ライフサイエンスコーパス: Jewish

1 onia, chorea, and Creutzfeldt-Jakob with and Jewish.

2 ge was 5 years, with 93.7% females and 77.6% Jewish.

3 Forty-seven percent were Catholic; 19% were Jewish; 16% were Protestant; and 6% were atheist or agno

4 try from North African (10.6%) and Sephardic Jewish (19.8%) sources.

5 ten the cause of FA in patients of Ashkenazi Jewish (AJ) ancestry, and we identified 2 novel FANCC mu

6 h Alzheimer's disease (AD), all of Ashkenazi Jewish (AJ) ancestry.

7 renia (SZ) susceptibility locus in Ashkenazi Jewish (AJ) and Han Chinese from Taiwan populations.

8 initis pigmentosa (RP) patients of Ashkenazi Jewish (AJ) descent, aiming to identify genotype-phenoty

9 ed better than the other models in Ashkenazi Jewish (AJ) families, BRCAPRO performed slightly better

10 o two densely typed data sets: 500 Ashkenazi Jewish (AJ) individuals and 56 Kenyan Maasai (MKK) indiv

11 rait with the highest frequency in Ashkenazi Jewish (AJ) individuals of Central European origin.

12 The Ashkenazi Jewish (AJ) population has long been viewed as a genetic

13 The Ashkenazi Jewish (AJ) population is a genetic isolate close to Eur

14 In the Ashkenazi Jewish (AJ) population of Israel, 11% of breast cancer a

15 IPD of a prevalent mutation in the Ashkenazi Jewish (AJ) population.

16 s and 1640 controls drawn from the Ashkenazi Jewish (AJ) population.

17 om European, African American, and Ashkenazi Jewish (AJ) reference case-control studies, and a meta-G

18 se locus in a French family and an Ashkenazi Jewish American family was also mapped to this region.

19 of pancreatitis (OR = 19, 95% CI: 3.1, 120), Jewish ancestry (OR = 1.8, 95% CI: 1.1, 3.1), and ABO bl

20 Whereas young age (P < .01), Ashkenazi Jewish ancestry (P < .01), triple-negative breast cancer

21 in unrelated affected persons, 3 of Georgian Jewish ancestry and 14 of Turkish ancestry.

22 individuals for BRCA testing: self-reported Jewish ancestry and family history of breast, ovarian, p

23 658 controls; both groups were of Ashkenazi Jewish ancestry and from New York, New York.

24 ics may reflect the presence of unrecognized Jewish ancestry in this population.

25 requency hearing loss in 2 families of Iraqi Jewish ancestry was due to homozygosity for the protein

26 Three siblings of Moroccan Jewish ancestry were compound heterozygotes for p.A33D a

27 0/172) of patients specifically of Ashkenazi Jewish ancestry were heterozygous for a nonsense, frames

28 Two families of Ashkenazi Jewish ancestry were homozygous for an 18 base pair in-f

29 atients belonging to 4 families of Ashkenazi Jewish ancestry were homozygous for either p.D104A or p.

30 founder alleles among patients of Ashkenazi Jewish ancestry with breast cancer.

31 entrosomal protein 78, in six individuals of Jewish ancestry with CRD and SNHL.

32 re much more common in patients of Ashkenazi Jewish ancestry with sporadic and familial PD than in th

33 almost exclusively individuals of Ashkenazi Jewish ancestry, is characterized by high levels of the

34 und almost exclusively in those of Ashkenazi Jewish ancestry.

35 mutations in patients with PD who are of non-Jewish ancestry.

36 All 21 affected probands are of Jewish ancestry.

37 ic white patients with and without Ashkenazi Jewish ancestry.

38 ncestry information, 21% did not self-report Jewish ancestry; of these individuals, more than half (6

39 Sixty-four Ashkenazi Jewish and 147 non-Jewish white families were studied.

40 pound haplotype frequencies for an Ashkenazi Jewish and a British sample.

41 This pattern was seen in Jewish and Bedouin children (the 2 ethnically distinct p

42 This pattern was seen in Jewish and Bedouin children (the two ethnically distinct

43 es, 48.3% were positive (42.0% and 52.8% for Jewish and Bedouin children, respectively; P < .001).

44 children from 2 distinct ethnic populations: Jewish and Bedouin.

45 pe 1 was present in 19 families of Ashkenazi Jewish and European ancestry, whereas haplotype 2 occurr

46 basis of studies in individuals of Ashkenazi Jewish and European ancestry.

47 Christian faith as well as Buddhist, Hindu, Jewish and Islamic perspectives.

48 yopathy has been obtained through studies of Jewish and Japanese patient cohorts carrying founder mut

49 All participants were Ashekanzi Jewish and most patients (98.1%) with GD carried at leas

50 erban, and Libyan) and comparison with other Jewish and non-Jewish groups demonstrated distinctive No

51 ish paternal lineages, as well as non-Levite Jewish and non-Jewish R1a samples.

52 this gene have been demonstrated in Tunisian Jewish and Palestinian kindreds with BCS.

53 emselves and all 4 grandparents as Ashkenazi Jewish and participated in the New York Breast Cancer St

54 our previous linkage results from Ashkenazi Jewish (ASHK) and African American (AFRAM) families.

55 nes in Old Order Amish (AMISH) and Ashkenazi Jewish (ASHK) families was investigated.

56 ore 1914 show the greatest increases in anti-Jewish attitudes.

57 These Jewish authorities reject the notion that generosity and

58 found to be more common among individuals of Jewish background.

59 yndrome trial, we genotyped 3,258 SNPs in 10 Jewish Bloom syndrome cases and 31 non-Bloom syndrome Je

60 ients were genotyped for the three Ashkenazi Jewish BRCA founder mutations (185delAG and 5382insC in

61 The findings in Ashkenazi Jewish BRCA1 mutation carriers should be confirmed.

62 Ninety-one percent of Jewish BRCA1/2-positive women carried a CJM.

63 ains another founder effect in all Ashkenazi-Jewish cases.

64 Here, in a cohort of Ashkenazi Jewish centenarians, their offspring, and offspring-matc

65 genetic variations in a cohort of Ashkenazi Jewish centenarians, their offspring, and offspring-matc

66 93%) for PCV7/13 serotypes among Bedouin and Jewish children <12 months old, respectively, and 32% (-

67 itored in prospective studies of Bedouin and Jewish children <3 years old in southern Israel between

68 ypes, rates of progression among Bedouin and Jewish children aged <12m declined 74% (55-85%) and 43%

69 tions), with steeper declines observed among Jewish children and children >12 months.

70 tions), with steeper declines observed among Jewish children and children aged >12 months.

71 dinal data from 369 Bedouin children and 400 Jewish children in Israel who were enrolled in a 7-valen

72 the first 4 Bedouin children and the first 4 Jewish children who were younger than 5 years old and at

73 icantly declined (33% and 11% in Bedouin and Jewish children, respectively).

74 otypes and among Bedouin children than among Jewish children.

75 gnificantly decreased among both Bedouin and Jewish children.

76 raeli individuals with CRC self-described as Jewish, Christian and Muslim.

77 e-wide scan in the largest to date Ashkenazi Jewish cohort of 1130 Parkinson patients and 2611 pooled

78 In the National Jewish cohort, the C allele at E375A was associated with

79 In the primary (National Jewish) cohort, these polymorphisms were also compared w

80 ts of studying complex diseases in Ashkenazi Jewish cohorts.

81 in this report occurred among U.S. Orthodox Jewish communities during 2009 and 2010.

82 e patients (93.4%) were part of the Orthodox Jewish community, and 473 of the patients (72.9%) reside

83 , its incidence is high within the Ashkenazi Jewish community.

84 e of international support from the Diaspora Jewish community; and a strong desire for acceptance by

85 ein 5 (FKBP5) intron 7, site 6 compared with Jewish comparison volunteers.

86 ific haplogroups suggests that the Sephardic Jewish component is the more ancient.

87 s from the 235 IBD pedigrees than in 149 non-Jewish controls (P=0.015).

88 elated, non-Jewish UC cases and 653 new, non-Jewish controls (P=0.021).

89 e two mutant DCXR alleles in 1,067 Ashkenazi Jewish controls was 0.0173, suggesting a pentosuria freq

90 trating possible applications in Islamic and Jewish countries.

91 % CI, 366.3-420.2 per 100,000) for Ashkenazi Jewish couples.

92 986A > C found in APBD patients of Ashkenazi Jewish decent.

93 benefited from the influx of several stellar Jewish dermatologists who were major contributors to the

94 likely to be women (53.1%) and of Ashkenazi Jewish descent (76.8%) in comparison with individuals wh

95 participants, four of whom were of Ashkenazi Jewish descent and three of whom did not meet family-his

96 0% of patients with familial PD of Ashkenazi Jewish descent likely carry the G2019S mutation in the L

97 The majority of families were of Ashkenazi Jewish descent, and the TP53 c.1000G>C allele was found

98 d on 44 large American families of Ashkenazi Jewish descent, each with at least two affected siblings

99 e genome sequencing of 97 trios of Ashkenazi Jewish descent, selecting "simplex" families with no fam

100 We focused on families of Ashkenazi Jewish descent, to reduce genetic heterogeneity, and, as

101 pulation of both non-Ashkenazi and Ashkenazi Jewish descent, using a sample set representative of the

102 Here, we report a family of Ashkenazi Jewish descent, with 2 out of 3 children affected by CDD

103 SZ cases and 490 controls, all of Ashkenazi Jewish descent.

104 ns, using 29 multiplex families of Ashkenazi Jewish descent.

105 h African Jews constitute the second largest Jewish Diaspora group.

106 ther; to European, Middle Eastern, and other Jewish Diaspora groups; and to their former North Africa

107 as a common Middle Eastern origin with other Jewish Diaspora populations, but also suggest that the A

108 ed at about the time of the beginning of the Jewish diaspora, explaining its presence in non-Ashkenaz

109 ttleneck in a.d. 75, at the beginning of the Jewish Diaspora.

110 understand its origin in the context of the Jewish diasporas and subsequent founder events.

111 beginning at a time that coincides with the Jewish Diasporas.

112 enome-wide association study on an Ashkenazi Jewish discovery group (n=428) was performed using Affym

113 ly ethical, ultimately its ethical status in Jewish ethics and law is inextricably connected to solvi

114 asians, African Americans, and the Ashkenazi Jewish ethnic group.

115 trol chromosomes were of confirmed Ashkenazi Jewish ethnicity.

116 s when the data were stratified by Ashkenazi Jewish ethnicity; however, there was some evidence of he

117 etic Research Study dataset and 19 Ashkenazi Jewish families collected at Johns Hopkins University.

118 families represent a combined dataset of 17 Jewish families from the Fred Hutchinson Cancer Research

119 The 36 Jewish families represent a combined dataset of 17 Jewis

120 We studied 2 large Ashkenazi Jewish families with a high prevalence of CD in an attem

121 prostate cancer susceptibility genes with 36 Jewish families, which represent a stratification of her

122 g exons 2-7 of TRPM1 present in 13 Ashkenazi Jewish families.

123 I was born into a Jewish family in Breslau, Germany, right before the rise

124 h autosomal recessive inheritance in a large Jewish family originating from Morocco.

125 igenetic investigation of a unique Ashkenazi Jewish family with monozygotic triplets, two of whom dev

126 mutation c.1034G>T p.G345V in the Ashkenazi Jewish family.

127 nd a genetically more homogeneous (Ashkenazi Jewish) family collection to perform a 9-cM autosomal ge

128 ) known to cause PCD, including an Ashkenazi Jewish founder mutation in DNAI2.

129 who carry one or more of the three Ashkenazi Jewish founder variants, evaluating two characteristics

130 than half (62%) do have detectable Ashkenazi Jewish genetic ancestry.

131 solve the issues of within and between-group Jewish genetic identity.

132 bly, gene ontology analysis of the Ashkenazi Jewish genetic signature revealed an enrichment of genes

133 Rapid decay of IBD in Ashkenazi Jewish genomes was consistent with a severe bottleneck f

134 ere part of a larger Ashkenazi and Sephardic Jewish group.

135 PMs at the IBD1 locus exist in the high-risk Jewish group.

136 Here, genome-wide analysis of seven Jewish groups (Iranian, Iraqi, Syrian, Italian, Turkish,

137 , genome-wide analysis of five North African Jewish groups (Moroccan, Algerian, Tunisian, Djerban, an

138 reek, and Ashkenazi) and comparison with non-Jewish groups demonstrated distinctive Jewish population

139 an) and comparison with other Jewish and non-Jewish groups demonstrated distinctive North African Jew

140 blood group and serum markers suggested that Jewish groups had Middle Eastern origin with greater gen

141 A from each of nine geographically separated Jewish groups, eight non-Jewish host populations, and an

142 n, Donna Bratton, and colleagues at National Jewish Health demonstrated that phagocytosis of apoptoti

143 She started her own laboratory at National Jewish Health in 2014, becoming a tenure-track Assistant

144 In response, the National Jewish Health Institutional Animal Care and Use Committe

145 ng Zbtb16(-/-) mice and R. O'Brien (National Jewish Health) for providing Vg4/6(-/-) mice.

146 g disease in the Adult Care Unit at National Jewish Health, Denver, Colorado, in the January 2006 to

147 We genotyped more than 1,300 Ashkenazi Jewish healthy volunteers from the Hebrew University Gen

148 Jewish heritage was overrepresented, and five multiplex

149 ncating mutation in exon 9 and had Ashkenazi Jewish heritage.

150 e HNPCC trial, we genotyped 8,549 SNPS in 13 Jewish HNPCC cases whose colon cancers exhibited microsa

151 al charts of all patients admitted to Barnes-Jewish Hospital (St Louis, MO, USA), a tertiary referral

152 submitted for enteric culture to the Barnes-Jewish Hospital and St.

153 men diagnosed with PPCM delivering at Barnes-Jewish Hospital between 2004 to 2014.

154 nducted a prospective cohort study in Barnes Jewish Hospital between June 2011 and May 2012 of hospit

155 ed in the heart transplant program at Barnes Jewish Hospital from 1994 to 2008.

156 y and receiving general anesthesia at Barnes-Jewish Hospital in St Louis.

157 The sepsis alert developed at Barnes-Jewish Hospital was shown to increase early therapeutic

158 Patients admitted to Barnes-Jewish Hospital without diarrhea were enrolled from June

159 for Candida species was conducted at Barnes-Jewish Hospital, a 1250-bed urban teaching hospital (Jan

160 Barnes-Jewish Hospital, Saint Louis, MO (January 15, 2015, to D

161 rogram for the Department of Surgery, Barnes Jewish Hospital, St. Louis, Missouri.

162 h cryptococcosis from 2002 to 2019 at Barnes-Jewish Hospital.

163 d S10OD026929; and the Foundation for Barnes-Jewish Hospital.

164 (2)) during gastric bypass surgery at Barnes-Jewish Hospital.

165 B admitted between 2008 and 2015 from Barnes-Jewish Hospital.

166 aphically separated Jewish groups, eight non-Jewish host populations, and an Israeli Arab/Palestinian

167 The cohort included all Jewish individuals born in Israel over 5 consecutive yea

168 n, Asian, Caucasian, Hispanic, and Ashkenazi Jewish individuals from the greater New York metropolita

169 ay-based genotype analyses of 1477 Ashkenazi Jewish individuals with CD and 2614 Ashkenazi Jewish ind

170 ewish individuals with CD and 2614 Ashkenazi Jewish individuals without CD (controls).

171 ;p.G334R is found predominantly in Ashkenazi Jewish individuals, causes a mild defect in p53 function

172 In a genetic analysis of Ashkenazi Jewish individuals, we associated CD with a frameshift m

173 done on NOD2/CARD15-translated regions in 12 Jewish individuals.

174 ed from structural MRI among 191 T2D elderly Jewish individuals.

175 national sampling of 3,225 healthy Ashkenazi Jewish individuals.

176 for any genetic studies involving Ashkenazi Jewish individuals.

177 ith CD in an independent cohort of Ashkenazi Jewish individuals.

178 ith CD in an independent cohort of Ashkenazi Jewish individuals.

179 orse saving Palestinian children than saving Jewish Israeli children, this proportion decreased when

180 e the lives of five children who were either Jewish Israeli or Palestinian.

181 We assessed Jewish-Israeli and Arab-Palestinian adolescents for brai

182 Furthermore, higher oxytocin levels in the Jewish-Israeli majority and tighter brain-to-brain synch

183 randomized field experiment, conducted among Jewish Israelis during widespread violence.

184 igious belief, changes the relative value of Jewish Israelis' lives (compared with Palestinian lives)

185 embers of the high-power group (in this case Jewish-Israelis) are more likely to associate peace with

186 ritings of major contemporary authorities of Jewish law and ethics whose halakhic positions on bioeth

187 In addition, Israeli Ashkenazi Jewish LRRK2 p.G2019S carriers (mean age at onset, 57.9

188 , as well as in 33.8% of other R1a Ashkenazi Jewish males and 5.9% of 303 R1a Near Eastern males, whe

189 Orthodox Jewish married women (N=380) ages 19 to 58 responded to

190 r seen between 1992 and 2004 at the National Jewish Medical and Research Center (n = 55).

191 e, showing no solidarity with its persecuted Jewish members.

192 7R ZnT-2 mutation in two unrelated Ashkenazi Jewish mothers with infants displaying TNZD.

193 We evaluated how these common Jewish mutations (CJMs) affect cancer risks and risk red

194 roups; and to their former North African non-Jewish neighbors has not been well defined.

195 est number of exposures occurring around the Jewish New Year.

196 rouped as Caucasian, Asian, Arabic, Turkish, Jewish or Afro-American.

197 from multiply affected families of Georgian Jewish or German ancestry.

198 diculoneuropathy in infants of North-African Jewish origin from 4 unrelated families.

199 in a separate study population of Ashkenazi Jewish origin suggests that variant(s) located near or w

200 le sources for lineages ascribed a Sephardic Jewish origin, these proportions attest to a high level

201 Ten of 11 families had Ashkenazi Jewish origins and the N48K CLRN1 mutation.

202 -Ashkenazi Levite R1a clade, other Ashkenazi Jewish paternal lineages, as well as non-Levite Jewish a

203 This is the largest study to date on a non-Jewish patient sample with a detailed genotype/phenotype

204 with 8.3% (95% CI, 3.1%-20.1%) in Ashkenazi Jewish patients (n = 41) and 2.2% (95% CI, 0.7%-6.9%) in

205 haplotype carrying only the 268S variant in Jewish patients (OR = 3.13, P=.0023) but not in non-Jews

206 of BRCA1 and BRCA2 in an unselected group of Jewish patients and to compare the clinical characterist

207 utation-specific) A636P testing in Ashkenazi Jewish patients at risk for Hereditary Nonpolyposis Colo

208 All the Georgian Jewish patients were homozygous for a mutation encoding

209 Of the 187 Jewish patients who underwent resection for PAC, tissue

210 Overall, 14.1% (142 of 1007) of Ashkenazi Jewish patients with breast cancer in the NYBCS carried

211 However, among Ashkenazi Jewish patients with breast cancer who do not carry one

212 e relevant genetic information for Ashkenazi Jewish patients with breast cancer.

213 Ashkenazi Jewish patients with CD and a positive family history we

214 incidence of BRCA mutations among Ashkenazi Jewish patients with fallopian tube carcinoma (FTC) or p

215 Substantial proportions of Ashkenazi Jewish patients with FTC or PPC are BRCA mutation carrie

216 Jewish patients with PAC resected between January 1986 a

217 nce of germline BRCA1 and BRCA2 mutations in Jewish patients with pancreatic adenocarcinoma (PAC) is

218 uding 6.1% in BRCA1/2 (5.1% in non-Ashkenazi Jewish patients) and 4.6% in other breast/ovarian cancer

219 A was fully sequenced for 1883 non-Ashkenazi Jewish patients, and mutations were identified in 7%, sh

220 SNPs with amygdalar volume among T2D elderly Jewish patients.

221 rmatics approach in a consanguineous Iranian-Jewish pedigree led to the identification of a homozygou

222 ed to define the relatedness of contemporary Jewish people.

223 Orthodox Jewish persons accounted for 97% of case patients.

224 oom syndrome cases and 31 non-Bloom syndrome Jewish persons as a comparison group.

225 d in German-speaking countries at that time, Jewish physicians were particularly vulnerable to persec

226 185delAG mutation is common in the Ashkenazi Jewish population and has been thought to result in loss

227 1307K allele is found in 6% of the Ashkenazi Jewish population and in 1%-2% of Sephardi Jews; it conf

228 s identified almost exclusively (99%) in the Jewish population and was mainly distributed in 3/7 Isra

229 roups demonstrated distinctive North African Jewish population clusters with proximity to other Jewis

230 h non-Jewish groups demonstrated distinctive Jewish population clusters, each with shared Middle East

231 aplotype in both and Caucasian and Ashkenazi Jewish population data sets, suggests that this haplotyp

232 SDs) at increased frequency in the Ashkenazi Jewish population has suggested to many the operation of

233 genic variants are enriched in the Ashkenazi Jewish population in gnomAD, a finding we confirmed with

234 The Ashkenazi Jewish population is of potential utility in disease-map

235 The Ashkenazi Jewish population represents a unique population for stu

236 l clustering and increased prevalence in the Jewish population support a role for a major genetic sus

237 e pulse model and show that in the Ashkenazi Jewish population the admixture fraction is correlated w

238 urpose, we selected cases from the Ashkenazi Jewish population, in which the mutant alleles are expec

239 In the endogamous Georgian Jewish population, the Gly47Arg carrier frequency was 0.

240 factor XI deficiency, outside the Ashkenazi Jewish population, to be highly heterogeneous.

241 ith sporadic and familial PD than in the non-Jewish population.

242 ccurred and that segregates in the Ashkenazi Jewish population.

243 and 1,640 controls drawn from the Ashkenazi Jewish population.

244 r diseases over-represented in the Ashkenazi Jewish population.

245 affects 1/3600 live births in the Ashkenazi Jewish population.

246 cell cycle regulator CHEK2 in the Ashkenazi Jewish population.

247 T (c.5946delT) - are common in the Ashkenazi Jewish population.

248 that is particularly common in the Ashkenazi Jewish population.

249 autosomal dominant mutation in the Ashkenazi Jewish population.

250 population clusters with proximity to other Jewish populations and variable degrees of Middle Easter

251 se in white populations, 13-30% in Ashkenazi Jewish populations, and 30-40% in North African Arab-Ber

252 mutation frequencies of white and Ashkenazi Jewish populations, and may not be applicable to other p

253 1L mutations in Middle Eastern and Ashkenazi Jewish populations, respectively.

254 o occurs at low frequencies in non-Ashkenazi Jewish populations.

255 th greater genetic similarity between paired Jewish populations.

256 (CD) has the highest prevalence in Ashkenazi Jewish populations.

257 L2307F is more frequent (4%) among Ashkenazi Jewish populations.

258 c.1000C>G;p.G334R is a pathogenic, Ashkenazi Jewish-predominant mutation associated with a familial m

259 i Levites, members of a paternally inherited Jewish priestly caste, display a distinctive founder eve

260 Forty-seven of the 115 (40%) Ashkenazi Jewish probands had point mutations; no genomic rearrang

261 In the 136 non-Ashkenazi Jewish probands, 36 (26%) BRCA point mutations and 8 (6%

262 In the non-Ashkenazi Jewish probands, genomic rearrangements constituted 18%

263 neages, as well as non-Levite Jewish and non-Jewish R1a samples.

264 ents of the West Bank and the Gaza Strip and Jewish residents of Israel.

265 ered Citrons and in those used in the Sukkot Jewish ritual [5] illuminates the path of domestication

266 Transmission was focused within Jewish schools for boys, where students spend many hours

267 ies among 260 Ashkenazi (AJ) and 80 Sephardi Jewish (SJ) individuals, we genotyped six CYP2C9 and eig

268 50 AJ and 53 members of 10 Sephardi/Oriental Jewish (SOJ) multiplex families with CD, in 36 AJ patien

269 t in non-Jews, suggesting the existence of a Jewish-specific additional disease-predisposing factor o

270 and Asian populations enabled the Ashkenazi Jewish-specific component of the variance to be characte

271 rging approaches, we identified an Ashkenazi Jewish-specific genetic signature that differentiated th

272 horectomy (RRSO), by CJM and self-identified Jewish status.

273 Patients 2-8 are of Oriental Jewish stock of Iraqi or Iranian origin with facial malf

274 esent in approximately 7% of older Ashkenazi Jewish study subjects (OR, 1.7; 95% CI, 1.2-2.4; P < 0.0

275 amilies and had a carrier rate of 1:66 among Jewish subjects of North-African origin.

276 Seventeen Jewish subjects were familiarized with biographies of ei

277 Among Ashkenazi Jewish subjects, either mutation was found in 15% of pat

278 and 3% of controls, and among non-Ashkenazi Jewish subjects, either mutation was found in 3% of pati

279 C1 mutations ranging from 0.56% in Ashkenazi Jewish to 3.26% in African/African Americans (5.8-fold d

280 read sequencing data from the GIAB Ashkenazi Jewish Trio son [NIST RM 8391/HG002].

281 ated in an association analysis of Ashkenazi Jewish type 2 diabetic (n = 275) and control (n = 342) s

282 Previously, in a genome scan of Ashkenazi Jewish type 2 diabetic families, we observed linkage to

283 icated in a second set of 258 unrelated, non-Jewish UC cases and 653 new, non-Jewish controls (P=0.02

284 allele was also more frequent in the 156 non-Jewish UC probands from the 235 IBD pedigrees than in 14

285 re adjusted for age and ethnicity (Ashkenazi Jewish vs others) as fixed effects and study center as a

286 ong-Term Care or self-reporting as Ashkenazi Jewish was significantly associated with BRCA mutation c

287 Sixty-four Ashkenazi Jewish and 147 non-Jewish white families were studied.

288 nd lower carriage of R702W compared with non-Jewish whites with CD.

289 In a study of 2 large Ashkenazi Jewish with multiple cases of CD, we found the genetic b

290 icantly more likely to undergo RRSO than non-Jewish women (54% v 41%, respectively; odds ratio, 1.87;

291 While observant Jewish women live in a culture defined by a high degree

292 Within BRCA1 mutation carriers, Ashkenazi Jewish women were about five times more likely to have T

293 Jewish women were significantly more likely to undergo R

294 t testing be considered in all non-Ashkenazi Jewish women with an estimated mutation prevalence >or=1

295 ovarian cancer were determined for Ashkenazi Jewish women with inherited mutations in the tumor suppr

296 Among Ashkenazi Jewish women, 3 mutations in BRCA1 and BRCA2 severely in

297 er risk approximately 2-fold among Ashkenazi Jewish women, whereas CHEK2.P85L is a neutral allele.

298 Of these women, 969 were self-identified Jewish women.

299 more likely to have TNBC than non-Ashkenazi Jewish women.

300 ports of a select group of married observant Jewish women.