PubMed Health⌕ Search

Biomedical subjects

B K Suarez

Publications and source records attributed to B K Suarez.

At least 19 recordsLinked to original sources
PubMed1992

Patterns of genetic variation in Native America.

Allele frequencies from seven polymorphic red cell antigen loci (ABO, Rh, MN, S, P, Duffy, and Diego) were examined in 144 Native American populations. Mean genetic distances (Nei's D) and the fixation index FST are approximately equal for the North and South American samples but are reduced in the Central American geographic area. The relationship between genetic distance and geographic distance differs markedly across geographic areas. The correlation between geographic distance and genetic distance for the North and Central American data is twice as large as that observed for the South American samples. This geographic difference is confirmed in spatial autocorrelation analyses; no geographic structure is apparent in the South American data but geographic structure is prominent in North and Central American samples. These results confirm earlier observations regarding differences between North and South American gene frequency patterns.

Blood Group Antigens↗
PubMed1991

Alcoholism and alleles of the human D2 dopamine receptor locus. Studies of association and linkage.

The association of the A1 allele of the D2 dopamine receptor gene with alcoholism was examined by comparing 32 unrelated white alcoholics with 25 unrelated white controls and by analysis of 17 nuclear families in multigenerational pedigrees of alcoholics in whom the A1 allele was segregating. All subjects had structured psychiatric interviews. Clinical assessment and genotyping were carried out independently. Thirteen (41%) of the 32 alcoholics carried the A1 allele compared with three (12%) of the 25 controls. The association with the A1 allele was significant when controls were compared with a subset of 10 alcoholics with severe medical problems (60% vs 12%), but not less severe cases. However, regardless of clinical severity or subtype, there was no evidence of linkage or cosegregation of the A1 allele and increased susceptibility to alcoholism in informative pedigrees. The possible association in the general population without linkage in families may be explained either by chance variation in our small samples or a modifying effect of the A1 allele that increases severity. Further study of the role of the D2 receptor gene in alcoholism is warranted.

Alcoholism↗
PubMed1988

Genes associated with the G2m(23) immunoglobulin allotype regulate the IgG subclass responses to Haemophilus influenzae type b polysaccharide vaccine.

We determined whether genes associated with the G2m(23) allotype, a genetic marker on IgG2 molecules, influence the subclass composition of the antibody response to Haemophilus influenzae type b polysaccharide vaccine. After immunizing 70 white adults, the geometric means (GMs) of the total, IgG, IgG1, and IgG2 antibody concentrations increased approximately 10-fold over preimmunization concentrations. There was no significant difference in the GMs of the total, IgG, or IgG1 antibody concentrations in postimmunization sera from subjects positive versus those negative for G2m(23). Adults positive for G2m(23) had a GM IgG2 concentration more than threefold higher than that of negative subjects (P less than .001). The antibody responses of 61 Amish adults immunized with type b polysaccharide vaccine were also analyzed. Those adults positive for G2m(23) had a higher GM serum IgG2 response to capsule than did those who were negative (P less than .01). These data indicate that genes associated with the G2m(23) locus regulate the IgG subclass composition of the antibody response to H. influenzae type b polysaccharide vaccine.

Adolescent↗
PubMed1986

Hemophilus influenzae type B disease in children vaccinated with type B polysaccharide vaccine.

We studied 55 cases of invasive Hemophilus influenzae type b disease occurring in children at least three weeks after vaccination with type b polysaccharide vaccine. Their mean age at the time of immunization was 27.8 months (range, 18 to 47). Meningitis developed in 39 patients, of whom 3 died and 6 had neurologic sequelae. We investigated certain host factors that may have contributed to the failure of the vaccine. The geometric mean concentration of antibody to type b polysaccharide in convalescent-phase serum from 31 of the vaccinated patients who had hemophilus disease was significantly lower than that in serum from 25 patients of similar age with the disease who had never been vaccinated (0.59 vs. 3.46 micrograms per milliliter, P less than 0.001). However, only 3 of 46 patients in whom the vaccine failed and who were tested for hypogammaglobulinemia had this finding, and none of 33 children tested for IgG2 had low serum concentrations of this immunoglobulin subclass, which is thought to be important in the immune response to polysaccharide antigens. In addition, all but 1 of the 46 patients in whom the vaccine failed and who were tested for IgG antibody to tetanus toxoid protein, a thymic-dependent antigen, had normal values, and 19 of 20 tested for hemolytic complement activity had normal levels. In white children, the presence of the Gm immunoglobulin phenotype (1,2,3, 17; ;5,13,21) was associated with a sevenfold increase in the relative risk of vaccine failure (P less than 0.003). We conclude that vaccine failure may be related in part to genetic factors, and that most vaccinated children in whom Hemophilus influenzae disease develops have deficient antibody responses to the type b polysaccharide despite normal serum concentrations of immunoglobulin and normal antibody responses to tetanus toxoid.

Antibodies, Bacterial↗
PubMed1986

Haemophilus influenzae type b disease in an Amish population: studies of the effects of genetic factors, immunization, and rifampin prophylaxis on the course of an outbreak.

In 1982, an outbreak of Haemophilus influenzae type b disease occurred in a 379-member Amish community. In an attempt to control the outbreak after the occurrence of the second case of disease, we investigated the combination of (1) rifampin chemoprophylaxis of all carriers of H influenzae type b and their household contacts from 1 month to 5 years of age and (2) H influenzae type b polysaccharide vaccine immunoprophylaxis of all community members 12 months of age and older. Despite our intervention, two additional cases of bacteremic H influenzae type b disease occurred in the ensuing 5 months, one in a 22-month-old infant who had been immunized at 19 months of age and the other in a child who had not been immunized because she was younger than 12 months of age. The outbreak ended following rifampin prophylaxis of all community members younger than 15 years of age. All of the children with disease were genetically related to one another, and three of the four were inbred. However, analysis of their coancestry revealed that neither the average level of kinship nor the average inbreeding level of the affected children differed significantly from those of the other children in the community. Furthermore, none of the four children with disease shared a human leukocyte antigen haplotype. Our observations suggest that inbreeding was not a risk factor in this community.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Genetic variation in North Amerindian populations: the geography of gene frequencies.

Ten-level synthetic gene frequency maps derived from a principal component analysis of seven polymorphic loci are displayed for a large sample of North Amerindian populations. These maps are useful for assessing population affinities over broad geographical regions and perhaps, as others have argued, for inferring recent migrations. The influence of European admixture is investigated by deleting highly admixed populations and regenerating the maps. In broad outline the resultant geographic patterning, while appearing more homogeneous, preserves many features of the maps that include the highly admixed samples--especially with respect to the Eskimo/non-Eskimo dichotomy. Further, in an effort to evaluate how varying the number of display levels affects patterning as well as interpretation, the maps were replotted at 5 and 20 levels. The 5-level maps are found to accentuate differences between the full data set and the less admixed data set, while the 20-level maps tend to obscure these differences.

Gene Frequency↗
PubMed1985

Genetic variation in North Amerindian populations: association with sociocultural complexity.

A survey of nine polymorphic loci for 82 North Amerindian populations was undertaken to test the hypothesis that increasing levels of sociocultural complexity are ineluctably accompanied by increased heterozygosity. The data reveal a significant relationship in the predicted direction. Moreover, the significant correlation between average heterozygosity and sociocultural complexity is substantially increased by the removal of 19 highly admixed samples. However, this relationship, at least among North Amerindian populations, may be more apparent than real since both mean heterozygosity and the level of sociocultural organization are significantly negatively correlated with latitude. When this latter variable is controlled for, all correlations between heterozygosity and sociocultural complexity are rendered nonsignificant.

Cultural Characteristics↗
PubMed1985

Genetic variation in North Amerindian populations: covariance with climate.

Allelic frequencies at seven polymorphic loci in 74 North Amerindian populations are examined relative to patterns of climatic variation. Canonical correlation analysis reveals strong and significant associations of heterozygosity at the ABO, Ss, Duffy, and P loci with climatic variability. Principal component analysis demonstrates that these loci tend to form correlated ensembles. Moreover, canonical correlation analysis of component scores provides support for an association between polymorphism at these loci and environmental variability. The results are concordant with two previous investigations which suggested a relationship between polymorphism for the ABO, Duffy, and Diego systems and climate. It is suggested that the examination of broad geographic patterns of genetic variation at multiple loci is a valuable, but underutilized, method of screening for the effects of long-term systematic pressures.

Climate↗
PubMed1985

Linkage analysis for psychiatric disorders. II. Methodological considerations.

Recent advances in molecular biology make genetic linkage analysis an increasingly attractive tool for the identification and characterization of genes involved in the etiology of psychiatric illnesses. However, the complex nature of psychiatric illnesses engenders a host of methodological difficulties not encountered in linkage analyses of simple, Mendelian genetic traits. A previous paper reviewed the basic concepts of genetic linkage analysis. This paper focuses on the methodological difficulties associated with the application of genetic linkage methods to psychiatric illnesses.

Age Factors↗
PubMed1985

Linkage analysis for psychiatric disorders. I. Basic concepts.

Within the last decade linkage analysis has become one of the most useful tools in the human genetics arsenal and is beginning to make substantial contributions in all areas of medicine. Its increasing popularity is a direct result of the burgeoning number of polymorphic markers that are now mapped to specific chromosomal locations. Within the near future the entire human genome is likely to be saturated. This paper is intended as an introduction to linkage analysis for non-geneticists. Basic methodological approaches, along with their strengths, weaknesses and assumptions are reviewed. A subsequent paper will critically review methodological difficulties in the application of linkage analysis to the psychiatric disorders.

Chromosome Mapping↗
PubMed1979

A simple method to detect linkage for rare recessive diseases: an application to juvenile diabetes.

A simple procedure designed specifically to detect linkage for rare recessive diseases is described. The method uses information on identity by descent scores for a pair of sibs at a marker locus conditioned on the number of affected sibs in the pair. A procedure for estimating the recombination fraction is described, and a table facilitating the likelihood ratio test of linkage is provided. The method, when applied to a collection of multiplex families segregating for juvenile diabetes mellitus, suggests the possibility that this disease is linked to the HLA complex. The method is found to compare favorably to the maximum likelihood approach, for which the computer program LIPED gives a maximum lod score of 2.48 at a male and female recombination fraction of theta = 0.20.

Diabetes Mellitus, Type 1↗
PubMed1979

Variability in sib pair genetic identity.

Using a realistic model of meiotic crossing over the variability in full sib genetic identity is estimated by simulating 200 independent pairs of sibs. The standard deviation of the percentage of the autosomal genome identical by descent (IBD) was found to be about 0.056. Simulations of sibships larger than size two revealed that the average within sibship standard deviation is between 0.054 and 0.056, thus indicating that sib pair variability is insensitive to the nonindependence structure present when considering all possible sib pairs contained in a large sibship.

Chromosomes, Human↗
PubMed1979

A three-dimensional model of dentin apposition.

Since we have found that conventional methods of dentin apposition measurements are inaccurate, we have devised a three dimensional model. This model allows the investigator to measure dentin apposition volumetrically, and simultaneously consider odontoblast activity and the geometric relationships which influence the configuration of the dentin.

Animals↗
PubMed1978

The affected sib pair IBD distribution for HLA-linked disease susceptibility genes.

The distribution of identity by descent (IBD) scores for sib pairs affected with a disease determined by a disease susceptibility (DS) locus tightly linked to the HLA complex is derived. It is shown that the sib pair IBD distribution differs from its a priori distribution and, moreover, is completely specified by three observable population parameters--the additive and dominance variances and the prevalence of the disease in the population. An application of the model is illustrated using data on juvenile diabetes mellitus.

Chromosome Mapping↗
PubMed1978

The generalized sib pair IBD distribution: its use in the detection of linkage.

General expression for the distribution of identity by descent (IBD) scores at a marker locus have been derived given neither, one or both sibs affected with a disorder determined by a linked trait locus with arbitrary gene frequency and penetrance vector. It is shown that the distirbution of IBD scores depends only on the additive and dominance variances and the population prevalence of the disorder. A one-sided test is suggested as an appropriate means of statistically testing the hypothesis that the recombination fraction is significantly less than 1/2. This sib pair approach is designed primarily to detect the presence of a critical disease susceptibility locus but when the assumptions of the incompletely penetrant single locus model are correct the methodology proposed here results in consistent estimates of the recombination fraction. The affected sib pair methodology seems especially suited to traits determined by single loci with non-Mendelian transmission.

Alleles↗