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Biomedical subjects

N Maeda

Publications and source records attributed to N Maeda.

At least 559 records · Page 31Linked to original sources
PubMed1986

A contribution of calmodulin to cellular deformability of calcium-loaded human erythrocytes.

The effect of intracellular calcium on the deformability of human erythrocytes was studied with a rheoscope, especially in relation to the dynamic structure of membrane cytoskeleton. The appropriate calcium-loading and calcium-depletion were performed to intact erythrocytes with A23187 in potassium buffer. The total calcium content was varied in the range of 0.25 to 3 times as much as normal content, without complete ATP depletion and shape change (the reduction of mean cell volume and the condensation of hemoglobin due to dehydration were avoided). Increasing the intracellular calcium content by about 1.5 times of normal, the deformability was distinctly decreased, while calcium depletion did not affect the deformability. Reduced deformability of the calcium-loaded erythrocytes was restored by the treatment with calmodulin inhibitors, W-7 or trifluoperazine. However, such an effect by calmodulin inhibitors was not detected on normal or calcium-depleted erythrocytes. In conclusion, the interaction between calcium-calmodulin complex and cytoskeletal proteins may affect the membrane stiffness which is regulated through the change of the cytoskeletal structure, and contributes to the deformability of erythrocytes.

Calcium↗
PubMed1986

Drift of an erythrocyte flow line due to the magnetic field.

Drifts of erythrocyte-flow lines due to inhomogeneous magnetic field in a laminar flow in a buffer solution are shown for the first time, and are interpreted as being due to the paramagnetism of hemoglobins included in the erythrocytes. The drifts were dependent on the hematocrit of the flowing erythrocyte suspension.

Buffers↗
PubMed1986

Structures of two HaeIII-type genes in the human salivary proline-rich protein multigene family.

Two members of the human salivary proline-rich protein (PRP) multigene family have been isolated and completely sequenced. These PRP genes, PRH1 and PRH2, are of the HaeIII-type subfamily and code for acidic PRP proteins. Both genes are approximately 3.5 kilobase pairs (kb) in length and contain four exons. Exon 3 encodes the proline-rich part of the protein and includes five 63-base pair (bp) repeats. CAT and ATA boxes and several possible enhancer sequences occur in a 1-kb region 5' to exon 1. Two sets of repeats occur in the sequenced region in addition to the 63-bp repeats: one pair of about 140 bp flanks 500 bp of DNA in the first intervening sequence, and the other pair of 72 bp is tandemly repeated 1.4 kb 5' to the PRH1 gene. The 4-kb region of sequenced DNA from PRH1 differs by an average of 8.7% from the same region in PRH2, but the nucleotide sequences of the exon 3 of the two genes differ by only 0.2%. This result suggests the occurrence of a recent gene conversion event. The regions containing the 5-fold repeated sequences of 63 bp are identical in the two genes, PRH1 and PRH2. A comparison of the human HaeIII and BstNI subfamily repeats and a comparison of the human, mouse, and rat repeats suggest that the individual repeats have evolved in a concerted fashion within each gene and within the PRP gene family as a whole.

Animals↗
PubMed1986

Increase of ATP level in human erythrocytes induced by S-adenosyl-L-methionine.

The effect of S-adenosyl-L-methionine (SAM) on the ATP level, the morphology and the deformability of human erythrocytes was investigated and compared with that of adenosine. (i) Upon incubation with SAM, the ATP level increased considerably in fresh cells (in both young and old cells in similar extent) and in stored (partially ATP-depleted) cells. But the incubation with adenosine increased ATP level to a lesser extent. (ii) The incubation of stored cells with SAM hardly affected (or rather decreased) the IMP level, while that with adenosine remarkably increased IMP (and ITP). (iii) The morphology and the deformability of stored erythrocytes were well conserved in spite of the treatment with SAM, as compared with the treatment with adenosine. The echinocytic transformation was induced in old cells to some extent by SAM, while did not in young cells.

Adenosine↗
PubMed1986

Opposite effect of albumin on the erythrocyte aggregation induced by immunoglobulin G and fibrinogen.

The effect of albumin on the immunoglobulin G (IgG)-induced and fibrinogen-induced aggregation of human erythrocytes was quantitatively examined by using a rheoscope combined with a television image analyzer and a computer. As albumin concentration in the medium was increased, the IgG-induced erythrocyte aggregation was inhibited, while the fibrinogen-induced erythrocyte aggregation was accelerated (albumin itself was not able to aggregate erythrocytes). These relations were empirically expressed by the equations, v = aG1.8/A and v = a'F1.5 (A + b'), respectively (v, the velocity of erythrocyte aggregation; A, G and F, the concentrations of albumin, IgG and fibrinogen, respectively; a, a' and b', constant). The IgG-induced erythrocyte aggregation was remarkably inhibited by the addition of poly(glutamic acid), but the fibrinogen-induced erythrocyte aggregation was not. A mechanism for the interaction of immunoglobulin G and fibrinogen with the surface of erythrocytes was proposed.

Adult↗
PubMed1986

Prostaglandin E2 stimulates DNA synthesis by a cyclic AMP-independent pathway in osteoblastic clone MC3T3-E1 cells.

The effect of prostaglandin E2 (PGE2) on osteoblastic cell proliferation was investigated using osteoblastic clone MC3T3-E1 cells cultured in serum-free medium. PGE2 at 2 micrograms/ml increased the number of the cells by 2 days after its addition. PGE2 raised the level of DNA synthesis in a dose-related fashion after a constant lag time, the maximal effect being at 2-10 micrograms/ml and the level about fourfold over that of the control at 36 hr after its addition. However, at low doses (below 0.2 microgram/ml), PGE2 rather depressed DNA synthesis. Isobutyl methylxanthine counteracted the stimulation of DNA synthesis by PGE2, and forskolin depressed the synthesis, which was inversely correlated with increasing intracellular cAMP content. These results indicate that an increase in cAMP content inhibits DNA synthesis. In addition, 2',5'-dideoxyadenosine did not negate the stimulatory effect of PGE2 on DNA synthesis, suggesting that PGE2 increases DNA synthesis, probably via a pathway different from the adenylate cyclase/cAMP system. Moreover, at a high dose, PGE2 stimulated both the production and degradation of cAMP; the elevation of cAMP content was rapidly depressed by the stimulated degradation system. Consequently, the stimulatory effect of PGE2 on DNA synthesis would be released from the inhibition by cAMP, resulting in an increase in DNA synthesis. Taken together with data from our previous reports, these results indicate that PGE2 enhances both the proliferation and differentiation of osteoblastic cells in vitro, which are probably mediated by two different second messengers dependent on the concentration of PGE2.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Mechanism of increased rate of de novo purine biosynthesis in rat liver after bilateral adrenalectomy.

The incorporation of [14C]glycine to hepatic purines increased proving the increased rate of de novo purine biosynthesis in rat liver after bilateral adrenalectomy in comparison to sham-operated controls. In the liver of adrenalectomized animals 24 hours after adrenalectomy when the rate of de novo purine biosynthesis is increased above control by 70% there was a 200% increase of 5-phosphoribosyl 1-pyrophosphate (PRPP) concentration. The concentrations of purine ribonucleotides showed a 33 and a 24% decrease of ATP and GTP, and 245 and 38% increase of AMP and ADP respectively associated with the unchanged total adenine and guanine nucleotide concentration and a 18% decrease of adenylate energy charge. The specific activity of amidophosphoribosyltransferase (ATase) was not changed. The replacement with corticosterone acetate to adrenalectomized animals for 24 hours partially restored the rate of de novo purine biosynthesis and the concentrations of purine ribonucleotides. These results suggest that the increased rate of de novo purine biosynthesis in adrenalectomized rat liver is compensatory against the increased catabolism of purine ribonucleotides as a result of the increased AMP concentration and that it is mediated by the increased concentration of PRPP. Our study has demonstrated the importance of the physiological amount of adrenocortical hormone to sustain the normal concentrations and the metabolism of purine ribonucleotides in liver.

Adrenalectomy↗
PubMed1986

In vivo inhibition of the rate of de novo purine synthesis in rat liver by glucagon.

The rates of de novo purine and protein synthesis were assessed in vivo in rat liver after bolus administration of glucagon. The specific activity of hepatic purines and the specific activity ratio of hepatic purine/protein were used as an index of the rate of de novo purine synthesis and the rate relative to protein. Glucagon at doses of 0.01 mg to 0.1 mg/200 g body weight (BW), administered as an intravenous bolus, inhibited dose-dependently the rate of de novo purine synthesis and the rate relative to protein although it increased dose-dependently the hepatic concentration of 5-phosphoribosyl 1-pyrophosphate (PRPP). The inhibition of the rate of de novo purine synthesis recovered to control levels during the period between 60 and 90 minutes after glucagon administration. Dibutyryl cyclic AMP (Bt2 cAMP) partially mimicked this effect of glucagon in that it did not increase the rate of de novo purine synthesis in spite of increased concentrations of PRPP. These results suggest that an intravenous bolus of glucagon inhibits the rate of de novo purine synthesis through increasing cAMP concentration. The data are consistent with inhibition of amidophosphoribosyltransferase (ATase) in spite of increased PRPP concentrations.

Animals↗
PubMed1986

Polymorphisms in the human haptoglobin gene cluster: chromosomes with multiple haptoglobin-related (Hpr) genes.

We have found polymorphisms for the number of tandemly arranged haptoglobin-related (Hpr) genes in the haptoglobin gene cluster of Blacks. Genomic mapping and nucleotide sequence analysis indicate that two copies of the Hpr gene first resulted from unequal but homologous crossing-over in a region 3' to the haptoglobin (Hp) and the haptoglobin-related genes. Subsequent increases in the number of Hpr loci have occurred in some chromosomes. Among 25 American Blacks studied (15 were unrelated), 2 related individuals have one extra copy of the Hpr gene and 5 unrelated individuals have more than two extra Hpr genes. None of 26 Whites and one Oriental studied have extra copies. In one of the Blacks, six tandemly arranged Hpr genes were demonstrated in one chromosome by pulsed field gradient electrophoresis. His other chromosome had one Hpr gene. The tandem Hpr genes were found in individuals with the haptoglobin genotypes Hp2/Hp2 (3 of 3 tested) and Hp2/Hp1 (4 of 11 tested), but none were found in the Hp1/Hp1 individuals (11 tested). Fibroblast cell cultures from two Hp2/Hp1 heterozygotes were fused to mouse cells to obtain cell lines retaining a human chromosome 16 on which the haptoglobin gene cluster is located. DNA analysis of the hybrid cells showed that in both individuals the tandemly arranged Hpr genes are linked to the Hp2 allele. These results suggest that the multiple copies are associated with the Hp2 gene.

Base Sequence↗
PubMed1986

Proton nuclear magnetic resonance analyses of the molecular conformations of unique long neurotoxins bearing Phe-25: Astrotia stokesii b, Astrotia stokesii c, and Acanthophis antarcticus b.

The 270-MHz proton NMR spectra of the unique long neurotoxins bearing Phe-25, Astrotia stokesii b (As b) and Astrotia stokesii c (As c) from Astrotia stokesii, and Acanthophis antarcticus b (Aa b) from Acanthophis antarcticus, have been analyzed. The aromatic proton resonances of Phe-25 in As b and Aa b were assigned on the basis of the nuclear Overhauser effects observed on irradiation of slowly exchanging amide protons. Phe-25 was found to be involved in hydrophobic interactions with Ile/Val-42, Ala-46 and Ile-58 in As b and As c, and with Ala-46 and Val-58 in Aa b. These hydrophobic interactions, instead of the hydrogen bond between Tyr-25 and Glu-42 found in other neurotoxins, appear to be important for maintenance of the biologically active tertiary structure. The pH dependency of the chemical shift and intensity of the Trp-72 N-1 proton resonance of As b indicates that the indole ring is not fully exposed to the solvent and that the extra tail segment of this long neurotoxin interacts with the main part of the molecule.

Circular Dichroism↗
PubMed1986

Effect of immunoglobulin preparations on the aggregation of human erythrocytes.

The aggregation of human erythrocytes induced by four kinds of immunoglobulin preparations was examined by a low shear rheoscope. After removing anti-A+ and anti-B+ activities contaminated in all preparations by incubating with erythrocytes of different blood groups, the facilitating effect on the rouleau formation of erythrocytes was compared: (i) The effect of polyethyleneglycol-treated preparation was the same in A+-, B+-, AB+- and O+-erythrocytes. (ii) Sulfonation did not affect the velocity of rouleau formation. (iii) Some of pepsin-treated preparations showed the strongest facilitation for A+-, B+- and AB+-erythrocytes, but the facilitation was much weaker for O+-erythrocytes. The others showed the weak facilitation for all types of erythrocytes (especially O+-erythrocytes). (iv) Plasmin treatment markedly decreased the velocity of rouleau formation of AB+- and O+-erythrocytes, but was not of A+- and B+-erythrocytes.

Adult↗
PubMed1986

Increased rate of purine biosynthesis in rat liver after bilateral adrenalectomy.

In bilaterally adrenalectomized rat liver the increased rate of de novo purine synthesis was shown by the increased [14C]glycine incorporation into hepatic acid-soluble purines with unchanged rapidly miscible glycine pool size and its turnover rate and by the increased rate of chasing of radiolabeled purines. At 24 h after adrenalectomy, the rate of de novo purine synthesis increased by 70%, 5-phosphoribosyl-1-pyrophosphate (PRPP) content increased by 200%, the specific activity of amidophosphoribosyltransferase (EC 2.4.2. 14; ATase) did not change, ATP and GTP showed a 33 and 24% decrease, and AMP and ADP showed a 245 and 38% increase. Combined, the metabolic pool size data reflected an unchanged total inhibitory potential on ATase. Replacement with corticosterone acetate for 24 h partially restored some of these abnormalities. These results suggest that the increase in the rate of de novo purine synthesis in adrenalectomized rat liver is secondary to increased catabolism of purine ribonucleotides and mediated by increased PRPP concentrations.

Adenosine Diphosphate↗
PubMed1986

Increased rate of de novo purine synthesis and its mechanism in regenerating rat liver.

In regenerating rat liver at 12 h after a 70% hepatectomy, [14C]glycine incorporation to hepatic acid-soluble purines increased by 2.4-fold with a 26% increase of the mean rapidly miscible glycine pool size and its comparable turnover rate. Amidophosphoribosyltransferase (EC 2.4.2.14, ATase) activity increased 1.8-fold at 18 h and 5-phosphoribosyl-1-pyrophosphate (PRPP) concentration increased 3.0-fold at 12 h after surgery. Decreases in ATP and GTP concentrations of 13 and 15%, respectively, in regenerating rat liver at 12 h after surgery were counterbalanced by increased AMP and GMP concentrations of 13 and 44%, respectively, with comparable inhibitory potentials on ATase. These results suggest than an increased rate of de novo purine synthesis in regenerating rat liver is mediated by the increased ATase activity and PRPP concentrations.

Adenosine Monophosphate↗
PubMed1986

Development of heart and aortic lesions in DBA/2NCrj mice.

The development of heart and aortic lesions was investigated in 3- to 8-week-old DBA/2NCrj mice. In the heart, small foci of myocardial calcification and severe calcification with subsequent inflammation were observed. Severe lesions were restricted to the myocardium below the right ventricular epicardium. Small foci of myocardial calcification were found from 4 to 8 weeks of age with almost the same frequency. The incidence of severe calcification showed a drastic increase between 6 and 7 weeks of age. Aortic lesions were observed from 3 weeks of age and characterized by focal calcification of the smooth muscle cells and elastic laminae. The frequency of aortic calcification was about 50% and not age-related.

Animals↗