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  • 1
    Electronic Resource
    Electronic Resource
    Diabetic nephropathy: a risk factor for diabetes mellitus in offspring (1995)
    Springer
    Diabetologia 38 (1995), S. 221-226 
    Details
    ISSN: 1432-0428
    Keywords: Key words Familial aggregation ; diabetes mellitus ; nephropathy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Both non-insulin-dependent diabetes mellitus and diabetic nephropathy show familial aggregation. If diabetes and renal disease have independent determinants (genetic or otherwise), offspring of parents with diabetic renal disease should have a similar risk of diabetes to those offspring of parents with diabetes alone. To test this hypothesis, the prevalence of diabetes was examined in a population-based pedigree study in Pima Indian offspring of three mutually exclusive parental types: 1) diabetic with renal disease, 2) diabetic, but without renal disease and 3) non-diabetic. Among offspring of one diabetic parent and one non-diabetic parent (n = 320) the prevalence of diabetes at ages 15–24 years and 25–34 years was 0 % and 11 %, respectively if the diabetic parent did not have renal disease compared with 6 % and 28 % respectively if the diabetic parent did have renal disease. Corresponding rates for offspring of two diabetic parents (n = 121) were 10 % and 17 %, respectively if neither parent had renal disease compared with 30 % and 50 %, respectively if one parent did have renal disease. The presence of renal disease in a parent with diabetes relative to diabetes alone was associated with 2.5 times the odds of diabetes (95 % confidence interval 1.4–4.3) in the offspring controlled for age, age at onset of parental diabetes and diabetes in the other parent using logistic regression. These findings provide support for parental diabetic renal disease, independent of age at onset of parental diabetes, conferring an increased risk for diabetes in the offspring. The results are compatible with the hypothesis that the susceptibility to renal disease in the parents and to diabetes in the offspring are due to shared familial environmental factors or to the same gene or set of genes. [Diabetologia (1995) 38: 221–226]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400098
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  • 2
    Electronic Resource
    Electronic Resource
    Diabetic nephropathy: a risk factor for diabetes mellitus in offspring (1995)
    Springer
    Diabetologia 38 (1995), S. 221-226 
    Details
    ISSN: 1432-0428
    Keywords: Familial aggregation ; diabetes mellitus ; nephropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Both non-insulin-dependent diabetes mellitus and diabetic nephropathy show familial aggregation. If diabetes and renal disease have independent determinants (genetic or otherwise), offspring of parents with diabetic renal disease should have a similar risk of diabetes to those offspring of parents with diabetes alone. To test this hypothesis, the prevalence of diabetes was examined in a population-based pedigree study in Pima Indian offspring of three mutually exclusive parental types: 1) diabetic with renal disease, 2) diabetic, but without renal disease and 3) non-diabetic. Among offspring of one diabetic parent and one non-diabetic parent (n=320) the prevalence of diabetes at ages 15–24 years and 25–34 years was 0% and 11%, respectively if the diabetic parent did not have renal disease compared with 6% and 28% respectively if the diabetic parent did have renal disease. Corresponding rates for offspring of two diabetic parents (n=121) were 10% and 17%, respectively if neither parent had renal disease compared with 30% and 50%, respectively if one parent did have renal disease. The presence of renal disease in a parent with diabetes relative to diabetes alone was associated with 2.5 times the odds of diabetes (95% confidence interval 1.4–4.3) in the offspring controlled for age, age at onset of parental diabetes and diabetes in the other parent using logistic regression. These findings provide support for parental diabetic renal disease, independent of age at onset of parental diabetes, conferring an increased risk for diabetes in the offspring. The results are compatible with the hypothesis that the susceptibility to renal disease in the parents and to diabetes in the offspring are due to shared familial environmental factors or to the same gene or set of genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400098
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  • 3
    Electronic Resource
    Electronic Resource
    Evidence for a role of HLA DRB1 alleles in the control of IgE levels, strengthened by interacting TCR A/D marker alleles (2000)
    Oxford BSL : Blackwell Science Ltd
    Clinical & experimental allergy 30 (2000), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: MHC class II alleles at human chromosome 6p21.1 and alleles in the TCR A/D locus at human chromosome 14q11.2 have been implicated in susceptibility to specific allergies and the modulation of total serum IgE. It has also been hypothesized that HLA and TCR allelic interactions may have a strong influence on predisposition to allergic disease.〈section xml:id="abs1-2"〉〈title type="main"〉ObjectiveThis study was performed to investigate the influence of HLA-DRB and DQB1 alleles and D14S50 alleles (adjacent to TCR A/D locus on 14q11.2), individually and in-combination, on total serum IgE levels, and on the development of specific allergies.〈section xml:id="abs1-3"〉〈title type="main"〉MethodsWe performed an association study between HLA-DRB, HLA-DQB1 polymorphisms, D14S50 alleles, total serum IgE expression and specific allergies to house dust mite, grass pollens and cat fur. A sample of 181 individuals was drawn from a larger set of 2415 adults, sampled at random from a district in Nottingham.〈section xml:id="abs1-4"〉〈title type="main"〉ResultsStrong association was observed between HLA-DRB1*0701 allele and high total serum IgE expression (P 〈 0.001). D14S50 alleles alone showed no evidence for independent association. However, there was a significant interaction between DRB1*0701 and D14S50 allele 170 such that, when both were present, there was a further increase in total serum IgE levels.〈section xml:id="abs1-5"〉〈title type="main"〉ConclusionThis study suggests that DRB1*0701 allele is involved in the modulation of total serum IgE, and that there is an interaction between DRB1*0701 and a marker adjacent to TCR A/D in the control of IgE expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2000.00944.x
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  • 4
    Electronic Resource
    Electronic Resource
    Association study of asthma and atopy traits and chromosome 5q cytokine cluster markers (1998)
    Oxford BSL : Blackwell Science Ltd
    Clinical & experimental allergy 28 (1998), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Linkage studies have provided evidence for the presence of gene(s) in the 5q cytokine cluster region which control total serum immunoglobulin E (IgE) concentration, and bronchial hyperreactivity (BHR). However, the identification of the gene(s) involved has been confounded by the lack of power of the published linkage studies and the presence of multiple candidate genes mapped to the region.〈section xml:id="abs1-2"〉〈title type="main"〉ObjectiveTo define the important loci on 5q31-33 which are implicated in the control of total serum IgE and BHR through a case/control study of association.〈section xml:id="abs1-3"〉〈title type="main"〉MethodsWe performed an association study between 11 polymorphic markers (spanning the region 5q31.1-33.1) and total serum IgE and BHR traits. A case/control sample of 181 individuals was drawn from a larger set of 2415 adults, sampled at random from a district in Nottingham, UK. Half of the subjects in this case/control sample were hyperreactive to methacholine and asthmatic (cases), while the other half were non-reactive and non-asthmatic (controls). Association analysis was performed using the non-parametric chi-squared and Mann–Whitney U-tests.〈section xml:id="abs1-4"〉〈title type="main"〉ResultsWe observed no evidence of strong allelic association between any of the above markers and the studied traits. Markers D5S404, interferon regulatory factor 1 (IRF-1) and D5S210 showed evidence of borderline association with BHR (P = 0.04, 0.03 and 0.04 respectively), and D5S404 showed borderline significance with IgE levels (P = 0.029).〈section xml:id="abs1-5"〉〈title type="main"〉ConclusionsThis study presents evidence against the presence of a strong association between markers mapped to 5q31-33 and either BHR or total serum IgE. The significance of the weaker associations observed with markers D4S404, IRF-1 and D5S210 is not clear. Whether this represents a type I error secondary to multiple hypothesis testing or a true association is uncertain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.1998.00229.x
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  • 5
    Electronic Resource
    Electronic Resource
    Hereditary susceptibility to colorectal cancer (1996)
    Springer
    Diseases of the colon & rectum 39 (1996), S. 739-743 
    Details
    ISSN: 1530-0358
    Keywords: Colorectal cancer ; Family history ; Hereditary nonpolyposis colorectal cancer ; Hereditary susceptibility
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Close relatives of patients with colorectal cancer are at an increased risk of developing a colorectal malignancy themselves. PURPOSE: A study was conducted to compare risks in relatives of patients diagnosed at different ages. METHODS: Family histories were taken from two cohorts of patients with colorectal cancer: Group A, a population group of 65 patients diagnosed at or under 45 (median, 42) years; Group B, 212 patients of all ages (median, 68 years) treated in a single surgeon's practice. RESULTS: Overall relative risk of colorectal cancer in first-degree relatives was 5.2 in Group A and 2.3 in Group B. There was familial clustering of colorectal cancers suggestive of hereditary nonpolyposis colorectal cancer in 13 (20 percent) families to Group A but to only 3 (1.5 percent) families in the second group. Cumulative incidence of colorectal cancer for relatives of the young cohort rose steeply from 40 years, reaching 5 percent at age 50 years and 10 percent at age 70 years. This contrasts with risk for relatives of older patients, in whom the shape of the curve resembles that of the overall population risk, reaching 5 percent at age 70 years and 10 percent at age 80 years. CONCLUSIONS: There appears to be a quantitative and qualitative increase in risk to relatives of patients diagnosed at a young age compared with those diagnosed later to life, at least part of which is likely to be the result of a hereditary susceptibility. Close relatives of early onset cases warrant more intensive endoscopic screening and at an earlier age than relatives of patients diagnosed at older ages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02054437
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  • 6
    Electronic Resource
    Electronic Resource
    Incidence of DNA replication errors in patients with multiple primary cancers (1998)
    Springer
    Diseases of the colon & rectum 41 (1998), S. 765-769 
    Details
    ISSN: 1530-0358
    Keywords: Multiple primary cancers ; Hereditary nonpolyposis colorectal cancer ; Replication errors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract PURPOSE: Multiple primary cancers are a feature of hereditary nonpolyposis colorectal cancer in which defects in DNA repair mechanisms result in accumulation of replication errors within tumor DNA. We assessed replication error incidence in multiple primary cancer patients who may have similar genetic defects. METHODS: DNA was obtained from 69 patients from the Yorkshire region who had developed colorectal cancer and one other primary tumor from the hereditary nonpolyposis colorectal cancer tumor spectrum (28 colorectal, 12 stomach, 15 ovary, and 14 uterus). DNA was also obtained from 86 sporadic, single primary cancer patients attending a colorectal cancer clinic. Replication error status was assessed at five microsatellite loci using fluorescent polymerase chain reaction and computer-assisted analysis. RESULTS: The replication error phenotype was observed in 7 of 86 (8 percent) of the sporadic single primary patients. This compared with 23 of 69 (33 percent) of the multiple primary group (P〈0.001). Replication error was also observed more frequently in each subgroup. Even excluding patients from families meeting the Amsterdam criteria (likely to be hereditary nonpolyposis colorectal cancer and have the replication error phenotype), this increased frequency remained in both the multiple primary group (P〈0.005) and multiple colorectal and colorectal/uterine subgroups (P〈0.001). CONCLUSIONS: Results suggest that genetic instability plays an important role in development of multiple primary cancers, particularly from certain cancer subsets. Testing for replication errors may be an appropriate way of identifying individuals at risk of multiple primary cancers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02236266
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  • 7
    Electronic Resource
    Electronic Resource
    BRCA1 and BRCA2 and Breast Cancer Incidence: A Review (1999)
    Springer
    Annals of oncology 10 (1999), S. 113-119 
    Details
    ISSN: 1569-8041
    Keywords: BRCA1 ; BRCA2 ; inherited susceptibility ; penetrance ; linkage mapping
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background. Epidemiological studies have repeatedly shown that having a family history is a risk factor for female (and male) breast cancer. Some rare families have many (4 or more) cases of early onset breast cancer (some of which also include women with ovarian cancer) which are most clearly explained by an autosomal dominant gene with high penetrance. Design. Families with multiple cases of early onset breast (and/or ovarian cancer) have been studied using linkage analysis with the intention of finding the chromosomal region containing such genes. Results. Two predisposition genes, BRCA1 and BRCA2, have been mapped and cloned. Mutations in these genes confer increased risks of cancer, although the precise level of the increased risk is still unclear. The majority of families with four or more cases of breast cancer diagnosed under the age of 60 years are due to mutations in BRCA1 or BRCA2. Conclusions. The importance of these two genes to familial breast cancer and to breast cancer incidence overall is becoming clearer, the current information is reviewed. The findings can be immediately translated into clinical practice for these multiple case families. The identification of such families raises a number of other important clinical questions concerning patient management.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008358419310
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  • 8
    Electronic Resource
    Electronic Resource
    Genetic epidemiology of cancer in utah genealogies: A prelude to the molecular genetics of common cancers (1984)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 121 (1984), S. 63-77 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041210409
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