors and cultured lymphoid cells showed a clonal rearrangement of T-cell receptor (TCR) gene C beta 1 with the molecular size of 9 kilobases. These findings suggested the T-cell origin of Ki-1+ cutaneous lymphoma cells and the occurrence of a clonal proliferation of tumor cells in culture.

Aged↗

Enhanced production of interleukin-2 in patients with progressive systemic sclerosis. Hyperactivity of CD4-positive T cells?

A significant enhancement of interleukin-2 production was observed in phytohemagglutinin-stimulated peripheral lymphocytes from patients with progressive systemic sclerosis (PSS). Their Leu-3a:Leu-2a ratio was also significantly higher than normal. Moreover, Leu-3a+ cells freshly purified from PSS patients' blood produced much more interleukin-2 than did cells from normal subjects. These results suggest that T cell hyperactivity, especially among Leu-3a+ T cells, occurs in patients with PSS.

Adult↗

An experimental approach to 31P spin-lattice relaxation time measurement in biological systems.

The accuracy of measurement of the spin-lattice relaxation time (T1) in biological systems using the variable nutation angle method is discussed using computer simulations. This method could reduce the time required for measurement to 10% of that using the inversion recovery method. In the perfused salivary gland of the rat (310 K), the T1 values of sugar phosphates, creatine phosphate, gamma-phosphate, and beta-phosphate of nucleotide triphosphates determined by this method were 5.2, 4.8, 0.9, and 0.8 s, respectively. During secretion of saliva, the T1 value of sugar phosphates decreased to 3.7 s, which could be due to an increased chemical exchange of phosphate in glycolysis.

Animals↗

C1q production and C1q-mediated immune complex retention in lymphoid follicles of rat spleen.

Involvement of C1q in retaining immune complexes in germinal centers in rat spleen was studied in vivo and in vitro. C1q production was found in fibroblastic reticulum cells in the peripheral mantle zone, in follicular dendritic cells in germinal centers, and in transitional forms between these two cells in the inner mantle zone. In passively immunized animals, immune complexes were found transiently on fibroblastic reticulum cells, then on the transitional forms and follicular dendritic cells. Extracellular C1q was detected by the presence of immune complexes on both the transitional forms and follicular dendritic cells, but not on fibroblastic reticulum cells. Thus, the fibroblastic reticulum cell appeared to trap immune complexes but not to retain either immune complexes or C1q. The morphology and function of the fibroblastic reticulum cell and the follicular dendritic cell suggest that they belong to the same lineage. Immune complexes were bound in vitro to germinal centers in cryostat spleen sections in the same manner as those retained in vivo. The binding required no complement in the incubation medium and was inhibited by C1q-suppressing factors. The extracellular C1q originating from the follicular cells may therefore play a role in retaining immune complexes in the germinal center.

Animals↗

Water intoxication in asthma assessed by urinary arginine vasopressin.

A 3-year-old girl with status asthmaticus developed a grand mal seizure in association with hyponatraemia after 16 h of fluid therapy. Urinary arginine vasopressin (AVP) was elevated during the attack and rose strikingly before the onset of the convulsion. In 13 of 17 other patients with moderately severe asthmatic attacks, increases in urinary AVP levels occurred before the initiation of treatment. Dilutional hyponatraemia (water intoxication) must be prevented in patients with severe asthmatic attacks in whom diuretic capacity is impaired.

Arginine Vasopressin↗

Molecular genetics of F1-ATPase from Escherichia coli.

We have reviewed recent molecular biological studies on F1-ATPase of Escherichia coli and emphasized the advantages of using the bacterium in studies on this important enzyme. All subunits had homologies of varied degrees with those from other organisms. Mutations of F1 subunits caused defects in catalysis and assembly. Defects of the mutant enzymes were studied extensively together with the determination of the amino acid substitutions. Extensive molecular biological studies may help greatly in understanding the normal mechanism and assembly of the complex.

Escherichia coli↗

Mechanism of F1-ATPase studied by the genetic approach.

E. coli F1-ATPase has been studied mainly by the genetic approach. Mutations in either the alpha or beta subunit modified the kinetics of multisite and uni-site hydrolysis of ATP. The mechanism of F1-ATPase and the essential amino acid residues of beta subunits are discussed.

Escherichia coli↗

Case of mixed connective tissue disease associated with autoimmune hepatitis.

A 56-year-old female with mixed connective tissue disease (MCTD) who developed autoimmune hepatitis is described. Hepatitis was controlled effectively by the corticosteroid therapy. Biopsy of the liver revealed swelling and hydropic degeneration of hepatocytes, accompanied by Councilman's body formation and focal necrosis. These histological findings differ from those in three previously described cases. A relationship between MCTD and liver involvement appears possible.

Autoimmune Diseases↗

Tricuspid regurgitation due to chest trauma: an unusual laceration around the annulus of the anterior leaflet.

A 70-year-old male with tricuspid regurgitation due to a blunt chest trauma inflicted 16 years previously underwent prosthetic valve replacement. At surgery, a tear, which produced tricuspid regurgitation, was found around the annulus of the anterior leaflet of the tricuspid valve. Since this area has not been reported as a location for heart trauma-producing tricuspid regurgitation, a possible mechanism of tricuspid regurgitation is discussed in this patient.

Aged↗