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1 l for the number of ASPs contributed by each nuclear family.
2 orithm-namely, genotype elimination within a nuclear family.
3 t residue 1126 of the mature receptor in one nuclear family.
4 rocesses that operate exclusively within the nuclear family.
5 ultiple parent-offspring pairs from the same nuclear family.
6 COME from 35 hospitals in the UK, and their nuclear family.
7 ated in our previous linkage analysis of 428 nuclear families.
8 ian population-based sample of 232 Caucasian nuclear families.
9 on the basis of data from arbitrary types of nuclear families.
10 t cases included 2,107 Pima Indians from 715 nuclear families.
11 xtended pedigrees were no more powerful than nuclear families.
12 grees and are not restricted to sib pairs or nuclear families.
13 nvolving 186 affected sibling pairs from 160 nuclear families.
14 Children expect saliva sharing to happen in nuclear families.
15 astic effects shared by cousins in different nuclear families.
16 ng of quantitative trait loci (QTL) based on nuclear families.
17 ix SNP and fed these into Transmit using 148 nuclear families.
18 d 29 SNP throughout this region in psoriatic nuclear families.
19 for quantitative traits and extended here to nuclear families.
20 relapsing individuals and 11 controls from 5 nuclear families.
21 aximum detection rate is 34% for four-person nuclear families.
22 hree of 18 unrelated BBS probands from small nuclear families.
28 ase and automated pedigree software, that 23 nuclear families affected with MCPHA are connected to a
30 EHR and geographical locations from 257,620 nuclear families and compile 1083 disease outcome measur
35 merican family-based study population (n=219 nuclear families) and two case-control populations--one
36 tions for a set of tightly linked markers in nuclear families, and the objective is to identify famil
37 ave implemented the basic model for use with nuclear families, and we illustrate its application thro
38 ng in rented homes; (iii) those belonging to nuclear families; and (iv) those with low monthly househ
39 esting, counseling, and risk calculation for nuclear families, as well as extended family members at
40 the MHC region on chromosome 6p21-22 in 225 nuclear families ascertained by African American proband
41 an based on 354 markers in 513 members of 92 nuclear families ascertained through extreme obesity and
43 hm for sequence location approximation using nuclear families (ASLAN) to identify the region of origi
44 sease associations for both case-control and nuclear family-based data-including application of corre
45 ide some guidance to investigators designing nuclear family-based linkage disequilibrium studies for
48 s, a few of them have been extended to small nuclear families, but none can be applied to large (e.g.
49 lso found in 12 Caucasian Amish kindreds (24 nuclear families) by both sib-pair and transmission dise
50 e phenotyping and genomic analysis utilizing nuclear families can provide a diagnosis in some cases a
51 st three carefully selected individuals in a nuclear family can recover >90% of the information avail
53 udy, we examined genome screen data from 148 nuclear families, collected without reference to phenoty
54 es in different family structures, including nuclear families commonly used in complex disease gene m
55 l clones (TCC) directed against MOG in three nuclear families, comprised of four individuals affected
56 e performed a genomewide linkage scan in 204 nuclear families comprising 853 individuals and 270 affe
57 ounding by environmental differences between nuclear families, consistent with a possible role for ev
61 -23 and 20p12 in a cohort of 115 multiethnic nuclear families containing 145 SLE-affected sibpairs.
63 We demonstrate this method on a four-member nuclear family, correctly assembling and phasing three g
64 inkage disequilibrium typically are based on nuclear-family data including affected individuals and t
66 mutation as an inheritance inconsistency in nuclear-family data, as a function of both the number of
67 packages for model-free linkage analysis of nuclear-family data, by applying them to single-marker d
68 d an extensive simulation study on simulated nuclear-family data, varying the number of trait loci, f
69 oach is applicable to either case/control or nuclear-family data, with case/control data modeled via
73 tism Symptom Scale (BPASS), were measured in nuclear families, each ascertained through two probands
74 were conducted in 3,369 individuals from 906 nuclear families enrolled, without selection, in a longi
75 types from Swedish national samples: intact nuclear families, families with a not-lived-with biologi
76 of complex disease we have regenotyped five nuclear families first studied in the 1996 UK multiple s
77 analysis to obesity, and 236 sib pairs in 82 nuclear families, for linkage analysis to energy metabol
79 ned 92 affected individuals, representing 82 nuclear families, for mutations, using single-strand con
81 l study included participants from 3 related nuclear families from an Amish community in the primary
82 blood assay in 392 children belonging to 135 nuclear families from an area hyperendemic for tuberculo
88 andard methods require selection of a single nuclear family from any extended pedigrees when testing
89 segregates with a disease phenotype in small nuclear families, from genome-wide oligonucleotide micro
90 Our previous genomewide linkage scan of 428 nuclear families (GeneQuest) identified a significant ge
92 e cousins; N = 10,913) to distinguish within-nuclear-family genetic-nurture effects from dynastic eff
94 me-wide linkage scans with hundreds of small nuclear families have identified new susceptibility gene
97 is of data on multigenerational extended and nuclear families identified the features of structural a
100 d depression and neuroticism using data from nuclear families in the UK Biobank, with data collected
102 rt comprised 1,037 predominantly white (82%) nuclear families in which at least 1 member had SLE.
104 transmission of memory disorders differs in nuclear families in which the AD-affected proband did ca
106 uencing was performed for 43 EoE cases in 18 nuclear families, including 6 relatives without EoE.
109 ies in 1465 American white subjects from 218 nuclear families indicated that allelic variation at, or
111 encing on the 3 affected puppies, along with nuclear family members (ie, sire, dam, 4 unaffected litt
112 families have larger correlations within the nuclear family members but smaller correlations outside
114 e storage rate after adjusting for age, sex, nuclear family membership, and percentage of body fat (P
115 o show that what we may regard as the simple nuclear family (mom, dad, and a few kids) is anything bu
116 investigated blood pressure in 1,183 Chinese nuclear families (mother, father, and first two children
118 In our previous genome-wide scan of Finnish nuclear families, obesity was linked to chromosome Xq24.
119 d nonsmokers, representing approximately 404 nuclear families of African American (AA) or European Am
120 tal of 2037 smokers and non-smokers from 602 nuclear families of African- or European-American (AA or
121 mple consisting of 2037 individuals from 602 nuclear families of African-American (AA) or European-Am
122 ruct a general approach that can accommodate nuclear families of any size, with or without parental i
123 ed out a complex segregation analysis in 636 nuclear families of consecutively ascertained and rigoro
124 found to be associated with total IgE in 420 nuclear families of Costa Rican children with asthma.
125 Participants were 2037 subjects from 602 nuclear families of either African-American (AA) or Euro
131 d to include only one affected offspring per nuclear family per extended pedigree; multiple three-mar
132 obese (BMI >or=35 kg/m(2)), and 84.8% of the nuclear families possessed >or=1 morbidly obese sibling
133 of 914 EoE probands (n = 2192 first-degree "Nuclear-Family" relatives) and an international registry
136 ample (187 families, 564 subjects), a German nuclear family sample (211 families, 751 subjects) and a
137 211 families, 751 subjects) and a Pittsburgh nuclear family sample (247 families, 729 subjects).
138 ilies (n=1240 individuals) were added to the nuclear family sample, and the Gln27Glu polymorphism in
142 region in a sample of 181 sib pairs from 82 nuclear families that were selected on the basis of a dy
143 e prediction intervals, and indeed, in large nuclear families, the majority of children top-scoring f
144 de meals especially for working parents in a nuclear family therefore it is imperative to determine t
145 icate this finding; combined analysis of 194 nuclear families through use of the transmission/disequi
146 ificate data dating back to 1967 and allowed nuclear families to be reconstructed by linking children
147 ssue and then perform simulation studies for nuclear families to compare the methods in terms of powe
148 wo approaches to segregation analysis in 102 nuclear families to estimate genetic models for componen
149 We collected 70 families, ranging from small nuclear families to extended multigenerational pedigrees
150 le-nucleotide polymorphism data collected in nuclear families to localize crossovers with high spatia
151 ypothesis, we resequenced two 3-4 generation nuclear families (totaling 29 individuals) of olive babo
152 d if indirect genetic effects reflect within-nuclear-family transmission ('genetic nurture') or inste
153 one heterozygous for DRD4*7R), including 12 nuclear family trios and 52 trios from four large TS kin
154 Canadian replication cohort consisted of 364 nuclear family trios with one type 1 diabetes-affected o
158 iduals of Chinese and Japanese descent, from nuclear families, was genotyped for two polymorphisms, r
159 ed data from 716 Pima Indians comprising 217 nuclear families, we have tested a number of polymorphic
160 Through whole-genome sequencing of large nuclear families, we identified the genomic locations of
161 g all possible affected sib pairs (ASPs) per nuclear family, we obtained a peak maximum LOD score bet
162 the hoarding phenotype in a data set with 53 nuclear families, which were collected by the Tourette S
163 of data simulated for 956 siblings from 263 nuclear families who had participated in a linkage study
164 re generated using 9,291 subjects from 2,900 nuclear families who participated in the National Heart,
167 enotyping these in an independent set of 636 nuclear families with 974 affected offspring revealed 75
169 sis of HLA class II alleles in 180 Caucasian nuclear families with at least two children with insulin
170 ng technology in finding causal mutations in nuclear families with dominantly inherited traits otherw
171 an also produce multimegabase haplotypes for nuclear families with just two children and can handle f
174 data on a polymorphism of the SDR5A2 gene in nuclear families with multiple cases of prostate cancer.
176 jects (815 siblings and 86 parents) from 222 nuclear families with multiple nicotine-addicted sibling
177 h rs2227476 (P = 0.01) was replicated in 240 nuclear families with one affected child from Mali.
179 The only LoF variant was identified in a nuclear family with the relatively milder syndrome of ge
182 in 38 702 offspring from 20 905 independent nuclear families, with most of these participants also r