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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Archives of Biochemistry and Biophysics 280 (1990), S. 346-351 
    ISSN: 0003-9861
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Solid state phenomena Vol. 89 (Feb. 2003), p. 315-320 
    ISSN: 1662-9779
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 117-118 (Jan. 1993), p. 501-506 
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-041X
    Keywords: Ascidians ; Egg fragments ; Muscle determinants ; UV-sensitivity ; Maternal messenger RNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The ascidian egg contains cytoplasmic determinants that specify the fate of larval muscle cells. In a previous study, we developed an experimental system to identify the molecular nature of muscle determinants, in which unfertilized Ciona savignyi eggs were fragmented into four pieces by centrifugation. When inseminated, only nucleated fragments (red fragments) develop into partial embryos that only show differentiation of epidermal cells. One type of enucleated fragment (black fragment) has the remarkable ability to promote muscle differentiation when fused with red fragments. In the present study, using this experimental system, we investigated the molecular nature of muscle determinants. UV irradiation of black fragments suppressed the ability to promote expression of the muscle-specific protein, myosin heavy chain. The wavelength of UV light responsible for the inactivation (250–275 nm) suggested that UV-sensitive targets are nucleic acids. Injection of poly(A)+ RNA isolated from an un-irradiated black-fragment-rich fraction into UV-irradiated black fragments partially recovered the ability to promote the expression of myosin heavy chain protein. Poly(A)+ RNA from a red-fragment-rich fraction did not rescue the suppression of UV-irradiated black fragments. These results suggest that maternal mRNAs enriched in black fragments are closely associated with muscle determinants in the ascidian egg.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Phosphodiesterase ; insulin receptor ; rat fat cell ; spontaneous obesity ; post-receptor defects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of insulin on insulin-sensitive phosphodiesterase were investigated in fat cells from rats aged 4, 8 and 16 weeks. The enzyme activities in rats aged 4 and 8 weeks higher at 0.1–30 nmol/l insulin concentrations than in rats aged 16 weeks, and half-maximum stimulations were obtained at 0.08 nmol/l in rats aged 4 weeks, at 0.15 nmol/l in rats aged 8 weeks and at 0.22 nmol/l in rats aged 16 weeks. Specific binding of insulin in fat cells from rats aged 4, 8 and 16 weeks was 3.3%, 5.0% and 11.6%/2×105 cells, respectively. Scatchard analysis indicated that increased insulin binding in fat cells from rats aged 16 weeks was due mainly to an increase of binding affinity. These results suggest that impairment of the phosphodiesterase activation system in fat cells from spontaneously obese rats is predominantly due to post-receptor defects.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Synthetic human connecting peptide ; C-peptide immunoreactivity (CPR) ; urine CPR ; blood CPR ; radioimmunoassay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A double-antibody radioimmunoassay method, using synthetic human connecting peptide as an immunizing antigen and standard, was evaluated for clinical assay of blood and urine samples. Normal fasting blood connecting peptide immunoreacivity (CPR) was 2.45±0.96 ng/ml, increasing promptly after a 50 g oral glucose load, but somewhat slower than insulin. Molar concentration of CPR exceeded that of insulin. CPR responses to glucose were subnormal in diabetics, very low in juvenile-type cases, and often poor in patients on insulin treatment. Fasting CPR levels were elevated in patients on corticosteroid treatment and with uraemia. A patient with insulin “auto-antibod” had high serum CPR. A considerable amount of CPR appeared in urine. Normal daily excretion of CPR was 1.52±0.55 μg/kg or 55.1±18.2 ng/mg creatinine. Urine CPR was very low in juvenile-type diabetics, and elevated in patients on corticosteroid treatment. The results confirm that blood and urine CPR are useful measures of the endocrine pancreatic function.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Insulin receptor ; type A insulin resistance ; deletion ; polymerase chain reaction ; insulin receptor gene ; direct sequence ; mRNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a previous report on a 16-year-old Japanese girl with type A insulin resistance, we found that one allele of the insulin receptor gene was inherited from her mother and contained a 1.2 kilobase pair deletion which removed the 14th exon in the β subunit. We extended investigation of the proband and found the deletion between two Alu sequences. To determine the effect of the deletion on the level of transcription and the splicing pattern of messenger ribonucleic acid (mRNA), we synthesized the complimentary DNA and used the polymerase chain reaction to amplify the region which included the deleted area. The deletion shifted the reading frame, resulting in a termination codon after amino acid 867 (Glu), thereby producing a truncated insulin receptor without a transmembrane region and cytoplasmic domain. We also sequenced each of 22 exons of the insulin receptor gene but found no mutation in exons of the insulin receptor gene, except for deletion of exon 14 of the maternal allele. Thus, the proband is a heterozygote for a single mutant allele. Abnormal mRNA transcribed from the mutant allele resulted in a decrease in insulin binding.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Insulin receptor ; type A syndrome of insulin resistance ; insulin binding ; autophosphorylation ; kinase activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Defects in insulin receptor function lead to impairment of the insulin response. We treated a patient with the typical phenotype of type A syndrome of insulin resistance whose insulin receptor seemed to lack the transmembrane region and cytoplasmic domain. Hyperinsulinaemia and resistance to exogenous insulin were evident, and insulin binding to cells and uptake of 2-deoxyglucose into fibroblasts were greatly decreased. Molecular weight of the α-subunit of the insulin receptor was normal, but autophosphorylation and kinase activity were impaired. In the pedigree analysis, defects in insulin binding were also observed in the mother, maternal grandfather and two maternal aunts, corresponding with the abnormality of the insulin receptor gene and mild insulin resistance. In the mother, much the same kinase defects as were seen in the patient became evident. However, no relatives had clinical symptoms similar to those seen in the patient. In the father there was a mild insulin resistance in the glucose clamp study and a borderline impaired glucose tolerance. Although insulin binding to cells was normal in the father, both autophosphorylation and kinase activity were reduced. Our findings suggest that insulin resistance in the patient may be caused by the defects in insulin receptor kinase activity as well as by a reduction in insulin binding activity.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Diabetes ; glucose transporter ; insulin receptor substrate-1 ; insulin ; genetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The beta-cell/liver glucose transporter (GLUT2) gene was screened for mutations using single-strand conformation polymorphism analysis (SSCP) in 30 Japanese subjects with non-insulin dependent diabetes mellitus (NIDDM). Analysis of all exons and adjacent intron regions identified six SSCP polymorphisms, three of which resulted in amino acid substitutions: V101I, T110I and G519E. The V101I and G519E substitutions represent new polymorphisms in this gene. The six polymorphisms were observed in both NIDDM and control groups and there were no significant differences in allele frequencies between groups. A portion of the insulin receptor substrate 1 gene in 30 NIDDM subjects and in normal control subjects was also screened for mutations. Two SSCP variants that change the sequence of the protein, δS686/687 (deletion of the codons for serine-686 and 687) and G972R, were identified in two different NIDDM subjects, both whom were also heterozygous for the V101I polymorphism in GLUT2. The GLUT2 and IRS1 amino acid polymorphisms did not show a simple pattern of co-inheritance with NIDDM in the families of these subjects suggesting that neither polymorphism is sufficient to cause NIDDM but may increase diabetes-susceptibility through their interaction with other loci and environmental factors.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0428
    Keywords: Glucokinase gene ; mutation ; Type 2 (non-insulin-dependent) diabetes mellitus ; polymerase chain reaction ; single stranded conformation polymorphism ; insulin secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mutations were screened for in the glucokinase gene of 25 Japanese patients with Type 2 (non-insulin-dependent) diabetes mellitus. Each exon was scanned by electrophoresis of enzymatically amplified DNA segments under non-denaturing conditions and variants were sequenced. A variant pattern was detected in exon 5 of one patient. Direct sequencing of this exon revealed a single nucleotide substitution in codon 188 (GCT→ACT) of one of two alleles resulting in the mutation of Ala188→Thr, an invariant residue in the sequence of all mammalian glucokinases and hexokinases. This mutation was not found in 40 normal control subjects. The proband had been diagnosed with Type 2 diabetes at the age of 62 years. Four other members of her family have the same mutation and all have Type 2 diabetes or impaired glucose tolerance. The youngest age at diagnosis of Type 2 diabetes in these other members was 13 years, suggesting that her pedigree was maturity-onset diabetes of the young (MODY). All subjects with the Thr188 mutation show a decreased insulin secretory response during oral glucose tolerance testing. Mutations in the glucokinase gene associated with Type 2 diabetes have been previously identified in Caucasian (French and British) subjects. This study indicates that mutations in this gene are also implicated in the development of Type 2 diabetes in Asians. Further studies are required to determine the frequency of mutations in glucokinase among Japanese patients with Type 2 diabetes.
    Type of Medium: Electronic Resource
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