戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 assessed using random-effects Cox regression survival analyses.
2 er operating characteristic (ROC) curves and survival analyses.
3 diagnosis were examined with descriptive and survival analyses.
4  remained significant in univariate-adjusted survival analyses.
5 re identified by univariate and multivariate survival analyses.
6 in 925 RTR using univariate and multivariate survival analyses.
7 orectomy were evaluated using time-dependent survival analyses.
8 variables in Cox regression and Kaplan-Meier survival analyses.
9 luated using Kaplan-Meier and Cox regression survival analyses.
10  years for renal outcomes and 11.2 years for survival analyses.
11 ssion and Kaplan-Meier methods were used for survival analyses.
12 ortional hazards regression and Kaplan-Meier survival analyses.
13 performed functional gene set enrichment and survival analyses.
14  dates of hospitalization were excluded from survival analyses.
15 ns with generalised estimating equations and survival analyses.
16 xamined through time-dependent covariates in survival analyses.
17 es was evaluated by parametric models and by survival analyses.
18 h age-period-cohort models and breast cancer survival analyses.
19 log-rank p=0.12) or 3-6 (log-rank p=0.98) in survival analyses.
20 dard descriptive statistics and Kaplan-Meier survival analyses.
21 w-up data available and were included in the survival analyses.
22 tional hazards models were used for adjusted survival analyses.
23 r AIDS Cohort Study by means of Kaplan-Meier survival analyses.
24 biased exposure effect estimates in standard survival analyses.
25 e of positive prognostic value in univariate survival analyses.
26       Polarity conversions were evaluated by survival analyses.
27 ombined to allow multivariate and stratified survival analyses.
28 t investigate the effect of interventions by survival analyses.
29 nth prospective follow-up were assessed with survival analyses.
30 er evaluated during long-term follow-up with survival analyses.
31 istries in 11 countries were included in the survival analyses.
32 019, was conducted using cross-sectional and survival analyses.
33 evaluated using t testing of proportions and survival analyses.
34 tistics and Kaplan-Meier curves when used in survival analyses.
35 ng Cox proportional hazards and Kaplan-Meier survival analyses.
36 thin and betanidin were also included in the survival analyses.
37 rs were correlated in uni- and multivariable survival analyses.
38 arisons, clinical prevalence assessments and survival analyses.
39 ding log-rank statistics were calculated for survival analyses.
40 ay followed by univariable and multivariable survival analyses.
41 re were constructed for transplantation-free survival analyses.
42 N, EGFR, and CDKN2A, were assessed alongside survival analyses.
43 x proportional hazards modeling was used for survival analyses.
44 ), version 1.1 and overall survival (OS) for survival analyses.
45 y aborted; these patients were excluded from survival analyses.
46 luded from overall survival and disease-free survival analyses.
47 -naive/acute) was treated as time-varying in survival analyses.
48 ups were analyzed using Kaplan-Meier and Cox survival analyses.
49 o R1/D1 and R2/D2 groups for comparative and survival analyses.
50  through Cox proportional hazards regression survival analyses.
51 dies accounted for socioeconomic position in survival analyses.
52 le inverse probability of treatment weighted survival analyses.
53 y univariate and multivariate shared frailty survival analyses.
54 al were performed, together with conditional survival analyses.
55 -cause mortality was the primary endpoint in survival analyses.
56   Statistical methods included discrete-time survival analyses.
57 re estimated with the use of competing-risks survival analyses.
58  completely the effect of FA on multivariate survival analyses.
59         The Kaplan-Meier method was used for survival analyses.
60 ariate logistic regression, and Kaplan-Meier survival analyses.
61 05 for all but 1 comparison) in Kaplan-Meier survival analyses.
62 rulopathy (TG) development were estimated in survival analyses.
63 -Tree were validated using tumor pathway and survival analyses.
64 of reaching the end points were estimated by survival analyses.
65 inic population through probability-weighted survival analyses.
66 in RFS analyses and 5606 patients in overall survival analyses); 3638 patients were analyzed by cytog
67                  Univariate and multivariate survival analyses adjusted for patient, disease, and tre
68                                           In survival analyses adjusted for patient, tumor, and treat
69                                              Survival analyses, adjusted for propensity score by usin
70 resonance imaging were modeled with midpoint survival analyses, adjusted for PS-quintile.
71                               Adjusted MSPHM survival analyses also found no significant difference i
72   Established clinical co-variates dominated survival analyses, although CCP and hypoxia may inform c
73  incidence of hyperglycemia was confirmed by survival analyses among C/C, C/T, and T/T carriers durin
74                                 Kaplan-Meier survival analyses and adjusted Cox proportional hazards
75                                              Survival analyses and adjusted hazard ratios (HRs) were
76                                              Survival analyses and binary logistic regression models
77 was tested using univariate and multivariate survival analyses and by receiver-operating-characterist
78                                 Kaplan-Meier survival analyses and Cox proportional hazards modeling
79 m mortality were assessed using Kaplan-Meier survival analyses and Cox proportional hazards modeling,
80 pe of event (ischemic or hemorrhagic), using survival analyses and Cox proportional hazards models.
81                                              Survival analyses and Cox regression models revealed tha
82                                   Stratified survival analyses and Cox regression were used to compar
83 urther data maturation is needed for overall survival analyses and evaluation of the full predictive
84                         We further performed survival analyses and identified 17 072 sQTLs associated
85                                              Survival analyses and inherent log-rank tests showed tha
86                                              Survival analyses and Kaplan-Meier analyses were used.
87                                        Final survival analyses and updated results are reported.
88  evaluated using adjusted propensity-matched survival analyses and weighted cumulative exposure model
89 multilevel spatiotemporal exposure model and survival analyses) and short-to-medium-term exposure-mor
90  clinical and sociodemographic factors using survival analyses, and conducted genome-wide association
91                      Descriptive statistics, survival analyses, and vaccine effectiveness were calcul
92 ed and results of the final progression-free survival analyses are presented here.
93 free survival and concurrent interim overall survival analyses are presented.
94                          Propensity-adjusted survival analyses assessed the association of perioperat
95 ks of mortality and survivorship (hazard and survival analyses) associated with 10 biomarkers and use
96                            Kaplan-Meier (KM) survival analyses based on complex patient categorizatio
97                   Analytical approaches (eg, survival analyses) commonly used to assess HIV care casc
98                                              Survival analyses compared the timing of anatomic change
99                                           In survival analyses, compared with people who were not lon
100 ring the following 7 years in sex-stratified survival analyses controlling for age.
101                                              Survival analyses, controlling for age, sex, number of g
102                                              Survival analyses, correlation analyses, and t tests wer
103                                              Survival analyses demonstrated that greater stressor-evo
104                                              Survival analyses demonstrated that the disease course i
105            All 554 patients were included in survival analyses during the follow-up period of 1 year.
106 sults were compared with those from standard survival analyses (e.g., Weibull regression) with time-u
107 on and disease progression were monitored by survival analyses, echocardiography, and electrocardiogr
108                              In multivariate survival analyses, elevated CRP was confirmed as an inde
109                             In contrast, for survival analyses, EPPs typically cause NDD to be undere
110                                Multivariable survival analyses evaluated (1) eGFR-low as a predictor
111                              In age-adjusted survival analyses for all causes of death, men who were
112                                  In adjusted survival analyses for breast cancer mortality, LRR was i
113  methylation, and contrast-enhancing volume) survival analyses for progression-free and overall survi
114                    We generated Kaplan-Meier survival analyses for the largest untreated Hutchinson-G
115                                              Survival analyses for time to development of dementia, p
116 itive time-lagged associations were found in survival analyses for virtually all temporally primary l
117  and 1749 [49%] female) were included in the survival analyses from 1972 onwards.
118                                              Survival analyses from datasets of commonly occurring hu
119           Retrospective cohort studies using survival analyses have reported that fewer than 25% of p
120                    Commonly used statistical survival analyses implicitly assume a constant ratio of
121 l-cause mortality by Cox Proportional Hazard survival analyses in 1840 stable RTR derived from the As
122 as the potential to improve the precision of survival analyses in a number of different sectors, incl
123                                           In survival analyses in ADNI-1, elevated plasma IGFBP2 was
124 een January 1980 and June 2005 that provided survival analyses in patients with breast cancer after a
125          The 1-, 2-, and 3-year Kaplan-Meier survival analyses in propensity-matched patients favored
126                                 Multivariate survival analyses included relevant variables identified
127                                              Survival analyses included unadjusted Kaplan-Meier plots
128 ant marker of poor prognosis in multivariate survival analyses, including classic prognostic markers,
129                                              Survival analyses indicate that arrest effects endured u
130                                Visual acuity survival analyses indicate that the optimal intervention
131                                              Survival analyses indicated that each 1g/dl increase in
132                                 Kaplan-Meier survival analyses indicated that IC significantly delaye
133                                 Kaplan-Meier survival analyses indicated that the survival estimate,
134 ting characteristic analysis, and subsequent survival analyses (Kaplan-Meier, hazard ratios [HRs]) of
135                                   Results of survival analyses may be biased by treatment indication
136 e response rate and interim progression-free survival analyses, median follow-up was 6.2 months (IQR
137                              In Kaplan-Meier survival analyses, neither severity of stenosis (P = .80
138  comprehensive clinicobiologic, genetic, and survival analyses of a large cohort of 213 adult patient
139                                              Survival analyses of groups defined by size of residual
140 verall survival and updated progression-free survival analyses of ICON8.
141                                              Survival analyses of incident AMD versus average running
142                     At 5 years in the pooled survival analyses of reconstructed time-to-event IPD, TA
143                                              Survival analyses of relapse/recurrence rates, as determ
144                               Interestingly, survival analyses of TDP or FUS models show no increase
145                                   Univariate survival analyses of the patients from whom the study sp
146  By excluding matched patients, KM plots and survival analyses of the unreported subgroups were retri
147                                              Survival analyses of time to recovery and, subsequently,
148                                              Survival analyses of treated patients with PEL were then
149                     In this work, we perform survival analyses on a large longitudinal dataset of Str
150 ll-cohort and propensity-matched comparative survival analyses on our 3-center database of Sprint Fid
151                                       In the survival analyses, only frailty (vs no frailty) showed s
152 on models have often relied upon traditional survival analyses or outcomes data failing to extend bey
153  the consideration of a continuous series of survival analyses over 7 decades at Massachusetts Genera
154                                 Kaplan-Meier survival analyses over a follow-up of 10 y revealed sign
155 ned significant in pairwise (p = 0.0003) and survival analyses (p = 0.02).
156                     All patients included in survival analyses received standard doxorubicin, bleomyc
157                            Insights from the survival analyses recommend possible inclusion of functi
158 d Harrell C-index in the cross-sectional and survival analyses, respectively.
159                                              Survival analyses reveal a subset of 3'-UTR alterations
160                                  Spatial and survival analyses reveal that an increased lipid-associa
161                                              Survival analyses revealed a set of approximately 70 gen
162                                              Survival analyses revealed that chromosome 1q and 11p ga
163                                              Survival analyses revealed that even when controlling fo
164                                              Survival analyses revealed that, in addition to these di
165                                              Survival analyses revealed the association between mesot
166 protein interaction network and Kaplan-Meier survival analyses revealed the importance of METTL14 and
167                             In this context, survival analyses show that BAX mutations are indicators
168                                              Survival analyses showed a significantly (P = 0.002) hig
169                                 The adjusted survival analyses showed a significantly higher survival
170                                              Survival analyses showed a time-dependent significant as
171                                              Survival analyses showed significant differences in PFS
172              For all data sets, Kaplan-Meier survival analyses showed significant differences in rela
173                                              Survival analyses showed significant effects of pretreat
174                        The Kaplan-Meier (KM) survival analyses showed that 69%, 54% and 44% of these
175                                              Survival analyses showed that a 1-point improvement on t
176                                              Survival analyses showed that patients who developed cut
177                                              Survival analyses showed that the estimated risk for eve
178 x and/or National Death Index, with adjusted survival analyses starting at 24 months after ART initia
179                         Lung cancer-specific survival analyses suggest that NSCLC tumor behavior may
180                                              Survival analyses suggest that symptomatic improvements
181                  Conditional recurrence-free survival analyses suggest that the risk of recurrence af
182            Main Outcomes and Measures: Using survival analyses techniques, incidence rate ratios were
183                                              Survival analyses that accounted for competing risks wer
184                                           In survival analyses that accounted for competing risks, pa
185                        Thus, time to disease survival analyses that censor disease-free individuals a
186 ically significant according to Kaplan-Meier survival analyses that included 131 (95%) of 138 POWs an
187                           For the purpose of survival analyses, the baseline survival time was set to
188 .012), and, when tropism was included in the survival analyses, the effect of the SDF1-3'A allele on
189                                           On survival analyses, the only variable associated with the
190        Propensity score matching was used in survival analyses to adjust for differences among recipi
191  Medical Center (CUMC) were used in separate survival analyses to compare those who did or did not re
192 ional hazards models along with Kaplan-Meier survival analyses to estimate outcomes at the end of 1,
193                             The authors used survival analyses to estimate the risk of natural menopa
194 sure records are available in TCGA, existing survival analyses typically did not consider drug exposu
195                                 We performed survival analyses using 10 FAMMM syndrome families (N =
196                                 We completed survival analyses using an as-treated approach.
197                                 We performed survival analyses using Cox proportional hazards models.
198 sequent hypomania or mania was determined in survival analyses using Cox proportional hazards regress
199 NTS: This prospective cohort study performed survival analyses using data from the Baltimore Longitud
200                                              Survival analyses using intent-to-treat principles and m
201  simple interface for conducting genome-wide survival analyses using VCF (outputted from Michigan or
202 al hazard regression models were applied for survival analyses, using register-based all-cause mortal
203                           Index date for the survival analyses was date of disease onset.
204                             For the maternal survival analyses, we compared 77 pregnant patients and
205 dence intervals when performing Kaplan-Meier survival analyses, we recommend adjusting for dependence
206  resonance imaging and histopathological and survival analyses, we show that tumor progression was si
207                                         Both survival analyses were adjusted for age, sex and years o
208                                              Survival analyses were adjusted for guarantee-time bias
209                                          All survival analyses were adjusted for sex, age, calendar y
210 receiver-operating characteristic curves and survival analyses were applied.
211                                      Overall survival analyses were based on the intention-to-treat p
212 tion of response, and overall and event-free survival analyses were by intention-to-treat.
213                             In both cohorts, survival analyses were carried out for the NHOC and for
214                                              Survival analyses were carried out in 112 patients.
215                                              Survival analyses were conducted for patients with adeno
216                                              Survival analyses were conducted to assess the prognosti
217              Kaplan-Meier and Cox regression survival analyses were conducted to estimate the associa
218                                              Survival analyses were conducted using an inverse probab
219 ghbor caliper matching of propensity scores, survival analyses were conducted using Cox proportional
220 d using generalized linear mixed models, and survival analyses were conducted using Cox proportional
221                                Multivariable survival analyses were conducted using Cox proportional
222                                              Survival analyses were conducted using Kaplan-Meier esti
223                               Differences in survival analyses were determined using the log-rank tes
224                                Retrospective survival analyses were done on 283 CCALD patients identi
225 haracteristics of patients were compared and survival analyses were done to evaluate the effect of in
226                          Bayesian multilevel survival analyses were done to examine the moderating in
227                                              Survival analyses were employed to identify variables as
228 ed in the first year after randomization, so survival analyses were landmarked as starting at 1 year
229                                              Survival analyses were largely consistent: controlling f
230 levels in this cohort, statistical power for survival analyses were limited.
231                                 Multivariate survival analyses were performed by proportional hazards
232                                 Kaplan-Meier survival analyses were performed for 80 patients from th
233                Univariable and multivariable survival analyses were performed for all patients and th
234                                     Log-rank survival analyses were performed for each trial, and ove
235                                              Survival analyses were performed for patients whose tumo
236                                 Response and survival analyses were performed on posttreatment sample
237                                              Survival analyses were performed separately for node-neg
238                                              Survival analyses were performed taking into account com
239                                      Several survival analyses were performed testing the association
240              Kaplan-Meier and Cox regression survival analyses were performed to assess cell clusters
241                                              Survival analyses were performed to determine cumulative
242 t viral pathogens in nasal wash samples, and survival analyses were performed to determine whether in
243          Cox proportional hazards regression survival analyses were performed to estimate the effect
244                                              Survival analyses were performed using Cox proportional
245                  Univariate and multivariate survival analyses were performed using Cox proportional
246                                 Multivariate survival analyses were performed using Cox proportional
247                                              Survival analyses were performed using Cox proportional
248                  Univariate and multivariate survival analyses were performed using Cox regression.
249                                              Survival analyses were performed using Cox's proportiona
250                        Uni- and multivariate survival analyses were performed using Cox-proportional
251                                              Survival analyses were performed using models adjusted f
252     LTL-stratified and medication-stratified survival analyses were performed using multivariable Cox
253                                 Multivariate survival analyses were performed using proportional haza
254 ssed using log-rank tests while multivariate survival analyses were performed using the Cox proportio
255                                              Survival analyses were performed using the Kaplan-Meier
256                                              Survival analyses were performed using the Kaplan-Meier
257                                              Survival analyses were performed with adjustment for bas
258                                              Survival analyses were performed with adjustment for bas
259                                              Survival analyses were performed with Cox proportional h
260                                              Survival analyses were performed with models adjusted fo
261                                 Kaplan-Meier survival analyses were performed with pairwise log-rank
262 re investigated at 3 mo after treatment, and survival analyses were performed with the Kaplan-Meier m
263                                              Survival analyses were performed with weighted Cox model
264                                          Cox survival analyses were performed, adjusting for potentia
265                                              Survival analyses were performed, including 451,151 part
266 eier and Cox proportional hazards regression survival analyses were performed.
267                  Univariate and multivariate survival analyses were performed.
268            Kaplan-Meier and Cox multivariate survival analyses were performed.
269 for quantitative variables, and Kaplan-Meier survival analyses were performed.
270 iptive statistics, correlation analyses, and survival analyses were performed.
271 variable logistic and linear regressions and survival analyses were performed.
272 l hazards regression model, and Kaplan-Meier survival analyses were performed.
273                              Comparative and survival analyses were performed.
274  using Cox regression models and incremental survival analyses were performed.
275                                              Survival analyses were repeated for tumor FASN expressio
276       These results were consistent when the survival analyses were restricted to stage III disease:
277                    Definitions of events for survival analyses were tooth loss, loss of > or = 2 mm c
278                                              Survival analyses were used to account for potential dif
279    Inverse probability of treatment weighted survival analyses were used to analyze posttransplant mo
280                                              Survival analyses were used to calculate the duration of
281                                              Survival analyses were used to calculate the RR of all-c
282                                 Kaplan-Meier survival analyses were used to compare survival times be
283                                 Kaplan-Meier survival analyses were used to compare the cumulative in
284                                Bivariate and survival analyses were used to delineate patterns and co
285                  Univariate and multivariate survival analyses were used to determine the predictive
286                                 Kaplan-Meier survival analyses were used to determine the rate of EK
287                                              Survival analyses were used to evaluate their prognostic
288 proportional hazards regression modeling and survival analyses were used to identify factors related
289 ng multivariable regression and Kaplan-Meier survival analyses were used to predict risk of relapse,
290 alysis of variance, multilevel modeling, and survival analyses, where appropriate.
291 y longer PFS and OS (both P 0.03; univariate survival analyses) whereas RANO criteria were not signif
292 onger PFS and OS (both P <= 0.03; univariate survival analyses) whereas RANO criteria were not signif
293 l age at miscarriage (GAM) to assign time in survival analyses, which overestimates duration of expos
294                                              Survival analyses with and without risk adjustment were
295 ing Cox proportional hazard and Kaplan-Meier survival analyses with censoring applied.
296  the limited software options for performing survival analyses with millions of SNPs, we developed gw
297                                              Survival analyses with respect to the rate of progressio
298                                       We did survival analyses with the Kaplan-Meier estimator and ev
299 ression and intervention were estimated from survival analyses, with risk factors determined by using
300 internalizing and externalizing disorders in survival analyses, with time-lagged associations consist

 
Page Top