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  • 1
    Electronic Resource
    Electronic Resource
    HLA-associated susceptibility to Type 2 (non-insulin-dependent) diabetes mellitus: the Wadena City Health Study (1993)
    Springer
    Diabetologia 36 (1993), S. 234-238 
    Details
    ISSN: 1432-0428
    Keywords: Genetics ; Type 2 (non-insulin-dependent) diabetes mellitus ; HLA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Epidemiologic data suggest that a parental history of Type 2 (non-insulin-dependent) diabetes mellitus increases the risk of Type 1 (insulin-dependent) diabetes in siblings of a Type 1 diabetes proband. This increase in risk is consistent with a shared genetic susceptibility between Type 1 and Type 2 diabetes. We have previously reported evidence that HLA-DR4-linked factors may represent a homogeneous subset of diabetes susceptibility. First, HLA-DR4 frequency was higher in Type 1 diabetic study subjects with a Type 2 diabetic parent than in Type 1 diabetic subjects whose parents were not diabetic. Second, a DR4-haplotype was transmitted from the Type 2 diabetic parent to the Type 1 offspring more often than expected. These data are consistent with the hypothesis that families with a Type 2 diabetic parent and Type 1 diabetic child, heavily determined by HLA-DR4 linked factors, may represent a homogeneous subset of diabetes susceptibility. In this report, we further explore the relationship between the high-risk HLA antigen (HLA-DR4) in study subjects with differing glycaemic status (National Diabetes Data Group criteria). In this community-based study, we find evidence that HLA-DR4 is increased in study subjects with Type 2 diabetes and may be a marker for Type 2 diabetes susceptibility.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399956
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Shared genetic susceptibility of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus: contributions of HLA and haptoglobin (1991)
    Springer
    Diabetologia 34 (1991), S. 350-355 
    Details
    ISSN: 1432-0428
    Keywords: Genetics ; Type 1 (insulin-dependent) diabetes mellitus ; Type 2 (non-insulin-dependent) diabetes mellitus ; HLA ; haptoglobin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Epidemiologic data suggest that having a parent with Type 2 (non-insulin-dependent) diabetes mellitus increases the risk for Type 1 (insulin-dependent) diabetes in siblings of a Type 1 diabetes proband. This increase in risk is consistent with a shared genetic susceptibility between Type 1 diabetes and Type 2 diabetes. We contrast genetic risk factors in three sets of families, consisting of (1) a single Type 1 diabetic child (proband) and non-diabetic parents, (2) multiple Type 1 diabetic siblings and non-diabetic parents, and (3) at least one Type 1 diabetic child and at least one Type 2 diabetic parent. Previous studies have demonstrated that HLA region genes, which elevate the risk in Type 1 diabetes, have no significant effect with respect to the risk for developing Type 2 diabetes. An earlier report cited a contribution by the haptoglobin locus to genetic susceptibility for Type 2 diabetes. We provide evidence that a high risk HLA antigen (HLA-DR3) is decreased to a greater extent in Type 1 patients with a Type 2 parent than in Type 1 patients in which the parents are not diabetic. The role of HLA-DR4 is maintained in these families, with an unexpectedly significant increased rate of transmission of the HLA-DR4 allele from Type 2 parent to Type 1 offspring. The role of haptoglobin in these families does not appear to be important, either with respect to association with diabetes or with respect to linkage with a secondary susceptibility locus. These results indicate that families with a Type 2 parent and Type 1 child, heavily determined by HLA-DR4 linked factors, may represent a homogeneous subset of diabetes susceptibility.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00405008
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Angiotensin I-converting enzyme (ACE): estimation of DNA haplotypes in unrelated individuals using denaturing gradient gel blots (1994)
    Springer
    Human genetics 〈Berlin〉 94 (1994), S. 117-123 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The angiotensin I-converting enzyme (ACE) gene (17q23) is a candidate gene for essential hypertension and related diseases, but investigation of its role in human pathology is hampered by a lack of identified polymorphisms. Currently, a 287-bp insertion/deletion (I/D) RFLP in intron 16 represents the only one known. Additional polymorphisms for the ACE gene would make most families informative for linkage studies and would allow haplotypes to be assigned in association studies. To increase the information provided by the ACE gene, we used a sensitive screening technique, denaturing gradient gel electrophoresis (DGGE) blots, to identify polymorphisms and combined this with gene counting to identify haplotypes. Five independent polymorphisms, restriction fragment melting polymorphisms (RFMPs), were identified by four probes (encompassing half of the ACE cDNA) in digests produced by three restriction enzymes (DdeI, RsaI, and AluI). One RFMP has three alleles while the others have two alleles. In a sample of 67 unrelated control subjects, minor allele frequencies ranged from 0.12 to 0.49. A significant level of linkage disequilibrium was found for all pairs of markers. The four most informative RFMPs, taken in combination, define 24 potential haplotypes. Based on gene counting, 11 of the 24 are rare or nonexistent in this population, and the estimated heterozygosity of the remaining 13 haplotypes approaches 80%. Under these conditions for the ACE locus, phase-unknown genotypes could be assigned to haplotype pairs in unrelated subjects with reasonable certainty. Thus, using DGGE blot technique for identifying numerous DNA polymorphisms in a candidate locus, in combination with gene counting, one can often identify DNA haplotypes for both related and unrelated study subjects at a candidate locus. These markers in the ACE gene should be useful for clinical and epidemiologic studies of the role of ACE in human disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00202855
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Absence of linkage between 5q markers and serum IgE levels in four large atopic families (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 26 (1996), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Both genetic and environmental influences have been suggested to control the immunoglobulin (Ig)E response to allergens and, as a result, provide susceptibility to atopic disease. Two recent reports suggested that a major gene controlling basal IgE levels in humans was transmitted in a pattern consistent with autosomal recessive inheritance and was located on the long arm of chromosome 5 in the interleukin (IL)-4 gene complex.Objective The purpose of this report is to evaluate evidence for linkage of IgE with polymorphic genetic markers in the candidate region of 5q in four large pedigrees originally selected for studies of atopy.Method Four large, highly characterized pedigrees in which IgE levels had been determined and genotypes at markers in the 5q candidate region were evaluated using both lod score and sib pair methods of analysis.Results In these pedigrees, we reject close to moderate hnkage (up to 5 cM) of an IgE locus with markers on 5q.Conclusion The genetic aspects of IgE regulation and its role in atopy remain controversial. The data suggest that should major genes be involved in the inheritance of atopy susceptibility, they are likely to be multiple in number and likely to involve interaction with other (exogenous) environmental exposures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1996.tb00623.x
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Genetic analysis of atopy in three large kindreds: no evidence of linkage to D11S97 (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 22 (1992), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Both genetic and environmental influences have been implicated in the pathogenesis of atopic disease. A recent report suggested that a major gene providing susceptibility to atopy was transmitted in a pattern consistent with autosomal dominant inheritance and evidence was presented that places the disease locus near the D11S97 marker on human chromosome 11q. In this report, we present three large, highly characterized pedigrees in which atopy is transmitted in a pattern consistent with autosomal dominant inheritance. Genotypes at the D11S97and HLA loci were evaluated using both lod score and sib pair methods of analysis. In these pedigrees, we reject close to moderate linkage (up to 10 cM) of atopy with both D11S97 and HLA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1992.tb00132.x
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    Paper (German National Licenses)
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