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Biomedical subjects

R C Go

Publications and source records attributed to R C Go.

At least 73 records · Page 4Linked to original sources
PubMed1982

Associations of properdin factor B with melanoma.

We investigated 98 melanoma patients and 135 normal controls for differences in phenotype and genotype frequencies at the properdin factor B locus. A significant negative association with the Bf-F allele and melanoma was found, resulting in an estimated relative risk of 0.5. The estimated relative risk for developing melanoma among people with the Bf-FF genotype is 0.07. The Bf-S phenotype was significantly increased among the melanoma sample, with an estimated risk of 6.5. The data suggest association of the Bf locus with a melanoma protection and/or susceptibility gene(s).

Complement Factor B↗
PubMed1982

HLA-A, -B, and -DR associations in type I diabetes mellitus with onset after age forty.

It remains to be convincingly demonstrated whether insulin-requiring, ketosis-prone, lean-at-onset, type I diabetics who develop their disease after age 40 have the same disease as the children with similar characteristics. To address this question, we examined the population HLA genetic associations of this group. One hundred forty white, insulin-using diabetics with onset of disease past age 40 yr and 268 normal white controls have thus far been analyzed for HLA type. In the group of patients who were lean-at-onset and/or ketosis-prone (N = 54), there was a significantly increased frequency of DR4 (RR = 4.63; P less than 0.01) and significantly decreased frequency of DR2 (RR = 0.18; P less than 0.05) after correction. DR4 was also significantly increased after correction (RR = 5.72; P less than 0.25) in the subgroup who were both lean and ketosis-prone (N = 23). No significant differences in HLA-DR frequencies were found between the obese and not-ketosis-prone group (N = 69) and controls. No significant associations of HLA-A or-B antigens with either group were observed after correction for the number of antigens tested. To our knowledge, this is the first such study in the United States, and the first demonstrating that late onset diabetics who are lean-at-onset and/or ketosis-prone exhibit HLA-DR antigen associations which are similar to early onset cases.

Adult↗
PubMed1982

Evidence for genetic admixture as a determinant in the occurrence of insulin-dependent diabetes mellitus in U.S. blacks.

In recent years, it has been proposed that genetic admixture may have played a role in the increased frequency of insulin-dependent diabetes mellitus (IDDM) in young U.S. blacks relative to African blacks. In support of this proposal, the similar associations of specific markers of the major histocompatibility complex (MHC) with IDDM in U.S. blacks with respect to U.S. whites have been cited. To determine whether racial admixture was a factor in the increased prevalence, we did three analyses of admixture. In the first we used nine genetic markers (ABO, Rh, Fy, Hp, Gc, Pl, OR, Tfr, and Gm) and determined that there was significantly greater than zero genetic contribution from whites in our sample of U.S. black IDDM patients (9.6 +/- 2.3%, P less than 0.01) when a sample of U.S. blacks without IDDM was used as one "parental" population. In the next two analyses, we estimated the amounts of genetic contribution from whites in the U.S. blacks with and without IDDM using reported gene frequencies for West African blacks for four genetic markers (ABO, Rh, Fy, and Hp). The estimate of admixture (21.4 +/- 2.8%) for the black IDDM sample was greater than that for the U.S. black controls (17.9 +/- 2.3%), although the difference was not significant. Our estimate of genetic contribution from whites, 21.4% for black IDDM patients, supports the assumptions of 20% admixture which MacDonald and Rotter and Hodge used to test their respective models for the inheritance of IDDM. These results support the hypothesis that admixture with the white population is, in part, responsible for the increase in prevalence of IDDM seen in U.S. blacks.

Black People↗
PubMed1981

Properdin factor B polymorphism in Black Americans.

Properdin factor B is a genetically-controlled polymorphism that can be demonstrated by agarose gel electrophoresis. The Bf gene frequencies were determined for 194 blacks from the south-eastern United States. The frequencies for Bf-F, Bf-S, Bf-F1, and Bf-S1 are 0.626, 0.034, and 0.013, respectively. The south-eastern blacks have similar Bf frequencies to the South African blacks; however, both these groups are different from blacks from Boston. The frequency differences between south-eastern blacks and Boston blacks may be due to racial admixture differences found in the two populations.

Black People↗
PubMed1980

Allele increasing susceptibility to human breast cancer may be linked to the glutamate-pyruvate transaminase locus.

The patterns of the occurrence of breast cancer in 11 high-risk families were evaluated by segregation and linkage analysis. These patterns were consistent with the hypothesis that increased susceptibility to breast cancer was inherited as an autosomal dominant allele with high penetrance in women. The postulated susceptibility allele in these families may be chromosomally linked to the glutamate-pyruvate transaminase (E.C. 2.6.1.2, alanine aminotransferase) locus. Confirmation of this linkage in other families would establish the existence of a gene increasing susceptibility to breast cancer. Since there is no association in the general population between a woman's glutamate-pyruvate transaminase genotype and her cancer risk, the glutamate-pyruvate transaminase linkage cannot be used as a screening test for breast cancer.

Alanine Transaminase↗
PubMed1979

Possible linkage between alpha-haptoglobin (Hp) and depression spectrum disease.

Depression spectrum disease is an unipolar depressive illness in which at least one member of the family has unipolar depression and at least one other first degree relative has alcoholism and/or antisocial personality; using this definition, 14 depression spectrum disease families are studied. Assuming, among other things, that variability in age of onset is environmentally caused and lognormally distributed, segregation analysis shows that the data are compatible with the dichotomy of 'affected' versus 'not affected' being due to an autosomal dominant gene. A simple environmental hypothesis in which the transmission of the illness does not depend upon the parents' type could be rejected (p less than 0.001). Linkage analysis is performed by the method of maximum likelihood, taking the best fitting Mendelian model found in the segregation analysis. The results show virtually no evidence of linkage between depression spectrum disease and C3, but suggestive evidence (lod score = 1.03) of linkage between depression spectrum disease and alpha-haptoglobin (both these linkages were previously suggested by significant results in sib-pair analyses).

Adolescent↗
PubMed1978

The malignancy of dementias.

Sruvival times were determined for 982 patients admitted over a ten-year period to the Geneva Psychiatric Clinic. Patients with dementia had one-third the life expectancy of controls. Among patients classed as having Alzheimer disease, the longest survival times were in those with neurofibrillary tangles involving the neocortex, while those lacking this anatomical abnormality had the shortest survival times. Except for women with Alzheimer disease, patients with dementia had less than 10% life expectancy from the time of their admission to the clinic compared to the life expectancy of Geneva's population.

Aged↗
PubMed1978

Efficiency and robustness of pedigree segregation analysis.

Different pedigree structures and likelihoods are examined to determine their efficiency for parameter estimation under one-locus models. For the cases simulated, family size has little effect; estimates based on unconditional likelihoods are generally more efficient than those based on conditional likelihoods. The proposed method of pedigree analysis under a one-locus model is found to be robust in the analysis of nuclear families: skewness of the data and polygenic inheritance will not lead to the spurious detection of major loci unless they occur simultaneously, and together with a moderate amount of environmental correlation among sibs.

Gene Frequency↗
PubMed1977

Linkage relationships of Lp and Ag serum lipoproteins with 25 polymorphic markers.

Linkage relations of Lp and Ag serum lipoproteins with 25 polymorphic marker systems are examined in a large kindred of over 100 persons. The results indicate that Lp and ESD are probably closely linked and so the Lp locus may also be assigned to chromosome 13. No significant linkage is detected between Ag and the other marker systems.

Chromosomes, Human, 13-15↗
PubMed1977

Possible linkage between group-specific component (Gc protein) and pure depressive disease.

Genetic linkage was studied in pure depressive disease, a subgroup of unipolar depression defined by absence of familial alcoholism and/or antisocial personality. Rigorous research criteria were used for diagnosis and the diagnoses were made blind, i.e. without the knowledge of the genetic marker results. Under the assumptions of full penetrance and of all examined individuals' having passed the risk period, two out of eight families investigated showed a possibility of linkage, using the lod score method, with the Group-Specific Component (Gc protein) locus, one of the 17 polymorphic markers tested. The results, being based on a small amount of data, are presented as a hypothesis only; important possible implications of Psychiatry, however, indicate the desirability of testing the hypothesis.

Alpha-Globulins↗
PubMed1976

A linkage study of depression spectrum disease: the use of the sib-pair method.

Genetic linkage was studied in depression spectrum disease, a subgroup of unipolar depressive illness defined by presence of familial alcoholism and/or antisocial personality, using a version of the sib pair method of Penrose. Rigorous research diagnostic criteria were used and the diagnoses were made blind, i.e., without knowledge of the genetic marker results. Possibility of linkage was suggested (p less than 0.005) with the alpha-haptoglobin (alpha-Hp) and third complement component (C3) loci. However, the likelihood that these two markers are not on the same chromosome, and the limitations of the sib pair method, permit these findings to be treated as suggestive only and indicate that these two promising markers should be investigated further, using a more definitive method of linkage detection such as the lod score method.

Adolescent↗