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1 COME from 35 hospitals in the UK, and their nuclear family.
2 l for the number of ASPs contributed by each nuclear family.
3 orithm-namely, genotype elimination within a nuclear family.
4 t residue 1126 of the mature receptor in one nuclear family.
5 ultiple parent-offspring pairs from the same nuclear family.
6 on the basis of data from arbitrary types of nuclear families.
7 t cases included 2,107 Pima Indians from 715 nuclear families.
8 xtended pedigrees were no more powerful than nuclear families.
9 grees and are not restricted to sib pairs or nuclear families.
10 nvolving 186 affected sibling pairs from 160 nuclear families.
11 relapsing individuals and 11 controls from 5 nuclear families.
12 ated in our previous linkage analysis of 428 nuclear families.
13 ng of quantitative trait loci (QTL) based on nuclear families.
14 ix SNP and fed these into Transmit using 148 nuclear families.
15 d 29 SNP throughout this region in psoriatic nuclear families.
16 for quantitative traits and extended here to nuclear families.
17 aximum detection rate is 34% for four-person nuclear families.
18 hree of 18 unrelated BBS probands from small nuclear families.
19 ian population-based sample of 232 Caucasian nuclear families.
24 ase and automated pedigree software, that 23 nuclear families affected with MCPHA are connected to a
30 merican family-based study population (n=219 nuclear families) and two case-control populations--one
31 tions for a set of tightly linked markers in nuclear families, and the objective is to identify famil
32 ave implemented the basic model for use with nuclear families, and we illustrate its application thro
33 esting, counseling, and risk calculation for nuclear families, as well as extended family members at
34 the MHC region on chromosome 6p21-22 in 225 nuclear families ascertained by African American proband
35 an based on 354 markers in 513 members of 92 nuclear families ascertained through extreme obesity and
37 sease associations for both case-control and nuclear family-based data-including application of corre
38 ide some guidance to investigators designing nuclear family-based linkage disequilibrium studies for
41 lso found in 12 Caucasian Amish kindreds (24 nuclear families) by both sib-pair and transmission dise
42 e phenotyping and genomic analysis utilizing nuclear families can provide a diagnosis in some cases a
43 st three carefully selected individuals in a nuclear family can recover >90% of the information avail
45 udy, we examined genome screen data from 148 nuclear families, collected without reference to phenoty
46 es in different family structures, including nuclear families commonly used in complex disease gene m
47 l clones (TCC) directed against MOG in three nuclear families, comprised of four individuals affected
48 e performed a genomewide linkage scan in 204 nuclear families comprising 853 individuals and 270 affe
52 -23 and 20p12 in a cohort of 115 multiethnic nuclear families containing 145 SLE-affected sibpairs.
54 inkage disequilibrium typically are based on nuclear-family data including affected individuals and t
56 mutation as an inheritance inconsistency in nuclear-family data, as a function of both the number of
57 packages for model-free linkage analysis of nuclear-family data, by applying them to single-marker d
58 d an extensive simulation study on simulated nuclear-family data, varying the number of trait loci, f
59 oach is applicable to either case/control or nuclear-family data, with case/control data modeled via
63 tism Symptom Scale (BPASS), were measured in nuclear families, each ascertained through two probands
64 were conducted in 3,369 individuals from 906 nuclear families enrolled, without selection, in a longi
65 of complex disease we have regenotyped five nuclear families first studied in the 1996 UK multiple s
66 analysis to obesity, and 236 sib pairs in 82 nuclear families, for linkage analysis to energy metabol
68 ned 92 affected individuals, representing 82 nuclear families, for mutations, using single-strand con
70 blood assay in 392 children belonging to 135 nuclear families from an area hyperendemic for tuberculo
76 andard methods require selection of a single nuclear family from any extended pedigrees when testing
77 segregates with a disease phenotype in small nuclear families, from genome-wide oligonucleotide micro
78 Our previous genomewide linkage scan of 428 nuclear families (GeneQuest) identified a significant ge
81 me-wide linkage scans with hundreds of small nuclear families have identified new susceptibility gene
84 is of data on multigenerational extended and nuclear families identified the features of structural a
88 rt comprised 1,037 predominantly white (82%) nuclear families in which at least 1 member had SLE.
90 transmission of memory disorders differs in nuclear families in which the AD-affected proband did ca
93 ies in 1465 American white subjects from 218 nuclear families indicated that allelic variation at, or
96 e storage rate after adjusting for age, sex, nuclear family membership, and percentage of body fat (P
97 investigated blood pressure in 1,183 Chinese nuclear families (mother, father, and first two children
99 In our previous genome-wide scan of Finnish nuclear families, obesity was linked to chromosome Xq24.
100 d nonsmokers, representing approximately 404 nuclear families of African American (AA) or European Am
101 tal of 2037 smokers and non-smokers from 602 nuclear families of African- or European-American (AA or
102 mple consisting of 2037 individuals from 602 nuclear families of African-American (AA) or European-Am
103 ruct a general approach that can accommodate nuclear families of any size, with or without parental i
104 ed out a complex segregation analysis in 636 nuclear families of consecutively ascertained and rigoro
105 found to be associated with total IgE in 420 nuclear families of Costa Rican children with asthma.
106 Participants were 2037 subjects from 602 nuclear families of either African-American (AA) or Euro
111 d to include only one affected offspring per nuclear family per extended pedigree; multiple three-mar
112 obese (BMI >or=35 kg/m(2)), and 84.8% of the nuclear families possessed >or=1 morbidly obese sibling
113 of 914 EoE probands (n = 2192 first-degree "Nuclear-Family" relatives) and an international registry
115 ample (187 families, 564 subjects), a German nuclear family sample (211 families, 751 subjects) and a
116 211 families, 751 subjects) and a Pittsburgh nuclear family sample (247 families, 729 subjects).
117 ilies (n=1240 individuals) were added to the nuclear family sample, and the Gln27Glu polymorphism in
120 region in a sample of 181 sib pairs from 82 nuclear families that were selected on the basis of a dy
121 de meals especially for working parents in a nuclear family therefore it is imperative to determine t
122 icate this finding; combined analysis of 194 nuclear families through use of the transmission/disequi
123 ificate data dating back to 1967 and allowed nuclear families to be reconstructed by linking children
124 ssue and then perform simulation studies for nuclear families to compare the methods in terms of powe
125 wo approaches to segregation analysis in 102 nuclear families to estimate genetic models for componen
126 We collected 70 families, ranging from small nuclear families to extended multigenerational pedigrees
127 le-nucleotide polymorphism data collected in nuclear families to localize crossovers with high spatia
128 one heterozygous for DRD4*7R), including 12 nuclear family trios and 52 trios from four large TS kin
129 Canadian replication cohort consisted of 364 nuclear family trios with one type 1 diabetes-affected o
132 iduals of Chinese and Japanese descent, from nuclear families, was genotyped for two polymorphisms, r
133 ed data from 716 Pima Indians comprising 217 nuclear families, we have tested a number of polymorphic
134 g all possible affected sib pairs (ASPs) per nuclear family, we obtained a peak maximum LOD score bet
135 the hoarding phenotype in a data set with 53 nuclear families, which were collected by the Tourette S
136 of data simulated for 956 siblings from 263 nuclear families who had participated in a linkage study
137 re generated using 9,291 subjects from 2,900 nuclear families who participated in the National Heart,
140 enotyping these in an independent set of 636 nuclear families with 974 affected offspring revealed 75
142 sis of HLA class II alleles in 180 Caucasian nuclear families with at least two children with insulin
143 ng technology in finding causal mutations in nuclear families with dominantly inherited traits otherw
144 an also produce multimegabase haplotypes for nuclear families with just two children and can handle f
147 data on a polymorphism of the SDR5A2 gene in nuclear families with multiple cases of prostate cancer.
148 jects (815 siblings and 86 parents) from 222 nuclear families with multiple nicotine-addicted sibling
149 h rs2227476 (P = 0.01) was replicated in 240 nuclear families with one affected child from Mali.
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