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1.
Genet Epidemiol ; 43(1): 102-111, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30334581

RESUMO

Results from association studies are traditionally corroborated by replicating the findings in an independent data set. Although replication studies may be comparable for the main trait or phenotype of interest, it is unlikely that secondary phenotypes will be comparable across studies, making replication problematic. Alternatively, there may simply not be a replication sample available because of the nature or frequency of the phenotype. In these situations, an approach based on complementary pairs stability selection for genome-wide association study (ComPaSS-GWAS), is proposed as an ad-hoc alternative to replication. In this method, the sample is randomly split into two conditionally independent halves multiple times (resamples) and a GWAS is performed on each half in each resample. Similar in spirit to testing for association with independent discovery and replication samples, a marker is corroborated if its p-value is significant in both halves of the resample. Simulation experiments were performed for both nongenetic and genetic models. The type I error rate and power of ComPaSS-GWAS were determined and compared to the statistical properties of a traditional GWAS. Simulation results show that the type I error rate decreased as the number of resamples increased with only a small reduction in power and that these results were comparable with those from a traditional GWAS. Blood levels of vitamin pyridoxal 5'-phosphate from the Trinity Student Study (TSS) were used to validate this approach. The results from the validation study were compared to, and were consistent with, those obtained from previously published independent replication data and functional studies.


Assuntos
Estudo de Associação Genômica Ampla , Simulação por Computador , Humanos , Modelos Genéticos , Fenótipo , Polimorfismo de Nucleotídeo Único/genética , Reprodutibilidade dos Testes
2.
Genet Epidemiol ; 42(4): 405-414, 2018 06.
Artigo em Inglês | MEDLINE | ID: mdl-29682794

RESUMO

Genome-wide association studies (GWASs) are unraveling the genetics of adult brain neuroanatomy as measured by cross-sectional anatomic magnetic resonance imaging (aMRI). However, the genetic mechanisms that shape childhood brain development are, as yet, largely unexplored. In this study we identify common genetic variants associated with childhood brain development as defined by longitudinal aMRI. Genome-wide single nucleotide polymorphism (SNP) data were determined in two cohorts: one enriched for attention-deficit/hyperactivity disorder (ADHD) (LONG cohort: 458 participants; 119 with ADHD) and the other from a population-based cohort (Generation R: 257 participants). The growth of the brain's major regions (cerebral cortex, white matter, basal ganglia, and cerebellum) and one region of interest (the right lateral prefrontal cortex) were defined on all individuals from two aMRIs, and a GWAS and a pathway analysis were performed. In addition, association between polygenic risk for ADHD and brain growth was determined for the LONG cohort. For white matter growth, GWAS meta-analysis identified a genome-wide significant intergenic SNP (rs12386571, P = 9.09 × 10-9 ), near AKR1B10. This gene is part of the aldo-keto reductase superfamily and shows neural expression. No enrichment of neural pathways was detected and polygenic risk for ADHD was not associated with the brain growth phenotypes in the LONG cohort that was enriched for the diagnosis of ADHD. The study illustrates the use of a novel brain growth phenotype defined in vivo for further study.


Assuntos
Encéfalo/crescimento & desenvolvimento , Estudo de Associação Genômica Ampla , Adolescente , Adulto , Transtorno do Deficit de Atenção com Hiperatividade/genética , Criança , Estudos de Coortes , Estudos Transversais , Feminino , Predisposição Genética para Doença , Humanos , Masculino , Herança Multifatorial/genética , Fenótipo , Polimorfismo de Nucleotídeo Único/genética , Fatores de Risco , Substância Branca/patologia
3.
Genet Med ; 20(5): 503-512, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-28933792

RESUMO

PurposeCaV3.2 signaling contributes to nociception, pruritus, gastrointestinal motility, anxiety, and blood pressure homeostasis. This calcium channel, encoded by CACNA1H, overlaps the human tryptase locus, wherein increased TPSAB1 copy number causes hereditary α-tryptasemia. Germ-line CACNA1H variants may contribute to the variable expressivity observed with this genetic trait.MethodsTryptase-encoding sequences at TPSAB1 and TPSB2, and TPSG1 and CACNA1H variants were genotyped in 46 families with hereditary α-tryptasemia syndrome. Electrophysiology was performed on tsA201 HEK cells transfected with wild-type or variant CACNA1H constructs. Effects on clinical phenotypes were interrogated in families with TPSAB1 duplications and in volunteers from the ClinSeq cohort.ResultsThree nonsynonymous variants in CACNA1H (rs3751664, rs58124832, and rs72552056) cosegregated with TPSAB1 duplications in 32/46 families and were confirmed to be in linkage disequilibrium (LD). In vitro, variant CaV3.2 had functional effects: reducing current densities, and altering inactivation and deactivation properties. No clinical differences were observed in association with the CACNA1H haplotype.ConclusionA previously unrecognized haplotype containing three functional CACNA1H variants is relatively common among Caucasians, and is frequently coinherited on the same allele as additional TPSAB1 copies. The variant CACNA1H haplotype, which in vitro imparts partial gain of function, does not result in detectable phenotypic differences in the heterozygous state.


Assuntos
Canais de Cálcio Tipo T/genética , Variações do Número de Cópias de DNA , Frequência do Gene , Haplótipos , Padrões de Herança , Triptases/genética , Canais de Cálcio Tipo T/metabolismo , Linhagem Celular , Duplicação Gênica , Estudos de Associação Genética , Loci Gênicos , Técnicas de Genotipagem , Humanos , Desequilíbrio de Ligação , Mutação , Fenótipo , Análise de Sequência de DNA , Triptases/metabolismo
4.
BMC Proc ; 10(Suppl 7): 385-388, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27980666

RESUMO

In this study, the effects of (a) the minor allele frequency of the single nucleotide variant (SNV), (b) the degree of departure from normality of the trait, and (c) the position of the SNVs on type I error rates were investigated in the Genetic Analysis Workshop (GAW) 19 whole exome sequence data. To test the distribution of the type I error rate, 5 simulated traits were considered: standard normal and gamma distributed traits; 2 transformed versions of the gamma trait (log10 and rank-based inverse normal transformations); and trait Q1 provided by GAW 19. Each trait was tested with 313,340 SNVs. Tests of association were performed with simple linear regression and average type I error rates were determined for minor allele frequency classes. Rare SNVs (minor allele frequency < 0.05) showed inflated type I error rates for non-normally distributed traits that increased as the minor allele frequency decreased. The inflation of average type I error rates increased as the significance threshold decreased. Normally distributed traits did not show inflated type I error rates with respect to the minor allele frequency for rare SNVs. There was no consistent effect of transformation on the uniformity of the distribution of the location of SNVs with a type I error.

5.
J Korean Neurosurg Soc ; 59(5): 466-70, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27651864

RESUMO

OBJECTIVE: To determine imaging features that may separate adamantinomatous and papillary variants of craniopharyngiomas given that tumors with adamantinomatous signature features are associated with higher recurrence rates, morbidity, and mortality. We specifically reviewed calcification on CT, T1 bright signal intensity, and cystic change on T2 weighted images for differentiating these two types. METHODS: We retrospectively reviewed the MRI and CT studies in 38 consecutive patients with pathologically proven craniopharyngiomas between January 2004 and February 2014 for the presence of calcification on CT scans, bright signal intensity on T1 weighted images, and cystic change on T2 weighted images. RESULTS: Of the 38 craniopharyngiomas, 30 were adamantinomatous type and 8 were papillary type. On CT scans, calcification was present in 25 of 38 tumors. All calcified tumors were adamantinomatous type. Twenty four of 38 tumors had bright signal intensity on T1 weighted images. Of these 24 tumors, 22 (91.7%) were adamantinomatous and 2 were papillary type. Cystic change on T2 weighted images was noted in 37 of 38 tumors; only 1 tumor with papillary type did not show cystic change. CONCLUSION: T1 bright signal intensity and calcification on CT scans uniformly favor the adamantinomatous type over papillary type of craniopharyngioma in children. However, these findings are more variable in adults where calcification and T1 bright signal intensity occur in 70.6% and 58.8% respectively of adult adamantinomatous types of craniopharyngiomas.

6.
AJR Am J Roentgenol ; 205(5): W512-8, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26496573

RESUMO

OBJECTIVE: The objective of this study was to test the hypothesis that bitemporal hemianopsia (BHA) is the most common visual field (VF) defect in patients with pituitary macroadenoma and to assess the degree of optic pathway compression necessary to produce visual defects. MATERIALS AND METHODS: We reviewed the MRI findings and medical records of 119 patients with pituitary macroadenoma who had undergone formal assessment of VFs. We then evaluated the degree of optic pathway displacement caused by the pituitary macroadenoma, as observed on MR images. The classifications of optic pathway displacement included no contact, abutment but no displacement, mild displacement (< 3 mm), and moderate displacement (≥ 3 mm). Qualitative analysis classified VFs as normal or as having defects that were monocular, bitemporal, mixed (bitemporal with additional defects), homonymous, or nonspecific. RESULTS: A total of 89 of 115 patients had an abnormal VF. Only one patient had true BHA. The most common defects were bitemporal or mixed defects (in 49 of 115 patients [42.6%]), likely because more than just the chiasm is often compressed by the pituitary macroadenoma. Classification of optic pathway displacement by the pituitary macroadenoma was as follows: 23 patients had no contact, eight had abutment but no displacement, 27 had mild displacement, and 57 had moderate displacement. In 78 of the 92 patients (84.8%) with pituitary macroadenoma that had contact with the optic pathway, contact was with the optic chiasm and the prechiasmal optic nerve. Of the 49 patients with bitemporal or mixed defects, 42 had moderate displacement of the optic pathway caused by their tumors. CONCLUSION: BHA is exceedingly uncommon in patients with pituitary macroadenoma. However, although bitemporal and mixed defects are the most common abnormal VF findings, they were found in only 42.6% of patients. Such defects rarely occur if the tumor displaces the optic pathway less than 3 mm from baseline.


Assuntos
Adenoma/complicações , Imagem por Ressonância Magnética/métodos , Quiasma Óptico/patologia , Neoplasias Hipofisárias/complicações , Transtornos da Visão/diagnóstico , Transtornos da Visão/etiologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos
7.
PLoS Genet ; 10(10): e1004575, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25329635

RESUMO

Neurofibromatosis type 1 (NF1) is an autosomal dominant, monogenic disorder of dysregulated neurocutaneous tissue growth. Pleiotropy, variable expressivity and few NF1 genotype-phenotype correlates limit clinical prognostication in NF1. Phenotype complexity in NF1 is hypothesized to derive in part from genetic modifiers unlinked to the NF1 locus. In this study, we hypothesized that normal variation in germline gene expression confers risk for certain phenotypes in NF1. In a set of 79 individuals with NF1, we examined the association between gene expression in lymphoblastoid cell lines with NF1-associated phenotypes and sequenced select genes with significant phenotype/expression correlations. In a discovery cohort of 89 self-reported European-Americans with NF1 we examined the association between germline sequence variants of these genes with café-au-lait macule (CALM) count, a tractable, tumor-like phenotype in NF1. Two correlated, common SNPs (rs4660761 and rs7161) between DPH2 and ATP6V0B were significantly associated with the CALM count. Analysis with tiled regression also identified SNP rs4660761 as significantly associated with CALM count. SNP rs1800934 and 12 rare variants in the mismatch repair gene MSH6 were also associated with CALM count. Both SNPs rs7161 and rs4660761 (DPH2 and ATP6V0B) were highly significant in a mega-analysis in a combined cohort of 180 self-reported European-Americans; SNP rs1800934 (MSH6) was near-significant in a meta-analysis assuming dominant effect of the minor allele. SNP rs4660761 is predicted to regulate ATP6V0B, a gene associated with melanosome biology. Individuals with homozygous mutations in MSH6 can develop an NF1-like phenotype, including multiple CALMs. Through a multi-platform approach, we identified variants that influence NF1 CALM count.


Assuntos
Proteínas de Ligação a DNA/genética , Regulação Neoplásica da Expressão Gênica , Neurofibromatose 1/genética , Polimorfismo de Nucleotídeo Único , Proteínas Adaptadoras de Transdução de Sinal/genética , Adulto , Estudos de Coortes , Grupo com Ancestrais do Continente Europeu/genética , Feminino , Variação Genética , Humanos , Masculino , Complexo Mediador/genética , Pessoa de Meia-Idade , Proteína 1 Homóloga a MutL , Proteína 2 Homóloga a MutS/genética , Neurofibromatose 1/patologia , Proteínas Nucleares/genética , Fenótipo , Proteínas/genética , ATPases Vacuolares Próton-Translocadoras/genética
8.
Hum Hered ; 74(1): 36-44, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-23154503

RESUMO

OBJECTIVE: Custom genotyping of markers in families with familial idiopathic scoliosis were used to fine-map candidate regions on chromosomes 9 and 16 in order to identify candidate genes that contribute to this disorder and prioritize them for next-generation sequence analysis. METHODS: Candidate regions on 9q and 16p-16q, previously identified as linked to familial idiopathic scoliosis in a study of 202 families, were genotyped with a high-density map of single nucleotide polymorphisms. Tests of linkage for fine-mapping and intra-familial tests of association, including tiled regression, were performed on scoliosis as both a qualitative and quantitative trait. RESULTS AND CONCLUSIONS: Nominally significant linkage results were found for markers in both candidate regions. Results from intra-familial tests of association and tiled regression corroborated the linkage findings and identified possible candidate genes suitable for follow-up with next-generation sequencing in these same families. Candidate genes that met our prioritization criteria included FAM129B and CERCAM on chromosome 9 and SYT1, GNAO1, and CDH3 on chromosome 16.


Assuntos
Cromossomos Humanos Par 16/genética , Cromossomos Humanos Par 9/genética , Ligação Genética , Escoliose/genética , Adulto , Mapeamento Cromossômico/métodos , Feminino , Heterogeneidade Genética , Predisposição Genética para Doença , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único
9.
Ann Hum Genet ; 76(1): 86-91, 2012 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-22091704

RESUMO

A large number of linkage and association studies of complex diseases focus on analysis of a more common or more easily measured disease endophenotype. The motivation for this approach is that there is a pleiotropic locus common to both the disease and the endophenotype and that this locus is a major genetic determinant of the endophenotype. In this paper, we determine the conditions under which the risk of the endophenotype in siblings of affected probands with disease equals the risk of the endophenotype in the offspring (parents) of affected parents (offspring) with disease. In doing so we prove that this equality holds if and only if the penetrance of either the endophenotype or the disease (but not necessarily both) is additive.


Assuntos
Endofenótipos , Pais , Irmãos , Família , Humanos , Matemática , Penetrância , Risco
10.
BMC Proc ; 5 Suppl 9: S83, 2011 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-22373393

RESUMO

Family-based study designs are again becoming popular as new next-generation sequencing technologies make whole-exome and whole-genome sequencing projects economically and temporally feasible. Here we evaluate the statistical properties of linkage analyses and family-based tests of association for the Genetic Analysis Workshop 17 mini-exome sequence data. Based on our results, the linkage methods using relative pairs or nuclear families had low power, with the best results coming from variance components linkage analysis in nuclear families and Elston-Stewart model-based linkage analysis in extended pedigrees. For family-based tests of association, both ASSOC and ROMP performed well for genes with large effects, but ROMP had the advantage of not requiring parental genotypes in the analysis. For the linkage analyses we conclude that genome-wide significance levels appear to control type I error well but that "suggestive" significance levels do not. Methods that make use of the extended pedigrees are well powered to detect major loci segregating in the families even when there is substantial genetic heterogeneity and the trait is mainly polygenic. However, large numbers of such pedigrees will be necessary to detect all major loci. The family-based tests of association found the same major loci as the linkage analyses and detected low-frequency loci with moderate effect sizes, but control of type I error was not as stringent.

11.
BMC Proc ; 5 Suppl 9: S104, 2011 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-22373484

RESUMO

Machine learning approaches are an attractive option for analyzing large-scale data to detect genetic variants that contribute to variation of a quantitative trait, without requiring specific distributional assumptions. We evaluate two machine learning methods, random forests and logic regression, and compare them to standard simple univariate linear regression, using the Genetic Analysis Workshop 17 mini-exome data. We also apply these methods after collapsing multiple rare variants within genes and within gene pathways. Linear regression and the random forest method performed better when rare variants were collapsed based on genes or gene pathways than when each variant was analyzed separately. Logic regression performed better when rare variants were collapsed based on genes rather than on pathways.

12.
BMC Proc ; 5 Suppl 9: S15, 2011 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-22373501

RESUMO

Tiled regression is an approach designed to determine the set of independent genetic variants that contribute to the variation of a quantitative trait in the presence of many highly correlated variants. In this study, we evaluate the statistical properties of the tiled regression method using the Genetic Analysis Workshop 17 data in unrelated individuals for traits Q1, Q2, and Q4. To increase the power to detect rare variants, we use two methods to collapse rare variants and compare the results with those from the uncollapsed data. In addition, we compare the tiled regression method to traditional tests of association with and without collapsed rare variants. The results show that collapsing rare variants generally improves the power to detect associations regardless of method, although only variants with the largest allelic effects could be detected. However, for traditional simple linear regression, the average estimated type I error is dependent on the trait and varies by about three orders of magnitude. The estimated type I error rate is stable for tiled regression across traits.

13.
BMC Med Genomics ; 3: 22, 2010 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-20529293

RESUMO

BACKGROUND: The inability of aspirin (ASA) to adequately suppress platelet aggregation is associated with future risk of coronary artery disease (CAD). Heritability studies of agonist-induced platelet function phenotypes suggest that genetic variation may be responsible for ASA responsiveness. In this study, we leverage independent information from genome-wide linkage and association data to determine loci controlling platelet phenotypes before and after treatment with ASA. METHODS: Clinical data on 37 agonist-induced platelet function phenotypes were evaluated before and after a 2-week trial of ASA (81 mg/day) in 1231 European American and 846 African American healthy subjects with a family history of premature CAD. Principal component analysis was performed to minimize the number of independent factors underlying the covariance of these various phenotypes. Multi-point sib-pair based linkage analysis was performed using a microsatellite marker set, and single-SNP association tests were performed using markers from the Illumina 1 M genotyping chip from deCODE Genetics, Inc. All analyses were performed separately within each ethnic group. RESULTS: Several genomic regions appear to be linked to ASA response factors: a 10 cM region in African Americans on chromosome 5q11.2 had several STRs with suggestive (p-value < 7 x 10-4) and significant (p-value < 2 x 10-5) linkage to post aspirin platelet response to ADP, and ten additional factors had suggestive evidence for linkage (p-value < 7 x 10-4) to thirteen genomic regions. All but one of these factors were aspirin response variables. While the strength of genome-wide SNP association signals for factors showing evidence for linkage is limited, especially at the strict thresholds of genome-wide criteria (N = 9 SNPs for 11 factors), more signals were considered significant when the association signal was weighted by evidence for linkage (N = 30 SNPs). CONCLUSIONS: Our study supports the hypothesis that platelet phenotypes in response to ASA likely have genetic control and the combined approach of linkage and association offers an alternative approach to prioritizing regions of interest for subsequent follow-up.


Assuntos
Afro-Americanos/genética , Plaquetas/fisiologia , Doença da Artéria Coronariana/genética , Grupo com Ancestrais do Continente Europeu/genética , Predisposição Genética para Doença , Ativação Plaquetária , Adulto , Aspirina/farmacologia , Cromossomos Humanos Par 5 , Doença da Artéria Coronariana/etnologia , Doença da Artéria Coronariana/etiologia , Feminino , Ligação Genética , Estudo de Associação Genômica Ampla , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Fenótipo , Polimorfismo de Nucleotídeo Único , Análise de Componente Principal
14.
J Neurolinguistics ; 23(3): 176, 2010 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-20161689

RESUMO

Thought disorder as well as language and communication disturbances are associated with schizophrenia and are over-represented in clinically unaffected relatives of schizophrenics. All three kinds of dysfunction involve some element of deviant verbalizations, most notably, semantic anomalies. Of particular importance, thought disorder characterized primarily by deviant verbalizations has a higher recurrence in relatives of schizophrenic patients than schizophrenia itself. These findings suggest that deviant verbalizations may be more penetrant expressions of schizophrenia susceptibility genes than schizophrenia. This paper reviews the evidence documenting the presence of thought, language and communication disorders in schizophrenic patients and in their first-degree relatives. This familial aggregation potentially implicates genetic factors in the etiology of thought disorder, language anomalies, and communication disturbances in schizophrenia families. We also present two examples of ways in which thought, language and communication disorders can enrich genetic studies, including those involving schizophrenia.

15.
BMC Proc ; 3 Suppl 7: S64, 2009 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-20018058

RESUMO

Random forests (RF) is one of a broad class of machine learning methods that are able to deal with large-scale data without model specification, which makes it an attractive method for genome-wide association studies (GWAS). The performance of RF and other association methods in the presence of interactions was evaluated using the simulated data from Genetic Analysis Workshop 16 Problem 3, with knowledge of the major causative markers, risk factors, and their interactions in the simulated traits. There was good power to detect the environmental risk factors using RF, trend tests, or regression analyses but the power to detect the effects of the causal markers was poor for all methods. The causal marker that had an interactive effect with smoking did show moderate evidence of association in the RF and regression analyses, suggesting that RF may perform well at detecting such interactions in larger, more highly powered datasets.

16.
Comput Stat Data Anal ; 53(5): 1829-1842, 2009 03 15.
Artigo em Inglês | MEDLINE | ID: mdl-20160849

RESUMO

A linkage study of a qualitative disease endophenotype in a sample of sib pairs, consisting of one disease affected proband and one sibling is considered. The linkage statistic compares marker allele sharing with the proband in siblings with an abnormal endophenotype to siblings with the normal endophenotype. Expressions for the distribution of this linkage statistic, in terms of the recombination fraction are derived and (1) the genetic parameter values (allele frequency and endophenotype and disease penetrance) and (2) the abnormal endophenotype rates in the population and in classes of relatives of disease affected probands. It is then shown that when either the disease or the abnormal endophenotype has additive penetrance, the expressions simplify to a monotonic function of the difference between abnormal endophenotype rates in siblings and in the population. Thought disorder is considered as a putative schizophrenia endophenotype. Forty sets of genetic parameter values that correspond to the known prevalence values for thought disorder in schizophrenic patients, siblings of schizophrenics and the general population are evaluated. For these genetic parameter values, numerical results show that the test statistic has>70% power (α = 0.0001) in general with a sample of 200 or more proband-sibling pairs to detect the linkage between a marker (θ = 0.01), and a locus pleiotropic for schizophrenia and thought disorder.

17.
BMC Genet ; 6 Suppl 1: S47, 2005 Dec 30.
Artigo em Inglês | MEDLINE | ID: mdl-16451658

RESUMO

In this paper we investigate the power of finding linkage to a disease locus through analysis of the disease-related traits. We propose two family-based gene-model-free linkage statistics. Both involve considering the distribution of the number of alleles identical by descent with the proband and comparing siblings with the disease-related trait to those without the disease-related-trait. The objective is to find linkages to disease-related traits that are pleiotropic for both the disease and the disease-related-traits. The power of these statistics is investigated for Kofendrerd Personality Disorder-related traits a (Joining/founding cults) and trait b (Fear/discomfort with strangers) of the simulated data. The answers were known prior to the execution of the reported analyses. We find that both tests have very high power when applied to the samples created by combining the data of the three cities for which we have nuclear family data.


Assuntos
Mapeamento Cromossômico/métodos , Doença/genética , Modelos Genéticos , Característica Quantitativa Herdável , Irmãos , Humanos
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