ライフサイエンスコーパス: family history

1 increased genetic risk of AAA independent of family history.

2 ic testing criteria on the basis of personal/family history.

3 e population risk for breast cancer based on family history.

4 h or without abnormal ultrasound findings or family history.

5 sociated positively with the presence of T2D family history.

6 age <21 years with a consistent personal or family history.

7 y histology, hormone receptor status, age or family history.

8 des children without an ASD diagnosis in the family history.

9 30-49 years and in low-risk patients with a family history.

10 ry; and "optimal control," healthy without a family history.

11 the clinical condition, the age at onset and family history.

12 of inherited genetic disease risk, including family history.

13 ated based on the infants' known clinical or family histories.

14 n obese individuals (BMI >= 30 kg/m2) with a family history (1.21-fold reduction, 95% CI 1.13-1.29).

15 -(1) medical history, (2) physical exam, (3) family history, (4) diagnostic phenotypic testing, and (

16 tors not specified in the Guidelines such as family history (50.2%) and conducting skin prick testing

17 consideration of risk enhancing factors (eg, family history), additional testing with measurement of

18 nsideration of risk enhancing factors (e.g., family history), additional testing with measurement of

19 re used to test the association between work-family histories and later-life cognition.

20 Women <50 years, with strong family histories and/or indicative tumour molecular feat

21 reasts, and optionally lifestyle factors and family history and a polygenic risk score, the model ide

22 ent in adulthood, typically with no apparent family history and a variable clinical phenotype of wide

23 nd SNCA in relation to age at symptom onset, family history and clinical features.

24 er (CRC) is largely driven by recognition of family history and early age of onset, the rates of such

25 Children with a positive family history and either confirmed or unknown disease s

26 articularly those with risk factors such has family history and high-grade dysplasia.

27 ociated with several risk factors, including family history and higher body mass index.

28 ers of genetic susceptibility to AF, such as family history and individual AF susceptibility alleles,

29 alue of integrating cancer-specific PRS with family history and modifiable risk factors for 16 cancer

30 -year risk trajectories after accounting for family history and modifiable risk factors.

31 data input (eg, restriction of the amount of family history and non-genetic information included) had

32 Additional family history and pathologic criteria garnered moderate

33 tic disease and for children with a negative family history and progressive disease.

34 -11) per SD increase in PRS), independent of family history and smoking risk factors (odds ratio(PRS+

35 s not previously studied in association with family history and uncover trait overlap, highlighting a

36 About 90% of these individuals have no family history and would have been considered average ri

37 tremor (ET) subjects (285 sporadic, 125 with family history, and 52 probands from well-characterized

38 gle, literacy, living in rural areas, having family history, and comorbidities, with a higher probabi

39 sease characteristics, including laterality, family history, and gene mutation status were analyzed.

40 iated with reduced diabetes risk across BMI, family history, and genetic risk categories, suggesting

41 llowing diabetes risk factors: BMI, diabetes family history, and genome-wide diabetes polygenic risk

42 In this study, we observed that age, family history, and histology are imprecise clinical cor

43 cted based on the infant's known clinical or family history, and the interpretation of results can su

44 ypotension, urinary/erectile dysfunction, PD family history, and the prodromal PD probability showed

45 diagnoses; "CHD-related," healthy with a CHD family history; and "optimal control," healthy without a

46 common in adult MDS/AML, often without known family history, arguing for systematic screening.

47 ble to identify 30% of individuals without a family history as having risk for CRC similar to those w

48 ex, a history of childhood maltreatment, and family history as well as more recent stressors are risk

49 Family history-based criteria to identify patients with

50 ve compared to several risk factors, such as family history, blood pressure, body mass index, and smo

51 e than it is among individuals with a strong family history but no identified mutation.

52 ncreatic cancer susceptibility gene; 345 met family history criteria for pancreatic surveillance but

53 Age at clinical onset, clinical syndrome and family history each strongly predict the likelihood of f

54 aScript widget to visualize and explore gene family history encoded in HOGs and python HOG analysis m

55 for these conditions is based on personal or family history, ethnic background or other demographic c

56 , previous eye trauma, large family size and family history eye problem were positively associated wi

57 However, although a family history (FH) of the same disease among close rela

58 R), captured by genetic risk score (GRS) and family history (FH).

59 x-wise according to APOE epsilon4 status and family history (FH).

60 kers, with alcohol dependence and a positive family history (FHP) of alcoholism, participated in a ra

61 Elevated lipoprotein(a) (Lp[a]) and family history (FHx) of coronary heart disease (CHD) are

62 story and outcome, particularly comorbidity, family history, food aversion, and poor body weight gain

63 preciably affected by limiting input data to family history for first-degree and second-degree relati

64 In the non-CD family history group, an association between delayed dis

65 pital record and questionnaire GWAS and that family history GWAS has better power to detect genetic a

66 We also show that family history GWAS using cases ascertained on family hi

67 -FH to genome-wide association without using family history (GWAS) and a previous proxy-based method

68 a previous proxy-based method incorporating family history (GWAX).

69 d spread risk was associated with a positive family history (HR=2.18, p=0.012) and self-reported alco

70 ical conditions, obstetric complications and family history in both the current and previous pregnanc

71 best-established way to reconstruct paternal family history in humans.

72 Family history included a brother with CF carrier status

73 Various factors-including age, family history, inflammation, reproductive factors, and

74 ighting a putative shared mechanism by which family history influences disease risk.

75 343 carriers who provided both ancestry and family history information, 44% did not have a first-deg

76 The results showed that family history is a risk factor for GCA.

77 Family history is a strong risk factor for many common c

78 early clinical diagnosis of probands without family history is not addressed by both diagnostic class

79 ls diagnosed with pancreatic cancer, even if family history is unremarkable.

80 odel, conditional on case-control status and family history (LT-FH).

81 ancreatic surveillance on the basis of their family history may better define those most at risk for

82 g should be discussed with individuals whose family history meets criteria for FPC and/or genetic sus

83 13) interaction with age at first diagnosis, family history, morphology, ER status, PR status, and HE

84 n Study (GWAS) of alcohol use/misuse and two family history (mother DSM-5 AUD and father DSM-5 AUD) f

85 enriched with women who have a breast cancer family history (N = 15,550).

86 m (CAC) = 0, CAC <=10, no carotid plaque, no family history, normal ankle-brachial index, test result

87 ors for developing pancreatic cancer include family history, obesity, type 2 diabetes, and tobacco us

88 information, 44% did not have a first-degree family history of a BRCA-related cancer and, in the abse

89 testinal symptoms, or patients solely with a family history of a penicillin allergy, symptoms of prur

90 o 75 years who have never smoked and have no family history of AAA outweigh the benefits.

91 y in women who have never smoked and have no family history of AAA.

92 5 to 75 years who have ever smoked or have a family history of AAA.

93 nalysis in a healthy middle-aged cohort with family history of AD (n = 68) and an older cohort (n = 1

94 enomics of Alzheimer's Project), 2) maternal family history of AD (UK Biobank), and 3) paternal famil

95 history of AD (UK Biobank), and 3) paternal family history of AD (UK Biobank).

96 Furthermore, patients with AD and a family history of AD had a higher risk of later aortic s

97 Furthermore, patients with AD with a family history of AD had a higher risk of later aortic s

98 A family history of AD in first-degree relatives was assoc

99 of this study was to evaluate the effect of family history of AD on the incidence and prognosis of A

100 GSMR applied to the maternal family history of AD UK Biobank dataset (SBP [beta(GSMR)

101 GSMR) = -0.10, p = .05]) and to the paternal family history of AD UK Biobank dataset (SBP [beta(GSMR)

102 A family history of AD was a strong risk factor for AD.

103 Marfan syndrome or bicuspid aortic valve, a family history of AD was associated with an RR of 6.56 (

104 ort comprising AD patients with or without a family history of AD was included to compare late outcom

105 k of later aortic surgery than those with no family history of AD.

106 patients with a high atherosclerotic burden, family history of AF is evident in >20% of patients and

107 adjustment for cardiovascular risk factors, family history of AF was associated with a higher risk o

108 Family history of AF was defined as the presence of AF i

109 Family history of AF was detected in 368 (21.4%) patient

110 rogressively decreased from patients without family history of AF, compared with those with single an

111 +/- 16 drinks per week and were balanced in family history of alcoholism (FH, 26 positive).

112 Information was collected on family history of allergic diseases, household size, soc

113 ort Study, a birth cohort of children with a family history of allergic diseases, we modeled the asso

114 atic C9(+) subjects older than 40 years with family history of ALS (as opposed to FTD) also exhibited

115 ontrols, the two other studies used parental family history of Alzheimer's disease to define proxy ca

116 nt, and including as potential confounders a family history of any allergy in parents, type of delive

117 A family history of any neuropsychiatric disorder was asso

118 ypertension (OR, 5.6; 95% CI, 1.4-22.3), and family history of aortic disease (mother: OR, 5.7; 95% C

119 ameter of 50 mm, but none in patients with a family history of aortic dissection.

120 s and more frequently had eosinophilia and a family history of asthma.

121 Term newborns with a family history of atopic disease were randomly assigned

122 To investigate the association between family history of atrial fibrillation (AF) with cardiova

123 n 2 years (odds ratio [OR], 6.30; P = .020), family history of autoimmune disease (OR, 5.12; P = .002

124 escent, selecting "simplex" families with no family history of BD and an early age of onset.

125 history of chest radiation (BRCA/RT group), family history of breast cancer (FH group), personal his

126 and mammographic features among women with a family history of breast cancer (N = 49,674) and a polyg

127 ldbirth were pronounced when combined with a family history of breast cancer and were greater for wom

128 All men undergoing screening had personal or family history of breast cancer and/or genetic mutations

129 (77.4%) had dense breasts, 247 (27.3%) had a family history of breast cancer in a first-degree relati

130 screening MRI performance in patients with a family history of breast cancer suggests that better ris

131 In addition, for MDC, having a family history of breast cancer was associated with slig

132 e extended model included menopausal status, family history of breast cancer, body mass index, hormon

133 : 0.65, 1.02) among women with and without a family history of breast cancer, respectively (P-interac

134 risk in both women with and those without a family history of breast cancer.

135 regnancy, abortion, or breastfeeding; and no family history of breast cancer.

136 the use of these supplements in women with a family history of breast cancer.

137 For unaffected women with family history of breast or ovarian cancer (n = 144), BO

138 For women with both personal and family history of breast or ovarian cancer (n = 241), al

139 A testing: self-reported Jewish ancestry and family history of breast, ovarian, prostate, or pancreat

140 e clinicians assess women with a personal or family history of breast, ovarian, tubal, or peritoneal

141 1 +/- 5.7 years, mainly men, smokers, with a family history of CAD or hypercholesterolemia.

142 dex, menopausal status, hormone therapy use, family history of cancer, and comorbidities.

143 linical and molecular diagnosis of TSC and a family history of cancer, presenting two rare associated

144 isk should include a comprehensive review of family history of cancer.

145 anted in UM patients with strong personal or family history of cancers, or both.

146 eased low-density lipoprotein cholesterol, a family history of cardiovascular disease, premature coro

147 The presence of a family history of CD was also considered.

148 ghtly between CD patients depending on their family history of CD.

149 c testing for individuals with a personal or family history of certain cancers.

150 significant associations between PTH-CH and family history of CH (OR 3.32, 95% CI 1.31 to 8.63), chr

151 usted OR [aOR]: 0.60, 95% CI: 0.36-0.99) and family history of Chagas disease (aOR: 0.58, 95% CI: 0.3

152 Older maternal age, family history of Chagas disease, home conditions, lower

153 rol groups, one with and the other without a family history of CHD, to explore the contribution of sh

154 A family history of childhood HCM was more common in those

155 ein epsilon4 (APOE epsilon4) carrier status, family history of cognitive impairment, and history of s

156 Risk factors for SSLs include white race, family history of colorectal cancer, smoking, and alcoho

157 A family history of conduction system disturbance or pacem

158 He had no other comorbidities and no family history of congenital heart disease, cardiomyopat

159 as more pronounced for those with additional family history of CRC (12-21 years earlier depending on

160 All participants with a family history of CRC are invited to a shared decision m

161 As there is evidence that individuals with a family history of CRC have an increased risk of developi

162 pulation patients with diabetes with/without family history of CRC reach the threshold risk at which

163 osing cholangitis, post-inflammatory polyps, family history of CRC, and ulcerative colitis versus Cro

164 included basic demographics, insurance, BMI, family history of CRC, smoking, diabetes, and aspirin us

165 having risk for CRC similar to those with a family history of CRC, whereas the PRS based on known GW

166 A family history of DCM identified only 34% (n=12/35) of h

167 A family history of DCM occurred in 11% (n=12) while clini

168 In humans, a first-degree family history of dementia (FH) is a well-documented ris

169 correlations between LOAD and traits such as family history of dementia and education.

170 APOE-epsilon4 and two other risk factors, a family history of dementia and obesity, on grey matter m

171 a positive family history of PD, a positive family history of dementia, non-smoking, low alcohol con

172 Family history of DGC and endoscopic findings therefore

173 pared between individuals with and without a family history of DGC.

174 carriers of PLP variants in CDH1 who lack a family history of DGC.

175 ers of PLP variants of CDH1 with and without family history of DGC.

176 (1.4-2.1 times), male gender (1.5 times) and family history of diabetes (1.4-3.4 times) were associat

177 smoking (aOR: 4.81, 95% CI: 2.27-10.21), and family history of diabetes (aOR: 4.60, 95% CI: 2.67-7.91

178 lder age and absence of either diabetes or a family history of diabetes in the ILS group, and higher

179 ', either elevated blood glucose levels or a family history of diabetes mellitus; 'K', the presence o

180 betes prevalence increased sharply with BMI, family history of diabetes, and genetic risk.

181 Twenty associated CEQTs were shared across family history of diabetes, asthma, and CHD, far more th

182 (7.0%), and 78 (17.1%) CEQTs associated with family history of diabetes, asthma, and CHD, respectivel

183 our method on 457 CEQTs for association with family history of diabetes, asthma, and coronary heart d

184 index, sleep duration, depressive symptoms, family history of diabetes, history of hypertension, and

185 eight individuals (BMI < 25 kg/m2) without a family history of diabetes, similar to that in obese ind

186 fatigue, or visual changes, and had no known family history of diabetes.

187 mily history GWAS using cases ascertained on family history of disease agrees with combined hospital

188 nic medical records, criminality, as well as family history of disease and crime were extracted from

189 ally includes risk factors such as age, sex, family history of disease and lifestyle (e.g. smoking st

190 Family history of disease can provide valuable informati

191 spital records, questionnaire responses, and family history of disease implicate similar disease gene

192 -FH greatly increases association power when family history of disease is available.

193 (iii) the independent information of PRS and family history of disease or monogenic mutations and (iv

194 how to best combine case-control status and family history of disease.

195 ve traits (CEQTs) for their association with family history of disease.

196 ncer, particularly among women with positive family history of early-onset breast cancer.

197 as more similar to the NS than the FA group: family history of eczema NS 44.6%, ST.

198 the proportion of affected individuals with family history of epilepsy on the maternal versus patern

199 n the likelihood of maternal versus paternal family history of epilepsy.

200 size > 5 (AOR: 4.44, 95% CI: 1.43-13.75) and family history of eye problem (AOR = 7.02, 95% CI: 1.95-

201 s early in life and often have a conspicuous family history of first- and second-degree relatives wit

202 Family history of gastric cancer and Helicobacter pylori

203 ge, sex, alcohol consumption, IBS diagnosis, family history of gastrointestinal cancer, smoking statu

204 of eye examination [AOR; 6.52: 3.37, 12.63]; family history of glaucoma [AOR; 12.08: 4.13, 35.30] and

205 sure >21 mm Hg, narrow drainage angles, or a family history of glaucoma were excluded.

206 Higher educational status, positive family history of glaucoma, eye examination and higher i

207 of deafness in individuals without previous family history of hearing loss is challenging and has be

208 We showed family history of heart disease was associated with a 20

209 Only 9 patients (27%) had a family history of hematological malignancy, and 15 (46%)

210 moking cessation or in aiding persons with a family history of HNC to evaluate their risks.

211 s per day, was a high school graduate, had a family history of HNC, and was non-Hispanic white.

212 rette smoking duration and intensity, and/or family history of HNC.

213 Controls either had a family history of Huntington's disease but a negative ge

214 ase but a negative genetic test, or no known family history of Huntington's disease.

215 r rectal bleeding are present, or there is a family history of inflammatory bowel disease or coeliac

216 ar risk factor and with neither personal nor family history of ischemic heart disease.

217 splant recipients and donors with a positive family history of kidney disease is discussed.

218 A family history of mood disorders was associated with poo

219 l cholesterol (2.85 [95% CI, 2.38-3.32]), or family history of myocardial infarction (2.71 [95% CI, 2

220 factors for myopia were collected, including family history of myopia, outdoor time, reading time, sc

221 hort of healthy controls with no personal or family history of neurological or psychiatric disorders

222 ther neuropsychiatric history, medication or family history of neuropsychiatric disorders predicted c

223 A family history of neuropsychiatric disorders was present

224 on patient neuropsychiatric, medication and family history of neuropsychiatric disorders.

225 A family history of neurotic disorders was associated with

226 A family history of OA, personal history of knee OA, or pa

227 Individuals with a family history of pancreatic cancer affecting two first-

228 Family history of pancreatic cancer and high-grade IPMN

229 duals (cancer affected or unaffected) with a family history of pancreatic cancer meeting criteria for

230 vidence and discuss whether a patient with a family history of pancreatic cancer should undergo scree

231 found that early onset cases and cases with family history of PCa were enriched in the genetically h

232 or exercise, increased fasting glucose and a family history of PCOS in at least one first degree rela

233 e <0.05) was found between PD and a positive family history of PD, a positive family history of demen

234 ng for environmental tobacco smoke exposure, family history of PD, and use of ibuprofen generated sim

235 kidney disease, hypertension and obesity; a family history of pre-eclampsia, nulliparity or multiple

236 es predictive of CAD in both models included family history of premature CAD, age, male sex, lower gl

237 ex, dyslipidemia, hypertension, smoking, and family history of premature cardiovascular disease contr

238 total-high-density lipoprotein cholesterol), family history of premature CVD, medical history (smokin

239 learning, information processing speed, and family history of psychosis.

240 with greater PLEs, even after accounting for family history of psychotic disorders, internalizing sym

241 rriers, only 25.2% of individuals reported a family history of relevant disease.

242 patients (20%) with bilateral disease had a family history of retinoblastoma.

243 act gradient had an inverse association, and family history of SCD had no association with SCD.

244 A family history of smoking was more often reported by ind

245 r adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomat

246 pia (2.0-<4.0 D) in preschool children, with family history of strabismus and maternal smoking during

247 panic and Hispanic white race and ethnicity, family history of strabismus, maternal smoking during pr

248 0 patient registry revealed highly prevalent family history of sudden cardiac death (51%) and cardiom

249 from a 13-year-old man (QTc, >480 ms) with a family history of sudden cardiac death.

250 She had no family history of sudden cardiac death.

251 Children referred for a family history of sudden death receive cardiac disease d

252 Patients referred for a family history of sudden death were evaluated in a retro

253 The two CD36 mutation carriers had no family history of T2D and no clustering of cardio-metabo

254 diabetes mellitus (T2DM; FH-) and 8 NGT with family history of T2DM (FH+) received an oral glucose to

255 patients with colorectal cancer (CRC) have a family history of the disease attributed to genetic fact

256 3 of 4 patients with early-onset CRC have no family history of the disease.

257 sk for keratoconus, even in people without a family history of the disease.

258 lly in patients with age-of-onset <50 years, family history of thoracic aortic disease, and no histor

259 erity and was higher in case subjects with a family history of tics than in simplex case subjects.

260 drome, BRIP1, and RAD51D genes, and 11 had a family history of TOC.

261 -fold higher in children with a first-degree family history of type 1 diabetes (FDR children) than in

262 Twelve NGT subjects without family history of type 2 diabetes mellitus (T2DM; FH-) a

263 ge at childbearing, previous history of GDM, family history of type 2 diabetes mellitus and ethnicity

264 Known family history of type 2 diabetes was identified in 25 i

265 acids demonstrated strong predictability for family history of type 2 diabetes.

266 In addition, family history of UC (2 studies, n = 557; P = .0004), ex

267 iligo cases are "simplex," where there is no family history of vitiligo, though occasional family clu

268 A family history of XP was present in 32 (27%) patients.

269 e, and deploy clinical predictors (including family history) of AF risk, to assess the utility of inc

270 characteristics and lack of appreciation of family history often result in a failure to diagnose ADT

271 For women whose personal or family history or ancestry is not associated with an inc

272 men at higher-than-average risk due to their family history or genetic susceptibility.See related com

273 eleterious germline variant include a strong family history or multiple cancers in a single patient,

274 hyperlipidemia (OR=4.36, P=.04) and diabetes family history (OR=5.38, P=.02) were independently assoc

275 and 125 UM patients with strong personal or family histories, or both, of cancer.

276 ersonal history (P < .001), and first-degree family history (P = .03) were associated with breast can

277 g age, obesity, prolonged standing, positive family history, parity and Caucasian ethnicity.

278 ent datasets comprising 676 cases and 35,675 family history proxy cases.

279 Meanwhile, a reduction in family history-related associations with altered white m

280 ricting testing to age <50 years, indicative family history (revised Bethesda guidelines or Amsterdam

281 genic risk component of BOADICEA and the non-family-history risk factors included in IBIS.

282 e of cancer or on other risk factors such as family history, sex, age and other lifestyle factors or

283 3, entirely asymptomatic and with a negative family history, showed an unexpected and practically com

284 ory and smoking risk factors (odds ratio(PRS+family history+smoking), 1.24 [95% CI, 1.14-1.35]; P(PRS

285 aortic surgery than those with AD without a family history (subdistribution hazard ratio: 1.40; 95%

286 t that models that include multigenerational family history, such as BOADICEA and IBIS, have better a

287 d in patients with pancreatic cancer without family histories suggestive of a familial cancer syndrom

288 Metastatic disease or family history suggestive of hereditary PCA was recommen

289 lable or poorly recorded and there is little family history to guide study.

290 Non-first-degree family history was not associated with cancer (P = .09).

291 those who do not; to determine the effect of family history, we compared those with genetic sporadic

292 Gastrointestinal comorbidities and family history were common in patients with FPIES.

293 ver, premorbid IQ in males and schizophrenia family history were significantly correlated with TRS an

294 Extensive work-up and family history were unremarkable.

295 An age-, sex- and APOE based risk score and family history were used to select cases most likely to

296 We developed a "family history-wide association study" (FamWAS) to syste

297 Some patients have a negative family history with apparently de novo mutations.

298 tory with allergic proctocolitis (23.2%) and family history with inflammatory bowel diseases (9.4%) a

299 However, the heritability and association of family history with late outcomes are unclear.

300 f CRC has been calculated largely by age and family history, yet 3 of 4 patients with early-onset CRC