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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 CTG repeats and the 1-kb Alu insertion/deletion polymorphism at the myotonin protein kinase gene in the Japanese population suggests a common Eurasian origin of the myotonic dystrophy mutation (1996)
    Springer
    Human genetics 〈Berlin〉 97 (1996), S. 145-147 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have studied linkage disequilibrium between CTG repeats and an Alu insertion/deletion polymorphism at the myotonin protein kinase gene (DMPK) in 102 Japanese families, of which 93 were affected with myotonic dystrophy (DM). All of the affected chromosomes are in complete linkage disequilibrium with the Alu insertion allele. Among the normal chromosomes, alleles of CTG repeats 5 and ≥ 17 are exclusively associated with the insertion allele. On the other hand, intermediate alleles of 11– 16 repeats show a significantly greater association with the deletion allele. A strikingly similar pattern of linkage disequilibrium observed in European populations suggests a common origin of the DM mutation in the Japanese and European populations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02265255
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  • 3
    Electronic Resource
    Electronic Resource
    Phenotypes ofdnaA mutants ofEscherichia coli sensitive to phenothiazine derivatives (1996)
    Springer
    Molecular genetics and genomics 252 (1996), S. 212-215 
    Details
    ISSN: 1617-4623
    Keywords: Escherichia coli ; Phenothiazine derivatives ; DnaA protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The activation of DnaA protein by cardiolipin is inhibited by fluphenazinein vitro. We therefore examined the sensitivity of temperature-sensitivednaA mutants ofEscherichia coli to fluphenazine and other phenothiazine derivatives. Among the eightdnaA mutants tested,dnaA5, dnaA46 dnaA602, anddnaA604, mutants with mutations in the putative ATP binding site of DnaA protein, showed higher sensitivities to phenothiazine derivatives than did the wild-type strain. ThednaA508 anddnaA167 mutants, which have mutations in the N-terminal region of DnaA protein, also showed higher sensitivities to phenothiazine derivatives. On the other hand, thednaA204 anddnaA205 mutants, with lesions in the C-terminal region of the DnaA protein, showed the same sensitivity to phenothiazine derivatives as the wild-type strain. Complementation analysis with a plasmid containing the wild-typednaA gene and phage P1-mediated transduction confirmed thatdnaA mutations are responsible for these sensitivity phenotypes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02173222
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  • 4
    Electronic Resource
    Electronic Resource
    Increase in synthesis and stability of σ 32 on treatment with inhibitors of DNA gyrase in Escherichia coli (1996)
    Springer
    Molecular genetics and genomics 253 (1996), S. 297-302 
    Details
    ISSN: 1617-4623
    Keywords: Key words Inhibitors of DNA gyrase ; Heat shock response ; σ32
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  We report here that in Escherichia coli, the anti-bacterial agent nalidixic acid induces transient stabilization and increased synthesis of σ32, accompanied by the induction of heat shock proteins (Dnak and GroEL proteins). The induction of heat shock proteins, increased synthesis of σ32, and stabilization of σ32 observed on treatment of wild-type cells with nalidixic acid were not observed in a nalA26 mutant, a strain that is resistant to nalidixic acid as the result of a mutation in the gyrA gene. Not only oxolinic acid, but also novobiocin, whose targets are the A and B subunits of DNA gyrase, respectively, also induced stabilization and increased synthesis of σ32. Thus, inhibition of the activity of DNA gyrase may cause stabilization and increased synthesis of σ32, resulting in turn in induction of heat shock proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00008596
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  • 5
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Ischemic preconditioning ; Na+/H+ exchange ; 5-(N-ethyl-N-isopropyl)amiloride (EIPA) ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6±2.8% of the risk zone to infarct in untreated Krebs buffer-perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4±2.0% and 7.0±1.0%, respectively (p〈0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1±1.5% infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50μM polymyxin B, a PKC inhibitor, or 1μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischemia caused 51.0±2.9% infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4±3.1% (p〈0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8±2.1% (p〈0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction in infarction was seen (23.8±3.5% infarction). To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia-induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which is quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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  • 6
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Key words Ischemic preconditioning – Na+/H+ exchange – 5-(N-ethyl-N-isopropyl)amiloride (EIPA) – protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6 ± 2.8 % of the risk zone to infarct in untreated Krebs buffer perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4 ± 2.0 % and 7.0 ± 1.0 %, respectively (p 〉 0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1 ± 1.5 % infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50 μM polymyxin B, a PKC inhibitor, or 1 μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischmia caused 51.0 ± 2,9 % infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4 ± 3.1 % (p 〉 0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8 ± 2.1 % (p 〉 0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction was seen (23.8 ± 3,5 % infarction) To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which ist quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Mapping of 20 polymorphic DNA markers in the rat by somatic hybrid and linkage analysis (1996)
    Springer
    Mammalian genome 7 (1996), S. 71-73 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900018
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