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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
    Hepatocyte nuclear factor-1a gene and non-insulin-dependent diabetes mellitus in the Japanese population (1998)
    Springer
    Acta diabetologica 35 (1998), S. 150-153 
    Details
    ISSN: 1432-5233
    Keywords: Key words Non-insulin-dependent diabetes mellitus ; MODY ; Hepatocyte nuclear factor-1α ; Genetics ; Microsatellite polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recently, hepatocyte nuclear factor-1α (HNF-1α, which is encoded by the TCF1 gene) mutations were reported in a subset of patients with maturity onset diabetes of the young (MODY3). We studied the contribution of TCF1 to genetic susceptibility to common non-insulin-dependent diabetes mellitus (type 2) in Japanese subjects by investigating allelic association with type 2 diabetes use of three markers. We also studied the frequency of the G191D mutation, the only mutation of TCF1 reported so far in late-onset type 2 diabetes. A total of 356 subjects were studied. There were no significant differences in allele frequency of the three markers between patients with type 2 diabetes and control subjects. A G191D mutation was not found in the subjects studied, giving a frequency of less than 0.4% in common type 2 diabetes. The lack of association of type 2 diabetes with three markers in and near TCF1 suggests that mutations in TCF1 derived from a limited number of founders are not a major cause of common type 2 diabetes even in the genetically homogeneous Japanese population. The data also indicate that the G191D mutation in TCF1 plays little, if any, role in susceptibility to common type 2 diabetes in the Japanese.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005920050120
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  • 3
    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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  • 4
    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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  • 5
    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: Key words 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. [Diabetologia (1995) 38: 983–985]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400589
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  • 6
    Electronic Resource
    Electronic Resource
    Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy (1998)
    Springer
    Diabetologia 41 (1998), S. 47-53 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Angiotensin I-converting enzyme gene ; I/D polymorphism ; meta-analysis ; diabetic nephropathy ; diabetic retinopathy ; genetic susceptibility.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene has repeatedly been shown to be associated with ischaemic heart disease, but the association of this genetic marker with diabetic microangiopathy is controversial. To assess the association of the genotypes with the development of diabetic nephropathy or retinopathy, we performed a meta-analysis of data from the literature, using Mantel-Haenszel method followed by the Breslow-Day test for assessing homogeneity among data. In a total of 4773 diabetic patients from 18 studies with (n = 2495) and without (n = 2278) renal complications, the D allele was significantly associated with diabetic nephropathy (p 〈 0.0001) in a dominant model (summary odds ratio 1.32, 95 % confidence interval: 1.15 to 1.51). There was no significant evidence against homogeneity of the odds ratios (χ 2 = 18.9, 20 df; p = 0.53). The association was significant both in non-insulin-dependent (p 〈 0.005) and in insulin-dependent diabetes mellitus (p 〈 0.05). Likewise, in a total of 2010 diabetic patients with (n = 1008) and without (n = 1002) retinopathy, there was no association of the I/D polymorphism with diabetic retinopathy. These data suggest that the ACE I/D polymorphism affects the risk for diabetic nephropathy, but not for diabetic retinopathy. [Diabetologia (1998) 41: 47–53]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050865
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  • 7
    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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  • 8
    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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  • 9
    Electronic Resource
    Electronic Resource
    The glycogen synthase gene in NIDDM and hypertension (1995)
    Springer
    Diabetologia 38 (1995), S. 1249-1250 
    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/BF00422377
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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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