ライフサイエンスコーパス: control population

1 the 12 months preceding ERP implementation (control population).

2 eas (LGAs) with another 12 LGAs serving as a control population.

3 ral, be preferred to models developed on the control population.

4 Specificity was calculated by using the control population.

5 us infections and compared them to a healthy control population.

6 ples were also collected from a matched lean control population.

7 472H, similar to the findings in the healthy control population.

8 mputees' contralateral skin and also for the control population.

9 comparison to homologous chest sites on the control population.

10 s, as well as on the chest and arm skin of a control population.

11 ion studies in a large African American case-control population.

12 ange of values measured on the chests of the control population.

13 of TCF7L2 in a larger African-American case-control population.

14 multisequence alignment and use of a normal control population.

15 , thromboembolism, and death compared with a control population.

16 MP exhibit more gingival inflammation than a control population.

17 patients with tuberculosis, compared to the control population.

18 ure (14.8%) was not different from that of a control population.

19 y in the rehabilitation group but not in the control population.

20 normal FP receptor expression, provided the control population.

21 ause some level of screening occurred in the control population.

22 relaxation time in patients compared with a control population.

23 ng changes to those in an ethnically matched control population.

24 icantly different from those measured in the control population.

25 WF glycan expression was seen in the healthy control population.

26 was higher in the LAgP group relative to the control population.

27 s, including the selection of an appropriate control population.

28 higher than that in the age- and sex-matched control population.

29 similar to the prevalence of IgG to CPS in a control population.

30 also elevated to a similar degree in the CHF control population.

31 ation and tirapazamine was equivalent to the control population.

32 s were identified, which were not found in a control population.

33 lignancy were also studied as a polymorphism control population.

34 n (at codons 26 and 389) was detected in the control population.

35 plotted against the allele frequency in the control population.

36 in either of the other 2 drug groups or the control population.

37 ipoprotein (APO E) gene when compared with a control population.

38 and C71W); these changes were not seen in a control population.

39 African-American SLE population than in the control population.

40 in a geographically matched African-American control population.

41 25 to 100 times greater than an age-matched control population.

42 and September 30, 1985, were included in the control population.

43 rom 200 volunteer blood donors was used as a control population.

44 quality of life than an age- and sex-matched control population.

45 ia over the follow-up were excluded from the control population.

46 study population were compared to a matched control population.

47 ients was determined relative to the healthy control population.

48 % of the nonfamilial cases and in <0.05 of a control population.

49 ease would differ from that of an uninfected control population.

50 between the SSTI patients and an uninfected control population.

51 similar to an age-matched and gender-matched control population.

52 ciles the occurrence of this mutation in the control population.

53 to continue with medical treatment formed a control population.

54 nedarone was 1.3% compared with 14.0% in the control population.

55 sed sample followed by replication in a case-control population.

56 170,139 patients who had not were used as a control population.

57 S from an endemic focus of FS and nonendemic control populations.

58 ning rates in RA patients compared to non-RA control populations.

59 on T2D and BMI in two European American case-control populations.

60 r in mutant bottlenecked populations than in control populations.

61 ontent, de novo inheritance and absence from control populations.

62 The variants were almost absent from control populations.

63 gen levels that are comparable with those of control populations.

64 ysical and emotional functioning relative to control populations.

65 association with AMD in two independent case-control populations.

66 housands of SNP markers between affected and control populations.

67 cDNA were found in both the patient and the control populations.

68 onal task-related activations in patient and control populations.

69 d the distributions of genotypes to those of control populations.

70 rheumatoid vasculitis in comparison with the control populations.

71 distributions previously reported in normal control populations.

72 mutations that are rare in both patient and control populations.

73 subjects, or group statistics for patient or control populations.

74 variant FcgammaR alleles in both disease and control populations.

75 DRbeta1*0401, both in the patient and in the control populations.

76 d from random distributions in these healthy control populations.

77 iated histone H1 kinase activity relative to control populations.

78 rent grades of CAS, or between the study and control populations.

79 nfluenzae type b (Hib) disease compared with control populations.

80 dle assembly checkpoint function relative to control populations.

81 lized type-IV collagen more rapidly than did control populations.

82 eased incidence of Hib disease compared with control populations.

83 onsistent with the clearance rates of normal control populations.

84 ence rates were found in Italian and Ugandan control populations.

85 t to reporting bias, and have lacked similar control populations.

86 ound levels were similar between airport and control populations.

87 machine learning using positive and negative control populations.

88 difficult when the variant is also found in control populations.

89 were detected between urchins from vent and control populations.

90 exposures than observed for the original and control populations.

91 This enrichment was absent in control populations.

92 cted carriers in heritable PAH families, and control populations.

93 All surgical procedures in the study and control populations.

94 0.95-2.13) in treatment groups compared with control populations.

95 7 controls), and Ghanaian (170 cases and 138 controls) populations.

96 ontrols) and European (4,036 cases and 6,959 controls) populations.

97 1365 controls) and Japanese (1484 cases/1188 controls) populations.

98 ds (2.7%), 8 novel variants not found in the control population (0%; P=0.001) were identified.

99 with the same effect directions in the case-control population (0.02 < or = P < or = 0.03).

100 0.07; OR 5.5; 95% CI 1.8-17.0) and a healthy control population (0.28 vs 0.11).

101 viation]) was 23.76% higher than that of the control population (1.08 +/- 0.08) (P < .0001), while th

102 Patients were matched by age and sex to a control population (1:4) in the SAIL database.

103 In our control population, 11.7% (9/77) of the individuals were

104 d for transplantation (31.8%) as compared to control population (13.5%, P < 0.001) and a lower freque

105 +/- 7.82) was 50.73% higher than that of the control population (14.95 +/- 4.83) (P < .0001).

106 was significantly higher than in the healthy control population (16.4 versus 8.7 pg/mL; P <.0001).

107 is was significantly higher than that in the control population (17.9% vs. 1.4%, P = 0.0032).

108 clinical symptoms n = 20) and two different control populations (20 poly-sensitized sedentary subjec

109 significantly greater proportion than in the control population (34 of 4300).

110 tumor aggressiveness in a family-based case-control population (439 cases and 479 sibling controls).

111 In the control population, 61.5% were homozygote wild type, 33.

112 duced frequency (1.1%) relative to a matched control population (7.0%), suggesting that I447V may be

113 ermination were free from AF, similar to the control population (87%,); P=not significant.

114 04L), or had not been reported previously in control populations (A572F and W1205C).

115 enetic database comprising data from a large control population) accounted for 67.7% of persons with

116 The PheWAS software generated cases and control populations across all ICD9 code groups for each

117 among patients was compared to that among a control population, adjusting for age and gender.

118 es except for the analyses that deliberately control population admixture.

119 was compared with the survival rates in two control populations: age- and sex-matched members of the

120 ters were compared to a published historical control population aged <=50 years.

121 cts with diabetes and the elderly and spouse control populations (all P > 0.087).

122 f 12 (17%) patients in the MGUS pretreatment control population also had detectable anti-PDC response

123 ingly, in the IPF population, but not in the control population, an increased frequency of cocarriage

124 There were 11,194 MIs (2.0%) within the control population and 2319 (1.8%) and 112 (2.9%) MIs wi

125 ccurred in 71 (1.7%) of 4139 patients in the control population and 88 (2.1%) in the low-molecular-we

126 Both mutations were excluded in both a control population and all unaffected family members tes

127 953 allele "1" was carried by >99% of the AA control population and by 100% of the AA LJP group, with

128 pe polymorphisms in an African-American (AA) control population and in 37 African-Americans with loca

129 biomarkers were compared with an age-matched control population and with 2-dimensional proteomic anal

130 enign copy number change well represented in control populations and copy number variation databases.

131 s to establish well-defined intervention and control populations and determine causal relationships b

132 tly associated in three distinct German case-control populations and in an additional German family s

133 human microbiota require carefully selected control populations and standardized protocols.

134 egation with the phenotype, low frequency in control populations and the application of stringent bio

135 are difficult to compare, due to suboptimal control populations and wide variations in follow-up tim

136 model and mixed linear model approaches for controlling population and family structure.

137 zed at the 50th percentile value in combined controls (population and hospital controls), a lower lev

138 ution of C-peptide concentration amongst the control population, and participants were classified as

139 oximately 20% faster than flies of ancestral control populations, and have evolved a number of other

140 tential false positives using frequencies of control populations, and identify novel candidate diseas

141 difference was observed between our case and control populations, and no difference was observed betw

142 uently encountered in PD than in age-matched control populations, and whereas operational definitions

143 A 4-year, double-blind, placebo-controlled, population-based randomized clinical trial i

144 eumatoid arthritis (RA), were evaluated as a control population because RA progression is not conside

145 vels were achieved over the long term in the control populations because some of the deleterious muta

146 ompared with the rates in several unscreened control populations born during the same period.

147 re similar to those reported in the Japanese control population, but none of these was associated wit

148 inferred allele frequencies in selected and control populations by pyrosequencing.

149 tissue of patients with ALS and compared to control populations by real-time polymerase chain reacti

150 panese population (6,244 RA cases and 23,731 controls) population by using HLA imputation, followed b

151 ation was independently replicated in a case-control population collected separately.

152 edict the presence of asthma in the two case-control populations (combined P=1.2 x 10(-5)) and serum

153 247 patients age 75 years or above, and the control population consisted of 2,304 patients below 75

154 A control population consisted of 363 women undergoing amn

155 The control population consisted of 50 patients undergoing C

156 A control population consisted of six patients who underwe

157 cantly larger tumors than those arising from control populations; conversely, RKO cells expressing re

158 ata obtained from an individual subject with control population data.

159 nce protects against infectious epidemics by controlling population density and increasing diversity

160 of small molecule signals, the ascarosides, controls population density sensing and mating behavior.

161 receiving no such inhibitors and two healthy control populations, despite similar social exposure.

162 in patients with SSc compared with those in control populations do not provide clear support for any

163 In healthy control populations, downregulation of emotional respons

164 that mediate the lineage fate decisions and control population dynamics.

165 ample size; presence/absence of well-defined controls), population (ethnic diversity; community-based

166 -based primary prophylaxis and served as the control population for assessing outcomes in the black A

167 r allele frequencies in the African American control population for each variation were 7.5%, 6.3%, a

168 Screening of a control population for novel coding variants in CACNA1C,

169 nce and gene-environment independence in the control population for the same data can lead to efficie

170 nfected adults with and without dementia and control populations for a polymorphic site located in th

171 ar importance of precisely matching case and control populations for association analyses of rare var

172 tive risks or odds ratios (ORs) from ALS and control populations for individual ATXN2 alleles.

173 ratio, 7.8 [95% CI, 0.02-1.0]) or among the control population from the Exome Aggregation Consortium

174 2020, with a parallel non-COVID-19 UK cancer control population from the UK Office for National Stati

175 d studies, followed by replication in 2 case-control populations from Brazil, involving 3162 individu

176 approach, we first typed 4,608 SNPs in case-control populations from four U.K. populations and an As

177 replicated in two independent European case-control populations from the Czech Republic (odds ratio,

178 28 of 716 people in the control population had a positive HIV test result (crude

179 as higher in the WPW group compared with the control population (hazard ratio, 1.55; 95% confidence i

180 Compared to the control population, HIV-infected patients exhibited rela

181 not significantly different than that of the control population; however, prognosis was not as good i

182 in the Zn-selected than in the original and control populations if the 20% effective concentration o

183 e of carotid atherosclerosis compared with a control population in order to assess the potential asso

184 isorder has been compared with an unaffected control population in terms of survival.

185 In contrast, the absence of c.6320G>A in the control population in the homozygous state, combined wit

186 nearly identical to that of the curated case-control population in the primary analysis, providing fu

187 To characterize the type profile of JCV in a control population in the United States, 54 females (10

188 The control population in this 1:2 case-control study consis

189 no significant differences between vCJD and control populations in frequencies of any MHC types, nor

190 sing studies and often show differences from control populations in language experiments using word p

191 are expenditures in these states compared to control populations in the rest of the US.

192 n deleterious mutations were disallowed with control populations in which such mutations were allowed

193 The control population included 69 community-dwelling twin,

194 stibular symptoms combined with those in the control population indicated that the positive predictiv

195 mutations were also found in 8% of a healthy control population, indicating that they do not confer a

196 Pathogenic alleles were also found in control populations, indicating that environmental trigg

197 on, while only approximately 10% of a normal control population is skewed.

198 studies found disease-associated variants in control populations, leaving the role of WDR36 in this d

199 idual cells and the information available to control population-level responses.

200 enome-wide significance in the European case-control populations, located on chromosomes 12q24.12 (rs

201 ower mitochondrial respiration, than did the control population maintained in ambient CO2 (400 muatm,

202 ssociation remains significant in a CAD case control population matched for age and sex.

203 k and only slightly higher than the risks in control populations matched for age.

204 current outbreaks (such as influenza) in the control populations may have improved test characteristi

205 Compared to the colonoscopy control population, MC was associated with similar odds

206 inferior to that of the age- and sex-matched control population; median survivals for patients younge

207 For the control population, more patients (55%) were in the low

208 with different forms of GBS and appropriate control populations must be obtained.

209 of the MPN cases plus V617F carriers in the control population (n = 1223) vs the remaining controls

210 children (n = 30) by using a shared healthy control population (n = 36) and in an independent popula

211 two cohorts, as well as with a statin-naive control population (n = 37).

212 ) for replication in stage II, a trauma case-control population (n = 778).

213 ) was significantly greater than that of the control population (n = 850, median 23, inter-quartile r

214 (ablation: 872, no ablation: 1461) and a 1:5 control population (n=11 175).

215 based fine-mapping of a multiethnic ALL case-control population (Ncases = 1,464, Ncontrols = 3,279) t

216 so more skilled than fox kits from a second, control population not bred for tame behavior (criticall

217 differed between PMF patients and 2 healthy control populations (odds ratio, 1.6 and 1.8).

218 This group was compared with a matched control population of 124 patients who did not experienc

219 tions were compared with those obtained in a control population of 15 HIV-1-positive men whose age, b

220 her-sister mating and compared to an outbred control population of 1945 families.

221 s were significantly higher than that of the control population of 240 North American white NIH blood

222 d in a multivariate logistic regression to a control population of 3047 subjects without Barrett's es

223 rams were also obtained at years 8 to 9 in a control population of age, race/ethnicity, and sex-match

224 ited CNV regions, of which 268 are rare in a control population of European origin but present in a l

225 ed to investigate biochemical variation in a control population of female rats over time in relation

226 The distribution of CCR5Delta32 in a control population of healthy United States Caucasian ra

227 .005) were tested in a stage III nested case-control population of mixed subjects in the intensive ca

228 n their mechanical thresholds and those of a control population of nociceptors.

229 ents with NSF were compared with data from a control population of patients with renal insufficiency

230 of an age-, sex-, and disease-matched (2:1) control population of residents who had not had an out-o

231 Individuals in a case-control population of RSV-infected children who were hom

232 For external validation, we used a control population of SAH patients from the CONSCIOUS-1

233 compared with a similar survey of a matched control population of subjects who participated in other

234 l group was composed of individuals from the control population of the Multiple Environmental and Gen

235 as well as the TNIP1 homolog TNIP2, in case-control populations of diverse ethnic origins.

236 ios or infer a fitness cost could be used to control populations of invasive alien species.

237 l be compared with concurrent and historical control populations of nonparticipants.

238 -infected patients who had tuberculosis with control populations of similar size.

239 As phage infection is known to control populations of V. cholerae and thus outbreaks of

240 Controlling populations of vector mosquito species in ur

241 llele frequency differences between case and control populations on a genomewide scale.

242 black case patients were matched to 3 white control populations on demographics (age, year of diagno

243 lation (n=219 nuclear families) and two case-control populations--one African American (n=295 pairs)

244 nal risk models were developed on either the control population only (internal controls only) or the

245 cessing steps for genotype liftOver, quality control, population outlier detection, haplotype pre-pha

246 ifferent DM and SOAM metrics relative to the control population (P < .05 for all; P value ranges for

247 months after transplantation compared with a control population (P = .0127).

248 REX1 were also associated in the second case-control population (P(a)=0.017-0.042).

249 roduction profile of IL-10 compared with the control population (P=0.04).

250 ariants in 46,XX DSD is enriched compared to control populations (P < 1.8 x 10(-4)).

251 Relative to the control population, patients who experienced abrupt clos

252 Compared with the control population, patients with BE had increased risks

253 ions derived from the spring relative to the control population, providing the first evidence that pl

254 Three independent case-control populations representing Caucasians and African

255 7.1%) deaths occurred in the syncope and the control population, respectively, yielding an event rate

256 olar disorder, in a northern Swedish patient/control population, resulted in the discovery of two fun

257 erformance, and superior future hybrids to a control population selected on inbred line performance w

258 ratified 3:1 propensity matching to select a control population similar to patients who underwent IVC

259 ulation to test the salience of airport, and control population specific songs.

260 phasing, imputation, post-imputation quality control, population stratification analysis, and genome-

261 Quality control, population stratification, and statistical anal

262 nique advantages in enriching rare variants, controlling population stratification, and improving gen

263 ed in BC susceptibility, we conducted a case-control population study and observed that germline occu

264 Therefore, we conducted a case-control population study and the allele and genotype fre

265 tched to control subjects from two different control populations: subjects who were in the general po

266 Compared with age- and sex-matched control populations, survivors of pediatric Hodgkin's di

267 mparing the newly infected population with a control population that was not infected, we show that d

268 egg production and activity than males from control populations that evolved with a polygamous matin

269 Compared with a normal control population, the frequencies of HLA-DR2 (50 vs 22

270 As compared with a normal control population, the IPF group showed no significant

271 Compared with a normal control population, the patients had significantly reduc

272 mographic and illness characteristics of the control population, the septic population was at signifi

273 In both the exposed and the control populations, there was an absolute increase of a

274 hereas such individuals represent 20% of the control population, this retrospective study determined

275 r analysis with mutation screening in larger control population to establish the true prevalence of N

276 ed playback experiments at the airport and a control population to test the salience of airport, and

277 epeats) in the SEN population with that in a control population, to determine if there was a possible

278 den real marker data to simulate patient and control populations under different genotypic risk ratio

279 dergoing CTS, to compare them with a matched control population undergoing similar surgical procedure

280 e equation, which we then calculated for the control population using multivariate linear regression

281 ere compared versus a predefined independent control population, using 3-dimensional stereotactic sur

282 tion subjects (age 50 or more) and a similar control population, using a standardized videotaping pro

283 enerally more common among patients than the control population, warranting long-term follow-up after

284 A screened healthy control population was used for comparison.

285 The unexposed (control) population was composed of patients with no his

286 for the frequency of de novo variants in the control population, we estimate that 15% of sporadic com

287 ages, the overall fitness gains observed for control populations were larger than fitness gains in mu

288 Ohnishi, except that three large homozygous control populations were maintained.

289 None of the control populations were positive for HGV.

290 atients were compared with a contemporaneous control population who did not experience AR.

291 portional to the within-line G matrix of the control population with a constant very close to the exp

292 the study period, similar to a Pennsylvania control population with full coverage.

293 These patients were compared against a control population with no known coronary atherosclerosi

294 age) with retrograde DAPs and an age-matched control population with nondecremental accessory pathway

295 population compared with an immunocompetent control population with similar cancers.

296 ts who completed colonoscopy compared with a control population, with absolute differences of -7.4 pe

297 DY discovery cohort compared to the European control population within ExAC (odds ratio = 131, P = 1

298 llular structures not observed in unselected control populations within ~750 asexual generations.

299 the SSR markers in the case (alcoholics) and control populations would have detected the ALDH2 marker

300 rgery compared with 162 (5%) patients in the control population, yielding an adjusted odds ratio of 0