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A Yoshimura

Publications and source records attributed to A Yoshimura.

At least 271 records · Page 15Linked to original sources
PubMed1988

[X-ray dosimetry using a charge injection type condenser].

An X-ray dosimeter has been investigated with the use of a charge injection type condenser. The detector is small size and is housed in an epoxy resin approximately 4.5 X 2.5 X 1.5 mm. The X-ray dose can be determined by decreasing the amount of electron injected into floating gate through X-ray irradiation. The X-ray irradiation dose can be measured by decreasing of the capacitance. This dosimeter shows good linearity but the X-ray energy response for low energy region is higher than high energy region.

Radiometry↗
PubMed1988

[X-ray dosimetry using SAMOS type read-only memory].

An X-ray dosimeter has been investigated with the use of a PROM of a SAMOS (stacked gate avalanche injection type MOS) structure. The SAMOS is employed as a memory IC. The SAMOS is different from a FAMOS (floating gate avalanche injection type MOS) in the presence of a control gate, with the use of this electrode, the analog amount of electrical charge accumulated in the floating gate can be measured. The X-ray dose can be determined by decreasing the amount of electron injected into floating gate by avalanche effect through X-ray irradiation. This dosimeter shows good linearity and flat energy response. The dosimeter has no effect on fading.

Radiometry↗
PubMed1988

[Improved performance of a waste water radiation monitor].

Gamma ray waste water radiation monitor has been improved by using multichannel analyzer. Maximum permissible concentrations of 125I are one thousandth lower than 51Cr. This condition, the radioactive waste water cannot be pumped out occasionally. Gamma ray energy spectrum is measured by microcomputer based multichannel analyzer by which 125I photo-peak counts is separated from other radionuclide counts. Also detecting vessel is washed with pressured fresh water to prevent contamination.

Environmental Monitoring↗
PubMed1988

[CHO].

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Animals↗
PubMed1987

Altered interaction between Sendai virus and a Chinese hamster cell mutant with defective cholesterol synthesis.

An amphotericin B-resistant mutant (AMBr-1) isolated from the Chinese hamster V79 cell line is defective in a pathway for sterol synthesis and contains a much reduced free cholesterol level as compared with the parental V79. The character of the plasma membrane of AMBr-1 was compared with that of V79 by measuring the fusion with the envelope of the Sendai virus and also by measuring membrane fluidity: AMBr-1 was found to be more sensitive to Sendai virus-induced cytolysis than V79. Both assays for membrane-permeability change and electron spin resonance (ESR) study showed an enhanced response to the fusion between viral envelope and plasma membrane in AMBr-1 cells. Measurement of the fluorescence polarization for 1,6-diphenyl-1,3,5-hexatriene suggested that the membrane of AMBr-1 was more fluid than that of V79. This aberrant nature of the cell membrane of AMBr-1 might be caused by the altered membranous sterol content.

Animals↗
PubMed1987

Altered function and structure of low-density lipoprotein receptor in compactin (ML236B)-resistant mutants of Chinese hamster cells.

Mutants resistant to compactin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, have been previously isolated from the Chinese hamster V79 cell line. Two compactin-resistant mutants, MF-1 and MF-2, show altered responses to human low-density lipoprotein (LDL). Accumulation of fluorescent-labeled LDL was much reduced. Ligand blotting showed LDL receptor activity in MF-1 and MF-2 cells of about one half to one third that of V79. Internalization and degradation of LDL in MF-1 or MF-2 cells were about one tenth those in V79 cells, suggesting that the LDL binding as well as the LDL internalization of the compactin-resistant clones was altered. Down-regulation of LDL receptor activity as well as hydroxymethylglutaryl CoA reductase was observed in V79 cells treated with LDL, while there appeared to be much less down-regulation in MF-1 and MF-2 cells. Using anti-LDL receptor antibody, MF-1 and MF-2 cells were found to produce smaller-sized mature forms of LDL receptor: the molecular mass of the mutant LDL receptor was 3-5 kDa smaller than that of the parental LDL receptor. Altered O-linked oligosaccharides or amino acid sequence might account for the decreased molecular mass and aberrant properties of the LDL receptor in MF-1 and MF-2.

Animals↗
PubMed1987

Low binding capacity and altered O-linked glycosylation of low density lipoprotein receptor in a monensin-resistant mutant of Chinese hamster ovary cells.

We have studied function and structure of the low density lipoprotein (LDL) receptors in a monensin-resistant (Monr-31) mutant isolated from Chinese hamster ovary (CHO) cells. To assay the ability of the receptor to bind LDL, we employed three methods, 125I-LDL binding to the cells at 4 degrees C, 125I-LDL binding to the receptor-phospholipid complex (Schneider, W.J., Goldstein, J.L., and Brown, M.S. (1980) J. Biol. Chem. 255, 11442-11447), and ligand blotting (Daniel, T.O., Schneider, W.J., Goldstein, J.L., and Brown, M.S. (1983) J. Biol. Chem. 258, 4606-4611). The LDL receptor number was similar in both CHO and Monr-31, but the binding affinity was reduced in the mutant. The semi-quantitative immunoblotting assay with an antibody directed against the COOH-terminal 14 amino acids and the ligand-blotting assay with LDL also showed that the relative steady-state level of the receptor in Monr-31 was comparable to that in CHO, whereas the binding capacity of the receptor in Monr-31 was lower than that in CHO. The precursor and degradation forms of the LDL receptors produced in the mutant cells were similar in size to those in the parental cells, but the apparent molecular mass of the mature receptor protein in sodium dodecyl sulfate-polyacrylamide gels was reduced about 5000 daltons in the mutant. These results suggest a structural change at the NH2-terminal LDL binding domain. Tests of the effects of tunicamycin, endo-alpha-N-acetylgalactosaminidase (O-glycanase), and sialidase (neuraminidase) on the molecular size of the mature receptors indicated that the reduced size of the receptor in the mutant cells resulted from altered oligosaccharide chain(s) linked to serine/threonine residues in the binding domain. We compared the molecular sizes and binding activity of human LDL receptors in several clones derived from CHO and Monr-31 cells which were transfected with human LDL receptor cDNA. The human LDL receptors produced in the transfected clones of Monr-31 were also smaller in molecular size and lower in binding capacity than those produced in the transfected clones of CHO. These results suggest that both structural and functional alteration of the LDL receptor of Monr-31 is not caused by a mutation in the structural gene of the LDL receptor but by altered processing or maturation of the receptor. The correlation of the decrease in molecular size and reduced binding capacity of the LDL receptor is discussed.

Animals↗
PubMed1987

Possible fusimotor innervation to frog muscle spindles.

In some muscle spindles located in or near the red area of semitendinosus muscle of the bull frog, a fine motor axon innervates the intracapsular compact zone, without any branches onto the extrafusal muscle fibers. The fine motor axon is 3.9 microns in mean diameter (measured in living axon) and 9.8 m X s-1 in mean conduction velocity at 20 degrees C. A ramp-and-hold stretch during 20 Hz repetitive stimulation of the fine motor axon markedly increased the rate of afferent discharges during static phase. Histochemical studies indicated depletion of glycogen in a compact zone along a small diameter intrafusal muscle fiber of the muscle spindles frozen immediately after tetanic stimulation of the fine motor axon. These results suggest that the fine motor axon is a fusimotor system in the frog muscle spindle.

Action Potentials↗
PubMed1987

Enhancement by a synthetic isoprenoid of the toxicity of conjugates of epidermal growth factor with Pseudomonas exotoxin.

A newly synthesized isoprenoid, N-solanesyl-N,N'-bis(3,4-dimethoxybenzyl)ethylenediamine, has a verapamil-like structure but no calcium channel blocking activity. The isoprenoid enhanced the cytotoxic effect of a conjugate of epidermal growth factor coupled with Pseudomonas exotoxin in human KB cells. By using iodinated epidermal growth factor ([125I]EGF), the effect of the isoprenoid on intracellular transport of EGF was examined. The isoprenoid did not affect the binding and uptake of [125I]EGF by KB cells. The release of radioactivity associated with [125I]EGF into medium was slow in the presence of the isoprenoid. Density gradient fractionation studies using cell homogenates suggest that [125I]EGF accumulates in an undegraded form in lysosomes when cells are treated with the isoprenoid. The pH value in lysosomes of KB cells was 5.5, and SDB did not affect significantly the pH value at the concentrations used to potentiate the cytotoxicity of chimeric toxins. Electron microscopy showed an increased number of electron-dense bodies in KB cells grown for 24 hr with 17-51 micrograms/ml isoprenoid. The potentiating action of chimeric toxins by the isoprenoid is discussed in relation to the altered lysosomal function in treated cells.

ADP Ribose Transferases↗
PubMed1987

Chinese hamster ovary cell mutant with defective down-regulation of low density lipoprotein receptors.

A monensin-resistant clone (Monr-31) shows a related series of differences from its parental Chinese hamster ovary (CHO) cell line in the cellular response to several ligands. The uptake and metabolism of low density lipoprotein (LDL) in the mutant cells are defective. Accumulation of fluorescent-labeled LDL as well as internalization and degradation of 125I-LDL are greatly reduced in Monr-31 cells. The receptor number for LDL on the cell surface of Monr-31 is about one-third that for CHO cells, but affinity constants for both cell lines are similar. Electrophoretic analysis shows a slightly reduced molecular weight of LDL receptor in Monr-31 cells in comparison to that in CHO cells. The internalization index (internalization plus degradation per binding) of LDL of the mutant is about one-half that of CHO cells, suggesting a failure of internalization of LDL as well as LDL binding. Hybrids (hyb-1, -2, and -3) between CHO and Monr-31 cells show LDL binding and LDL internalization activities comparable to that of CHO cells, suggesting that the altered LDL response in Monr-31 cells is recessive. Addition of exogenous LDL to culture medium down-regulates the LDL receptor activity of CHO, hyb-2, and hyb-3 cells, whereas no such down-regulation is seen in Monr-31 cells. Probably as a result of the failure of down-regulation, the prominent inhibition of sterol synthesis from acetate and 3-hydroxy-3-methylglutaryl-coenzyme A reductase observed in CHO cells is scarcely detectable in Monr-31 cells. As a correlated result, sterol synthesis from acetate is 6-fold higher in the mutant. The failure of down-regulation of LDL receptors in Monr-31 cells is discussed in relation to the altered binding and internalization of LDL.

Animals↗
PubMed1987

Coronary angiographic characteristics in Japanese patients with heterozygous familial hypercholesterolemia.

Coronary angiographic findings were analyzed in 51 consecutive patients (36 males and 15 females) with heterozygous familial hypercholesterolemia (FH) and 279 consecutive patients (216 males and 63 females) without FH (non-FH). The coronary stenosis index and over 75% stenosis vessel subset were almost three times as high in the FH group. The incidence of myocardial infarction was almost twice as high in the FH group. Levels of total cholesterol and its lipoprotein fractions, except HDL-cholesterol, were almost twice as high in the FH group. In the FH group aged under 50 years, the two parameters of coronary angiogram and the incidence of myocardial infarction were significantly higher in males than in females. However, in the group aged over 50 years, all three parameters were not significantly different between those in males and females. The level of HDL-cholesterol was significantly lower in males than in females. A significantly higher incidence (18%) of coronary ectasia was observed in the FH group compared with the incidence (2%) in non-FH. All patients with coronary ectasia were males, except one female with FH. On comparison of the males among the FH patients with those among the non-FH patients matched for total cholesterol, age and other risk factors, the FH patients were associated with a significantly higher degree of coronary atherosclerosis and lower level of HDL-cholesterol. Seven FH patients with a normal coronary angiogram were observed. However, any factors as regards age, total cholesterol, HDL-cholesterol and Achilles tendon thickness failed to distinguish between the FH patients with a normal coronary angiogram and those without.(ABSTRACT TRUNCATED AT 250 WORDS)

Achilles Tendon↗
PubMed1987

Analysis of kinetic rate constants in [18F]fluorodeoxyglucose model using a least square fitting package SALS (statistical analysis with least squares).

The analysis of kinetic rate constants in the compartment model for [18F]fluorodeoxyglucose (FDG) was undertaken. Four kinetic rate constants were determined with a least square fitting package SALS (Statistical Analysis with Least Squares), using the measured data of 18F activity as a function of time. SALS calculations were found to be easy and quick with high precision. The rate constants and the curves fitted by the k3 and the k4 models were compared in situations with various degree of cerebral glucose metabolism during positron emission tomography (PET) studies. The k4 model in the determination of cerebral metabolic rate for glucose (CMRglu) was much superior than the k3 model in any given situation as it always underestimates the metabolic rate. However, the k3 model produces less variation when the cerebral radioactivity curve shows steady rising pattern.

Brain↗
PubMed1987

[A molecular basis for multidrug-resistance and reversal of resistance with human malignant cells].

Development of cellular resistance to multiple types of anticancer agents has been recognized as one of the major obstacles for the effective cancer chemotherapy. Increased expression of mdr 1 mRNA seems to be a common mechanism for multidrug resistance (MDR) in human malignant cells. The product of the mdr 1 gene is P-glycoprotein. The predicted membrane orientation of the protein and homology with bacterial active transport proteins, and capability of the protein to bind hydrophobic anticancer agents are consistent with the function of P-glycoprotein as an energy-dependent efflux pump responsible for MDR phenotype. Most of the hydrophobic agents which overcome MDR are cationic and amphipathic. These agents interact with certain polar lipids and inhibit also the binding of hydrophobic anticancer agents with P-glycoprotein. They might directly bind to the binding site of anticancer agents on P-glycoprotein and competitively inhibit the binding of anticancer agents. Alternatively, they might bind to polar lipids of membrane vesicles and indirectly inhibit the binding ability of the protein to anticancer agents by perturbing the membrane function.

ATP Binding Cassette Transporter, Subfamily B, Mem↗