ライフサイエンスコーパス: family history

1 ine in social functioning, baseline age, and family history).

2 d families had no corneal signs but positive family history.

3 were identified in sporadic patients without family history.

4 continuous measure of genetic risk based on family history.

5 ancer risks and to investigate the impact of family history.

6 f subjects with normal corneas, but positive family history.

7 rward on clinical grounds with the help of a family history.

8 specialist sarcoma clinics without regard to family history.

9 re onset zone and were more likely to have a family history.

10 t diagnosis and were not selected for age or family history.

11 est, extreme QT prolongation, and a negative family history.

12 There was no relevant surgical or family history.

13 ients were diagnosed by newborn screening or family history.

14 on in younger women, Latinas, and those with family history.

15 Likewise, the patient had no relevant family history.

16 er loss of function had MPMs and/or positive family history.

17 He had no significant family history.

18 or alcohol abuse, nor was there any relevant family history.

19 tomatic white individuals without a relevant family history.

20 riteria on the basis of age of diagnosis and family history.

21 s were stratified by age at onset and cancer family history.

22 ts) or after screening because of a positive family history (13/36 subjects) or by another ophthalmol

23 posing mutation and available information on family history, 23 (40%) had a family history of cancer.

24 P = .01) and more often reported a positive family history (35 of 79 [44.3%] vs 367 of 1201 [30.6%];

25 by risk factor (56 years for patients with a family history, 59 years for those with many nevi, and 6

26 r race, age at menarche, age at first birth, family history, alcohol consumption, and smoking status,

27 Data were linked with family histories and findings from clinical and patholog

28 th EOC risk from 15,437 cases unselected for family history and 30,845 controls and from 15,252 BRCA1

29 For men with no family history and a high genetic risk score (90%), the

30 Cancer family history and demographic and clinical features wer

31 ed with breast cancer in other categories of family history and folate intake (P-interaction = 0.55).

32 d breast cancer was found among women with a family history and folate intake less than 400 mug/day (

33 When the association was stratified by family history and folate intake, a positive association

34 5 patients were assessed for personal and/or family history and genotype.

35 and demonstrate the potential importance of family history and mutation location in risk assessment.

36 We hypothesized that a negative family history and no sarcomere mutations represent a no

37 ceive genetic counseling regardless of their family history and phenotype.

38 atus, number of pregnancies, breast feeding, family history and receptor status also did not reveal a

39 he BAP1 cancer syndrome through personal and family history and TBSE for the presence of possible MBA

40 mptom onset, higher prevalence of a positive family history, and AMD phenotype.

41 no consensus on what constitutes a positive family history, and ascertainment is unreliable for many

42 s provided blood for DNA analysis and cancer family history, and cancer treatment records were review

43 density of less than 75%, for women with no family history, and for postmenopausal women.

44 t density of less than 75%, for women with a family history, and for women who were postmenopausal.

45 sub-Saharan African ethnic origin, positive family history, and high myopia.

46 and further tailored based on clinical data, family history, and immunophenotyping.

47 ications of cardiovascular disease, a benign family history, and normal electrocardiogram accounted f

48 vels, questionnaires about child medical and family history, and review of medical records.

49 ed mutational distribution, association with family history, and risk for multiple primary malignanci

50 major predisposing risk factors are obesity, family history, and sedentary lifestyle.

51 ethnic origin, exercise, educational level, family history, and smoking, the hazard ratio (HR) for T

52 on on skin, hair, and eye color; skin cancer family history; and sun exposure history, such as tannin

53 Exposures: Single nucleotide polymorphisms, family history, anthropometric factors, menstrual and/or

54 ith a primary IPMN with HGD or with positive family history are at an increased risk to develop subse

55 e and outcomes of adding WGS to standardized family history assessment in primary care.

56 anding of individual risk is found, a simple family history assessment of major depression as part of

57 r a familial BRCA1/2 mutation (breast cancer family history [BCFH] positive, n = 208; n = 69 with BRC

58 association of risk factors (age, ethnicity, family history, body mass index, medication use) with pr

59 adenocarcinoma and describe the clinical and family history characteristics.

60 .02) and at surgery (chi2 = 7.77; P = .005), family history (chi2 = 6.26; P = .01), and smoking habit

61 n multiply affected families with a positive family history compared with families with only a single

62 mographic information, clinical history, and family history data were obtained at enrollment.

63 Family history did not predict the presence of an underl

64 er tumors and higher proportions of positive family history, estrogen receptor+, progesterone recepto

65 ivity C-reactive protein (hsCRP) levels, and family history (FH) of ASCVD to the PCE in participants

66 ness (CIMT) among asymptomatic adults with a family history (FH) of premature coronary heart disease

67 leotide polymorphisms (SNPs) associated with family history (FH) of upper gastrointestinal cancer (UG

68 beyond using coronary artery calcium (CAC), family history (FH), and high-sensitivity C-reactive pro

69 moderate the association between a positive family history for depression and the later manifestatio

70 lected and matched 1:4 to controls without a family history for estimating MACE-free survival.

71 etinogram in at least 1 eye), and a negative family history for retinitis pigmentosa.

72 ically targetable, will be missed if current family history guidelines are the main criteria used to

73 hout classic clinical stigmata or suspicious family history has led to increased reliance on genetic

74 absolute risk owing to nonmodifiable (SNPs, family history, height, and some components of menstrual

75 ies, including the importance of an accurate family history in interpreting genetic variants associat

76 Pertinent family history included breast cancer in both her mother

77 Family history indicated dominant (43%), recessive (10%)

78 n pertaining to specific subjects (including family history, individual genetic and other biometric i

79 Obtaining a detailed family history is critical to identify families who will

80 Family history is thus an important factor to take into

81 idelines for cancer genetic testing based on family history may miss clinically actionable genetic ch

82 Therefore, family history may not be particularly informative in th

83 ative FH phenotype definitions incorporating family history, more stringent age-based low-density lip

84 In an adoption cohort of 561 families, history of severe antisocial behavior assessed

85 n in individuals with strong personal and/or family histories of breast and/or ovarian cancer, while

86 e for screening in subjects with and without family histories of CRC.

87 l trial used archived DNA samples and cancer family history of 315 patients with TNBC enrolled betwee

88 However, a family history of a specific subtype is most strongly as

89 High subjective risk of AD, a family history of AD, and minimal attendance at research

90 n of AF and to estimate the association of a family history of AF with major adverse cardiovascular e

91 ironmental factors, and the association of a family history of AF with prognosis are unclear.

92 stronger in those with than those without a family history of alcohol use disorder.

93 factors for alcohol use disorder, including family history of alcoholism, male sex, impulsivity, and

94 Infants with a family history of allergic disease were randomized (stra

95 e gender (except for single egg allergy) and family history of allergic disease, whilst exposure to p

96 initis and asked about sociodemographics and family history of allergies.

97 The importance of the family history of allergy may decrease with age.

98 ion persisted when children with and without family history of allergy were considered separately.

99 7-8 years was independently associated with family history of allergy, OR 2.1 (95% CI 1.6-2.8), urba

100 ter age 11-12 years was associated only with family history of allergy.

101 neurodegenerative condition or if they had a family history of ALS in a first- or second-degree blood

102 dy documents an association between EMAP and family history of AMD and glaucoma, a clear female predo

103 Except for positive family history of AMD with rs3750846, all genotype-pheno

104 re variants in age at onset of symptoms, the family history of AMD, complement activation levels (C3d

105 cular drusen on fluorescein angiography, and family history of AMD.

106 dependent predictors of mortality, including family history of aortic dissection and age, can be incl

107 ensity lipoprotein cholesterol >/=160 mg/dL; family history of ASCVD; high-sensitivity C-reactive pro

108 g with ASD, and 122 were at low risk with no family history of ASD.

109 is mother had asthma, but there was no other family history of asthma or other lung disease.

110 s in early term-born children persisted when family history of atopy and delivery by means of cesarea

111 even when stratified by mode of delivery and family history of atopy.

112 reduced subcortical volumes in those with a family history of AUD compared to those without; and (4)

113 increase in first AUD onset in those with a family history of AUD or with prior externalizing behavi

114 mpared with healthy control subjects with no family history of autoimmunity.

115 Of patients with a personal or family history of breast and colorectal cancer, 10.7% (9

116 obands were selected from 3 strata, based on family history of breast and/or ovarian cancer, pancreat

117 early-onset breast cancer (</=40 years) or a family history of breast and/or ovarian cancer.

118 h images in healthy control subjects with no family history of breast cancer (n = 10).

119 Family history of breast cancer (P-het = .008) had modes

120 cancer risk in younger women, overall and by family history of breast cancer and folate intake, we pr

121 isk of breast cancer among those with both a family history of breast cancer and lower folate intake.

122 were performed in women with a first-degree family history of breast cancer, 46% in women with a per

123 mammographic density, polygenic risk score, family history of breast cancer, and BRCA mutations.

124 irst birth, body mass index at age 18 years, family history of breast cancer, and prior benign breast

125 ered fibroglandular densities), first-degree family history of breast cancer, body mass index (>25 vs

126 he relative hazards for age, race/ethnicity, family history of breast cancer, history of breast biops

127 reast cancer, bilateral breast cancer, and a family history of breast cancer.

128 years and did not have a personal or strong family history of breast cancer.

129 f biopsy were lowest in women who had only a family history of breast cancer.

130 er for women with risk factors, particularly family history of breast cancer; previous benign breast

131 negative breast cancer (TNBC) unselected for family history of breast or ovarian cancer to determine

132 triple-negative breast cancer (P = .01), and family history of breast/ovarian cancer (P = .01) predic

133 1 mutations exhibited increased frequency of family history of cancer (100% vs 65.9%, P = .06), parti

134 higher income, being unmarried, and having a family history of cancer (all P values < 0.05).

135 Interactions between family history of cancer and HL treatment were evaluated

136 cal features in mesothelioma patients with a family history of cancer has not been reported.

137 atic prostate cancer who were unselected for family history of cancer or age at diagnosis.

138 atures (eg, early age at diagnosis, personal/family history of cancer or polyps, tumor microsatellite

139 that mesothelioma patients presenting with a family history of cancer should be considered for BAP1 g

140 n status of 150 mesothelioma patients with a family history of cancer, 50 asbestos-exposed control in

141 he extent of hereditary cancer syndromes and family history of cancer, in patients diagnosed with CRC

142 also analyzed data on patients' personal and family history of cancer, including fulfillment of clini

143 n nine of 150 mesothelioma cases (6%) with a family history of cancer.

144 nformation on family history, 23 (40%) had a family history of cancer.

145 ly, the risk is higher in individuals with a family history of cancer.

146 L survivors with and without a site-specific family history of cancer.

147 with pancreatic cancer without a significant family history of cancer.

148 asbestos-exposed control individuals with a family history of cancers other than mesothelioma, and 1

149 duals with isolated LVNC in the absence of a family history of cardiomyopathy.

150 ake), health history and medication use, and family history of cardiovascular disease.

151 after adjustment for gender, age, education, family history of cardiovascular diseases, body mass ind

152 A borderline association between family history of CD and surgical recurrence (P = .054)

153 g sex, country of origin, housing materials, family history of CD, and awareness of CD.

154 groups included healthy individuals with no family history of celiac disease or antibodies against t

155 IECs from subjects with a family history of celiac disease, but not from subjects

156 r country, human leukocyte antigen genotype, family history of celiac disease, maternal education, an

157 th normal findings from colonoscopies and no family history of colorectal cancer (unexposed; mean age

158 for a 3-year surveillance interval included family history of colorectal cancer and detection of 1-2

159 ellitus, hypertension, hypercholesterolemia, family history of coronary artery disease, and known cor

160 peptide <100 pg/mL, no microalbuminuria, no family history of coronary heart disease (any/premature)

161 Among clinical features, absence of any family history of coronary heart disease was the stronge

162 Persons with a family history of CRC or a documented advanced adenoma i

163 model, we found that for individuals with a family history of CRC, it is cost effective to gradually

164 Neither proband age at CRC diagnosis, family history of CRC, nor personal history of other can

165 decreases with age among individuals with a family history of CRC.

166 A family history of cutaneous melanoma ('melanoma') is a w

167 rogresses to anterior cerebral regions and a family history of dementia is present.

168 based on age, APOE genotype, sex, education, family history of dementia, vascular risk, subjective me

169 , poorer baseline cognitive performance, and family history of dementia.

170 ala reactivity was assessed as a function of family history of depression and severity of stressful l

171 uggesting the potential value of determining family history of depression in children and adolescents

172 found between development of gray matter and family history of depression or experiences of traumatic

173 n (OR, 3.67), high ALT level (OR, 1.86), and family history of diabetes (OR, 3.43) were associated wi

174 ic-naive schizophrenia, after adjustment for family history of diabetes and other potential confounde

175 ependent of age, body mass index, education, family history of diabetes, cigarette smoking, alcohol d

176 tus, alcohol consumption, physical activity, family history of diabetes, homeostasis model assessment

177 ther lifestyle factors, body mass index, and family history of diabetes.

178 itability of 12 complex human diseases using family history of disease in 1,555,906 individuals of wh

179 ere MFS (p = 0.04), age at presentation, and family history of dissection.

180 nnaires concerning general health, including family history of DM.

181 the orbitofrontal cortex was associated with family history of drug use.

182 ded age, sex, anxiety or mood disorders, and family history of drug, alcohol, and behavioral problems

183 , race/ethnicity, anxiety or mood disorders, family history of drug, alcohol, and behavioral problems

184 opology between LD patients with and without family history of dystonia.

185 a height of more than 190 cm, obesity, and a family history of end-stage renal disease.

186 ileptic drugs before withdrawal, female sex, family history of epilepsy, number of seizures before re

187 ic glomeruli were older age, shorter height, family history of ESRD, higher serum uric acid level, an

188 ified in a small fraction of patients with a family history of FSGS.

189 There were no systemic features, or family history of genetic conditions.

190 After multivariate adjustment, family history of glaucoma or AMD was strongly associate

191 ; and any ethnicity over age 40 years with a family history of glaucoma or diabetes.

192 >/=40 years, ED aged >/=50 years, diabetes, family history of glaucoma, and/or pre-existing diagnosi

193 ctive error, number of glaucoma medications, family history of glaucoma, diabetes, hypertension, visu

194 Medical and ocular history, family history of glaucoma, visual acuity, and intraocul

195 e any other adult aged >/=60 years, or had a family history of glaucoma.

196 transferase, previous chronic liver disease, family history of HCC, and cumulative smoking had good d

197 ere were 251 (61%) probands with no reported family history of HCM, including 166 (40% of total) prob

198 similar phenotype of LQTS plus a personal or family history of HCM-like phenotypes and identified 2 a

199 ac output" for a patient with a longstanding family history of heart disease, "decreased circulating

200 such as targeted screening of persons with a family history of hyperlipidemia vs. general screening)

201 Cox regression models were adjusted for age, family history of hypertension, body mass index, physica

202 85.8 vs 26.3 in controls, p < 0.0001), but a family history of hypertension, diabetes, myocardial inf

203 ion models adjusted for age, sex, ethnicity, family history of hypertension, smoking, alcohol use, ph

204 ent hypertension, hypertension duration, and family history of hypertension.

205 ng the latter, F8 gene mutations, ethnicity, family history of inhibitors, and polymorphisms affectin

206 a greater than additive interaction between family history of lung cancer and HL treatment was shown

207 ory and nicotine addiction, medical history, family history of lung cancer, and lung function (forced

208 By integrating risk factors such as family history of lung cancer, CEA and AFP for light smo

209 n analysis, age, gender, smoking pack-years, family history of lung cancer, personal cancer history,

210 f cancer, personal history of pneumonia, and family history of lung cancer.

211 , duration, and quit-years; body mass index; family history of lung cancer; and self-reported emphyse

212 e trunk (41% vs 29%, P < .001), those with a family history of melanoma were more likely to have mela

213 inic keratoses, were more likely to report a family history of melanoma, and had tumors that were mor

214 (39%) were defined as higher risk owing to a family history of melanoma, multiple primary melanomas,

215 uded hair color, nevus density, first-degree family history of melanoma, previous nonmelanoma skin ca

216 many nevi, history of previous melanoma, and family history of melanoma, to assist with improving the

217 al of 5 of 29 probands (17.2%) with a strong family history of neuropsychiatric conditions (>/=3 firs

218 The risk factors of family history of NMSC (OR, 1.66 [95% CI, 0.90-3.07]) an

219 diseases (AOR = 4.0 (95 % CI: 1.92, 8.33)), family history of non-ocular allergic diseases (AOR = 3.

220 Family history of ovarian cancer (hazard ratio [HR], 1.5

221 patients with noninvasive IPMNs showed that family history of pancreatic cancer (P = 0.027) and high

222 risk of pancreatic cancer (eg, those with a family history of pancreatic cancer and chronic pancreat

223 or first-degree relative (P < .01), but not family history of pancreatic cancer, age at diagnosis, o

224 ly three of these 33 patients had reported a family history of pancreatic cancer, and most did not ha

225 Olfactory function, genetic risk, family history of Parkinson's disease, age, and gender w

226 omy patients was stratified into men with no family history of PCa (NFH); a first-degree relative wit

227 All participants had a family history of PD.

228 %), whereas CAE was found less frequently in family history of positive MI patients (21%), sporadic M

229 We ascertained family history of premature (<60 years) death from cardi

230 l lipid disorders in a patient with a strong family history of premature atherosclerotic cardiovascul

231 ity lipoprotein cholesterol and personal and family history of premature atherosclerotic cardiovascul

232 A family history of premature cardiomyopathy death was ass

233 of hypertension, diabetes, or dyslipidemia; family history of premature coronary artery disease; nev

234 In contrast, a family history of premature death from other cardiac or

235 encies did not differ according to whether a family history of prostate cancer was present or accordi

236 nign prostatic hyperplasia, and those with a family history of prostate cancer were more likely, and

237 gnificantly according to age at diagnosis or family history of prostate cancer.

238 majority (87%) of case subjects reported no family history of pulmonary fibrosis.

239 ent "at risk" was defined as a person with a family history of retinoblastoma in a parent, sibling, o

240 A 12-month-old female child without a family history of retinoblastoma presented with unilater

241 ophysiological study results (p < 0.0001), a family history of SCD (p = 0.03), and AF (p < 0.0001).

242 Stressful life events, trauma, and family history of schizophrenia were not significant pre

243 Our study demonstrated that family history of schizophrenia/psychoses is partly medi

244 including sociodemographic characteristics, family history of substance use disorder, disturbed fami

245 lling for sex, age, other substance use, and family history of substance use disorder.

246 confidence interval, 0.92-0.98; P=0.004) and family history of sudden cardiac death (odds ratio, 3.5;

247 ustained ventricular tachycardia, syncope, a family history of sudden cardiac death, and severe cardi

248 tients with HCM, age, NYHA functional class, family history of sudden death (FHSD), syncope, atrial f

249 4.0; 95% confidence interval, 1.6-9.7) and a family history of sudden death (odds ratio, 3.2; 95% con

250 Prior syncope and family history of sudden death are predictors of a posit

251 Age, sex, clinical presentation, family history of sudden death, ethnicity, and deprivati

252 not different among those with or without a family history of T1D (P = 0.39) or HLA-DR-DQ genotypes

253 me, accompanied by a mutation in DCTN1; or a family history of the disease, parkinsonism and a mutati

254 e risk for retinoblastoma in children with a family history of the disease.

255 cases, and less than 10% of patients have a family history of the disease.

256 (19%) were diagnosed in individuals with no family history of the disease.

257 esence or absence of systemic symptoms, or a family history of the disease.

258 ut who do not have syndromic features have a family history of thoracic aortic disease.

259 ty, stratifying by country and adjusting for family history of type 1 diabetes, HLA-DR-DQ genotypes,

260 One patient without a family history of uveal melanoma had a single nucleotide

261 Both had a family history of uveal melanoma in at least 1 relative.

262 ed body mass index, those with a personal or family history of venous thromboembolism, and those rece

263 ther these risk factors are independent of a family history of VTE in first-degree relatives.

264 These results were independent of a positive family history of VTE.

265 V Leiden mutation (FVL) depend on a positive family history of VTE.

266 of gestational VTE independent of a positive family history of VTE.

267 r antenatal thromboprophylaxis regardless of family history of VTE.

268 toma harbor germline VHL mutations without a family history or additional features of VHL disease.

269 e numbers on newborn screening or a positive family history or clinical suspicion of SCID or other se

270 ely understood, even in patients with strong family history or early age at onset.

271 teral cases, and the unilateral cases with a family history or germline RB1 mutation) we found a tril

272 vs leaky SCID/Omenn syndrome, diagnosis via family history or newborn screening, use of preparative

273 ational level (OR, 1.69; 95% CI, 1.20-2.40), family history (OR, 1.63; 95% CI, 1.22-2.17), and privat

274 preselection for age at diagnosis, personal/family history, or MSI/MMR results.

275 co-occurring cardiac features, pathogenesis, family history, or myocardial dysfunction.

276 t start, duration, and pack-years), alcohol, family history, oral contraceptive, hormones, physical a

277 raction between the polygenic risk score and family history (P = .03).

278 Controlling for age, family history, presentation, nuclear grade, number of e

279 ct gene detection for patients with positive family history prior to refractive surgeries.

280 Possibly influenced by patients' family history, race, quality of bowel preparation, or n

281 collected included age at presentation, sex, family history, RB1 mutation status, 8th edition TNMH ca

282 Patients were randomly assigned to receive a family history report alone (FH group) or in combination

283 nt of potential demographic, anthropometric, family history, reproductive, and lifestyle confounders.

284 he central idea of the PGC is to convert the family history risk factor into biologically, clinically

285 ple with 1 affected FDR (92% of those with a family history), screening every 3 years beginning at an

286 Twin and family history studies show a high heritability for esse

287 The number of patients with a family history suggestive of LS was highest among women

288 Twenty per cent had a family history, the remaining having sporadic ataxia.

289 eatic cancer, and most did not have a cancer family history to suggest an inherited cancer syndrome.

290 xamination including an ocular, medical, and family history; visual acuity testing, intraocular press

291 of 13 subjects having no signs but positive family history was 69.2%.

292 Family history was pertinent for breast cancer in her mo

293 Family history was positive in all patients.

294 Her family history was remarkable for an aunt who died of sy

295 A recent analysis using family history weighting and co-observation classificati

296 Her otologic, birth, and family histories were limited, given that she was adopte

297 enazi Jewish patients with CD and a positive family history were recruited from the University Colleg

298 used for risk prediction, including age and family history, were not associated with breast cancer r

299 n both risk groups, it is the offspring with family history who go on to have recurrences and a poor

300 atic castration-resistant PCA, regardless of family history, with stronger agreement to test BRCA1/2