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  • 1
    Electronic Resource
    Electronic Resource
    Space and time-resolved measurements of plasma density by a lithium neutral beam probe in NBT-1M (1985)
    [S.l.] : American Institute of Physics (AIP)
    Review of Scientific Instruments 56 (1985), S. 1050-1052 
    Details
    ISSN: 1089-7623
    Source: AIP Digital Archive
    Topics: Physics , Electrical Engineering, Measurement and Control Technology
    Notes: A lithium neutral beam probe has been improved for space and time-resolved measurements of plasma density in NBT-1M. A lithium neutral beam (4 keV, 10–30 μA) is injected into the plasma and photon flux emitted from the injected lithium atoms by electron impact excitation is detected. This cross section is not sensitive to the electron temperature in a wide range (10 eV〈Te 〈200 eV) and the photon flux intensity is proportional to the electron density. Typical spatial and temporal resolutions are 1 cm and a few milliseconds, respectively. Beam attenuation is not severe for plasmas with n1〈1014 cm−2 unless the ion temperature is very high (Ti 〉1 keV), where the attenuation through charge-exchange process becomes dominant. This method is not influenced by the magnetic field and can be applied to plasmas in any magnetic field configuration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1138265
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  • 2
    Electronic Resource
    Electronic Resource
    The cataract Shionogi mouse, a sister strain of the non-obese diabetic mouse: similar class II but different class I gene products (1988)
    Springer
    Diabetologia 31 (1988), S. 254-258 
    Details
    ISSN: 1432-0428
    Keywords: Major histocompatibility complex ; non-obese diabetic mouse ; non-obese non-diabetic mouse ; cataract Shionogi mouse ; insulin-dependent diabetes ; restriction fragment length polymorphisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied with a series of monoclonal antibodies and restriction fragment analysis the K, D, and class II region of the major histocompatibility complex of the non-obese diabetic mouse in comparison with its sister strains, the non-obese non-diabetic and cataract Shionogi mouse. (1) K region: Monoclonal antibody 31-3-4S (anti-Kd) reacted with splenocytes from non-obese diabetic mice while other anti-K (Kb, Kk, Kq) monoclonals did not react. Splenocytes from non-obese non-diabetic mice reacted with both anti-Kb and Kk monoclonals while splenocytes from cataract Shionogi mice reacted with anti-Kd and Kk monoclonals. Both sister strains, therefore, differ from the non-obese diabetic and other known mice strains by monoclonal analysis of H-2K. (2) D region: Splenocytes from both non-obese diabetic and non-obese non-diabetic mice reacted with monoclonal antibody 28-14-8S (anti-Db) while splenocytes from cataract Shionogi mice did not react with any anti-D monoclonal antibody tested. (3a) Class II region (non-obese diabetic and non-obese non-diabetic mice): Three of 11 monoclonal antibodies to class II molecules reacted with splenocytes of the non-obese diabetic mouse. The 3 reacting monoclonals have I-Ak primary specificities though additional anti-I-Ak monoclonal antibodies were negative. Among these monoclonals, 39B and 40A reacted with the non-obese diabetic mouse but not with the non-obese non-diabetic mouse, while 10-2-16 reacted with non-obese diabetic, non-obese non-diabetic and cataract Shionogi mice. Monoclonal MKD6 (anti-I-Ad) reacted with non-obese non-diabetic but not non-obese diabetic mice. In crosses of non-obese diabetic with non-obese non-diabetic mice, splenocytes from all diabetic backcrosses studied (6/6) were positive with monoclonal 40A but negative with MKD6 indicating that the major histocompatibility complex of non-obese non-diabetic mice is not diabetogenic and confirming major histocompatibility complex-linkage of the diabetogenic gene in this additional cross. (3b) Class II region (cataract Shionogi mice): Utilising 11 anti-class II monoclonal antibodies the pattern of reactivity of the cataract Shionogi mouse was identical to the non-obese diabetic mouse. Splenocytes from both non-obese diabetic and cataract Shionogi mice fail to express I-E (no reaction with monoclonal 14-4-4). In addition, using an I-A alpha probe with restriction endonuclease HindIII or I-A beta probe with BamHI, the restriction fragment length polymorphism pattern of the cataract Shionogi mouse was identical to the non-obese diabetic mouse. In summary, the cataract Shionogi mouse appears to have a similar I-A region to the non-obese diabetic mouse but differs at both the K and D region. With the hypothesis that the unique I-A beta of the non-obese diabetic mouse is diabetogenic, the cataract Shionogi mouse should provide a new strain for further characterisation of diabetogenic genes of the non-obese diabetic mouse since it is similar at I-A, fails to express I-E, but differs at both class I loci.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00290594
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  • 3
    Electronic Resource
    Electronic Resource
    Class I HLA is associated with age-at-onset of IDDM, while class II HLA confers susceptibility to IDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 1493-1495 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400620
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  • 4
    Electronic Resource
    Electronic Resource
    The NSY mouse: a new animal model of spontaneous NIDDM with moderate obesity (1995)
    Springer
    Diabetologia 38 (1995), S. 503-508 
    Details
    ISSN: 1432-0428
    Keywords: NSY mouse ; non-insulin-dependent diabetes mellitus ; animal model ; insulin secretion ; isolated islets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The NSY (Nagoya-Shibata-Yasuda) mouse was established as an inbred strain of mouse with spontaneous development of diabetes mellitus, by selective breeding for glucose intolerance from outbred Jcl∶ICR mice. NSY mice spontaneously develop diabetes mellitus in an age-dependent manner. The cumulative incidence of diabetes is 98% in males and 31% in females at 48 weeks of age. Neither severe obesity nor extreme hyperinsulinaemia is observed at any age in these mice. Glucose-stimulated insulin secretion was markedly impaired in NSY mice after 24 weeks of age. In contrast, fasting plasma insulin level was higher in male NSY mice than that in male C3H/He mice (545±73 vs 350±40 pmol/l, p〈0.05, at 36 weeks of age). Pancreatic insulin content was higher in male NSY mice than that in male C3H/He mice (76±8 vs 52±5 ng/mg wet weight, p〈0.05, at 36 weeks of age). Morphologically, no abnormal findings, such as hypertrophy or inflammatory changes in the pancreatic islets, were observed in NSY mice at any age. These data suggest that functional changes of insulin secretion in response to glucose from pancreatic beta cells may contribute to the development of non-insulin-dependent diabetes mellitus (NIDDM) in the NSY mouse. Although insulin sensitivity was not measured, fasting hyperinsulinaemia in NSY mice suggests that insulin resistance may also contribute to the pathogenesis of NIDDM. Since these findings are similar to the pathophysiologic features of human NIDDM patients, the NSY mouse is considered to be useful for investigating the pathogenesis and genetic predisposition to NIDDM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400717
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  • 5
    Electronic Resource
    Electronic Resource
    The NSY mouse: a new animal model of spontaneous NIDDM with moderate obesity (1995)
    Springer
    Diabetologia 38 (1995), S. 503-508 
    Details
    ISSN: 1432-0428
    Keywords: Key words NSY mouse ; non-insulin-dependent diabetes mellitus ; animal model ; insulin secretion ; isolated islets.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The NSY (Nagoya-Shibata-Yasuda) mouse was established as an inbred strain of mouse with spontaneous development of diabetes mellitus, by selective breeding for glucose intolerance from outbred Jcl:ICR mice. NSY mice spontaneously develop diabetes mellitus in an age-dependent manner. The cumulative incidence of diabetes is 98 % in males and 31 % in females at 48 weeks of age. Neither severe obesity nor extreme hyperinsulinaemia is observed at any age in these mice. Glucose-stimulated insulin secretion was markedly impaired in NSY mice after 24 weeks of age. In contrast, fasting plasma insulin level was higher in male NSY mice than that in male C3H/He mice (545 ± 73 vs 350 ± 40 pmol/l, p 〈 0.05, at 36 weeks of age). Pancreatic insulin content was higher in male NSY mice than that in male C3H/He mice (76 ± 8 vs 52 ± 5 ng/mg wet weight, p 〈 0.05, at 36 weeks of age). Morphologically, no abnormal findings, such as hypertrophy or inflammatory changes in the pancreatic islets, were observed in NSY mice at any age. These data suggest that functional changes of insulin secretion in response to glucose from pancreatic beta cells may contribute to the development of non-insulin-dependent diabetes mellitus (NIDDM) in the NSY mouse. Although insulin sensitivity was not measured, fasting hyperinsulinaemia in NSY mice suggests that insulin resistance may also contribute to the pathogenesis of NIDDM. Since these findings are similar to the pathophysiologic features of human NIDDM patients, the NSY mouse is considered to be useful for investigating the pathogenesis and genetic predisposition to NIDDM. [Diabetologia (1995) 38: 503–508]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400717
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  • 6
    Electronic Resource
    Electronic Resource
    Association of distal chromosome 2q with IDDM in Japanese subjects (1998)
    Springer
    Diabetologia 41 (1998), S. 228-232 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Genetic susceptibility ; linkage disequilibrium ; association ; positional cloning ; microsatellite marker.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An insulin-dependent diabetes mellitus (IDDM)-susceptibility gene (IDDM13) has recently been mapped to a region of distal chromosome 2q, which is syntenic to the region of mouse chromosome 1 containing a murine susceptibility gene for IDDM, Idd5. To determine the contribution of this region to IDDM disease susceptibility further and to narrow the region for positional cloning of susceptibility genes, we have studied the association of distal chromosome 2q with IDDM in the genetically distinct Japanese population. A 137 mobility unit (mu) allele at D2S137 locus was significantly associated with IDDM (odds ratio 1.92, p = 0.0016). Other markers, D2S301 and D2S143, located in the same region were not associated with IDDM, indicating that IDDM13 is in linkage disequilibrium with D2S137, but not with D2S301 or D2S143. The association of D2S137 with IDDM was observed in patients lacking one of two high risk HLA alleles, DQB1 * 0303 and DQB1 * 0401, but not in patients with either of these alleles. The frequency of high risk HLA alleles was significantly lower in patients with the susceptible allele at D2S137, suggesting that IDDM13 contributes to IDDM susceptibility in subjects without high risk genotypes at IDDM1. Demonstration of allelic association of D2S137 with IDDM localizes IDDM13 in the close vicinity (〈 2 centiMorgans) of D2S137, greatly facilitating fine structure mapping and positional cloning of IDDM13. [Diabetologia (1998) 41: 228–232]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050894
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  • 7
    Electronic Resource
    Electronic Resource
    Age-dependent changes in phenotypes and candidate gene analysis in a polygenic animal model of Type II diabetes mellitus; NSY mouse (2000)
    Springer
    Diabetologia 43 (2000), S. 932-938 
    Details
    ISSN: 1432-0428
    Keywords: Keywords NSY mouse, ageing, animal model, insulin resistance, glucose transporter 4.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The Nagoya-Shibata-Yasuda (NSY) mouse closely mimics human Type II (non-insulin-dependent) diabetes mellitus in that the onset is age-dependent, the animals are not severely obese, and both insulin resistance and impaired insulin response to glucose contribute to disease development. The aim of this study was to clarify the influence of age on the pathogenesis of diabetes and to analyse a candidate gene for Type II diabetes in this strain.¶Methods. Several phenotypic characteristics related to diabetes mellitus were monitored longitudinally in male NSY and control C3H/He mice. The nucleotide sequence of Glut4, a candidate gene for Nidd1nsy (a susceptibility gene for Type II diabetes) on Chromosome 11, encoding insulin-sensitive glucose transporter, was determined in NSY and C3H mice.¶Results. Glucose intolerance worsened with age, and fasting blood glucose and fasting plasma insulin concentration increased with age in NSY mice. Pancreatic insulin content increased until 24 weeks of age but then decreased at 48 weeks of age in NSY mice. The hypoglycaemic response to insulin was statistically significantly smaller in NSY than in C3H/He mice. The nucleotide sequence of GLUT4 cDNA was identical in NSY and C3H/He mice, but both were different from the sequence reported previously.¶Conclusion/interpretation. Insulin secretion and insulin resistance, as well as ageing possibly play an important part in the disease development in NSY mice. A decline of pancreatic insulin content in older age might cause the relative insulin deficiency in this strain. Nucleotide sequencing suggests that Glut4 is unlikely to be a candidate gene for Nidd1nsy. [Diabetologia (2000) 43: 932–938]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051472
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  • 8
    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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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    A mutation in the glucagon receptor gene (Gly40Ser): heterogeneity in the association with diabetes mellitus (1995)
    Springer
    Diabetologia 38 (1995), S. 983-985 
    Details
    ISSN: 1432-0428
    Keywords: Glucagon receptor gene ; susceptibility ; missense mutation ; non-insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible pathogenic mutation in the glucagon receptor gene causing a Gly to Ser change at codon 40 (Gly40Ser) was reported to be associated and linked with non-insulin-dependent diabetes mellitus (NIDDM), in France and Sardinia, Since the frequency of the mutation (Gly40Ser), about 5% in the French population of familial NIDDM and 8% in randomly chosen diabetic patients in Sardinia, was much higher than that of any of the previously reported mutations in candidate genes, it is important to clarify whether the contribution of this mutation to NIDDM is universal. In this study, we investigated the association of this mutation with diabetes mellitus in a large number of Japanese diabetic patients (383 NIDDM and 53 insulin-dependent diabetic patients) by polymerase chain reaction-restriction fragment length polymorphism analysis. None of the Japanese diabetic patients showed Gly40Ser mutation and the association of this mutation with NIDDM was significantly different (p〈4·10−5 vs French, p〈3·10−6 vs Sardinian by Fisher's exact test). The results not only indicate that the mutation plays little, if any, role in susceptibility to diabetes in Japan, but also indicate the genetic heterogeneity in NIDDM and further emphasize the importance of studies on genetic susceptibility to NIDDM and other complex traits in different ethnic groups.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400589
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