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  • 1
    Electronic Resource
    Electronic Resource
    A novel microsatellite polymorphism in the human OB gene: a highly polymorphic marker for linkage analysis (1996)
    Springer
    Diabetologia 39 (1996), S. 1398-1401 
    Details
    ISSN: 1432-0428
    Keywords: KeywordsOB gene ; microsatellite ; genetics ; obesity ; diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mouse ob gene and its human homologue OB have recently been cloned. The mutations in the ob gene are known to be associated with extreme obesity. The relationship between the human OB gene and disease, however, is largely unknown due to the lack of suitable markers within or adjacent to the OB gene. To obtain informative markers, we searched for simple tandem repeat polymorphisms in the genomic sequence of the human OB gene and identified a novel tetranucleotide repeat in the 3′ flanking region. Fifteen alleles were detected in this marker with a heterozygosity of 0.85 and polymorphism information content of 0.83, indicating a highly informative nature of this marker. Two-point linkage mapping in two Centre Etude Polymorphisme Humaine (CEPH) reference families suggested that this marker is located in the interval between D7S514 and D7S530, the same interval where the OB gene is located (recombination fractions with D7S514 and D7S530 were 0.026 and 0.034, respectively). Although allele frequency distributions of this marker did not differ between 84 control subjects and 69 NIDDM patients, there was a tendency to higher body weight in control subjects with class I/class I genotype than in those without this genotype (68.8 ± 11.1 vs 60.8 ± 10.3 kg, p = 0.05). The highly polymorphic nature of this marker and its location in the OB gene makes this marker useful for linkage studies of the OB gene with a number of phenotypes, such as obesity, non-insulin-dependent diabetes mellitus, hypertension and the insulin resistance syndrome. [Diabetologia (1996) 36: 1398–1401]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050589
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  • 2
    Electronic Resource
    Electronic Resource
    Association of Trp64Arg mutation of the β3-adrenergic-receptor with NIDDM and body weight gain (1996)
    Springer
    Diabetologia 39 (1996), S. 349-352 
    Details
    ISSN: 1432-0428
    Keywords: Β3-adrenergic-receptor gene ; susceptibility ; missense mutation ; non-insulin-dependent diabetes mellitus ; insulin resistance syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible pathogenic mutation in the Β3-adrenergic-receptor gene (Trp64Arg) has been reported to be associated with an earlier age of onset of non-insulin-dependent diabetes mellitus (NIDDM) and clinical features of the insulin resistance syndrome in Pima Indian, Finnish and French subjects. Since marked heterogeneity has been reported in the association of mutations of candidate genes with NIDDM between Japanese and other ethnic groups, we investigated the association of Trp64Arg with NIDDM in Japanese subjects. The allele frequency of the mutation (Arg) was slightly, but not significantly, higher in NIDDM than in control subjects (70 out of 342 alleles [20.5%] vs 40 out of 248 [16.1%], respectively, p〉0.2). When our data were combined with those of Pima Indian and Finnish subjects, however, the Arg/Arg genotype was significantly associated with NIDDM as compared with the other two genotypes (p〈0.005, relative risk [RR] 2.13, 95% confidence interval [CI] 1.28–3.55). The Arg allele was also associated with NIDDM (p〈0.05, RR 1.27, 95% CI 1.06–1.52). Japanese subjects homozygous for the mutation had a significantly higher body mass index (mean ± SD∶25.5±3.9 kg/ m2) than heterozygotes (22.6±4.1, p〈0.05) and normal homozygotes (22.8±3.8, p〈0.05). NIDDM patients homozygous for the mutation tended to have an earlier age of onset of NIDDM than those with other genotypes. These data suggest that the Trp64Arg mutation not only contributes to weight gain and age-at-onset of NIDDM but is also associated with susceptibility to NIDDM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418352
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Association of Trp64Arg mutation of the b3-adrenergic-receptor with NIDDM and body weight gain (1996)
    Springer
    Diabetologia 39 (1996), S. 349-352 
    Details
    ISSN: 1432-0428
    Keywords: Keywordsβ 3-adrenergic-receptor gene ; susceptibility ; missense mutation ; non-insulin-dependent diabetes mellitus ; insulin resistance syndrome.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible pathogenic mutation in the β 3-adrenergic-receptor gene (Trp64Arg) has been reported to be associated with an earlier age of on-set of non-insulin-dependent diabetes mellitus (NIDDM) and clinical features of the insulin resistance syndrome in Pima Indian, Finnish and French subjects. Since marked heterogeneity has been reported in the association of mutations of candidate genes with NIDDM between Japanese and other ethnic groups, we investigated the association of Trp64Arg with NIDDM in Japanese subjects. The allele frequency of the mutation (Arg) was slightly, but not significantly, higher in NIDDM than in control subjects (70 out of 342 alleles [20.5 %] vs 40 out of 248 [16.1 %], respectively, p 〉 0.2). When our data were combined with those of Pima Indian and Finnish subjects, however, the Arg/Arg genotype was significantly associated with NIDDM as compared with the other two genotypes (p 〈 0.005, relative risk [RR] 2.13, 95 % confidence interval [CI] 1.28–3.55). The Arg allele was also associated with NIDDM (p 〈 0.05, RR 1.27, 95 % CI 1.06–1.52). Japanese subjects homozygous for the mutation had a significantly higher body mass index (mean ± SD: 25.5 ± 3.9 kg/m2) than heterozygotes (22.6 ± 4.1, p 〈 0.05) and normal homozygotes (22.8 ± 3.8, p 〈 0.05). NIDDM patients homozygous for the mutation tended to have an earlier age of onset of NIDDM than those with other genotypes. These data suggest that the Trp64Arg mutation not only contributes to weight gain and age-at-onset of NIDDM but is also associated with susceptibility to NIDDM. [Diabetologia (1996) 39: 349–352]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418352
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Identification of genes regulated by glucose in a pancreatic beta-cell line by a new method for subtraction of mRNA (1996)
    Springer
    Diabetologia 39 (1996), S. 1293-1298 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Glucose-regulated gene ; cDNA subtraction ; gene expression ; polymerase chain reaction ; expressed sequence tag.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Various genes are differentially expressed in cells during cell differentiation, development, aging, and in pathological conditions. To identify and isolate the genes that are specifically and differentially expressed in cells, we established a ligation-mediated polymerase chain reaction (PCR)-based method for cDNA subtraction. As this method is PCR-based, when target genes are expressed at high levels relative to the driver (a control pool for subtraction), even a small amount of target genes can be amplified. By this newly developed PCR-based subtraction method, a set of genes regulated by glucose were identified in a mouse insulinoma cell line. This PCR-based and non-radioactive subtraction method will be a powerful tool for identification of novel genes, specifically and differentally expressed in cells. [Diabetologia (1996) 39: 1293–1298]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050572
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Properties of utricular nerve-activated vestibulospinal neurons in cats (1996)
    Springer
    Experimental brain research 112 (1996), S. 197-202 
    Details
    ISSN: 1432-1106
    Keywords: Utricular nerve ; Vestibulospinal neuron ; Lateral and medial vestibulospinal tracts ; Vestibular nuclei ; Cat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The axonal pathway, conduction velocities, and locations of the cell bodies of utricular nerve-activated vestibulospinal neurons were studied in decerebrated or anesthetized cats using the collision test of orthodromic and antidromic spikes. For orthodromic stimulation, bipolar tungsten electrodes were placed on the utricular nerve and the other vestibular nerve branches were transected. Monopolar tungsten electrodes were positioned on both sides of the upper cervical segments (C2–4), caudal end of the cervical enlargement (C7-T1), and from the lower thoracic to the upper lumbar segments (T12-L3) and were used for antidromic stimulation of the spinal cord. Another monopolar electrode was also placed in the oculomotor nucleus to study whether utricular nerve-activated vestibulospinal neurons have ascending branches to the oculomotor nucleus. Of the 173 vestibular neurons orthodromically activated by the stimulation of the utricular nerve, 46 were second-order vestibulospinal neurons and 5 were third-order neurons. The majority of the utricular nerve-activated vestibulospinal neurons were located in the rostral part of the descending vestibular nucleus and the caudal part of the ventral lateral nucleus. Seventy-three percent of the utricular nerve-activated vestibulospinal neurons descended through the ipsilateral lateral vestibulospinal tract. Approximately 80% of these neurons reached the cervicothoracic junction, but a few reached the upper lumbar spinal cord. Twenty-seven percent of the utricular nerve-activated vestibulospinal neurons descended through the medial vestibulospinal tract or the contralateral vestibulospinal tracts. Those axons terminated mainly in the upper cervical segments. Almost none of the utricular nerve-activated vestibular neurons had ascending branches to the oculomotor nucleus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227638
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    Paper (German National Licenses)
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