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1                              A wide range of interpatient absorbed doses was delivered to normal orga
2 ence in CD19-mediated signaling unfolds both interpatient and intraclonal diversity in CLL.
3 bevacizumab is high in mRCC, with remarkable interpatient and intrapatient heterogeneity.
4 ing has become increasingly used to evaluate interpatient and intrapatient tumor heterogeneity.
5                                              Interpatient and intrapatient variabilities in apparent
6 sporin (Neoral) exhibited significantly less interpatient and intrapatient variability than tacrolimu
7                                              Interpatient and intrapatient variability was similar (i
8                       PK studies showed wide interpatient and intrapatient variability.
9 s nonmalignant immune cells with significant interpatient and intrapatient variability.
10              We show that a unified model of interpatient and intratumor heterogeneity describes hist
11 atient cohorts demonstrated the intercancer, interpatient, and intratumoral heterogeneity of interact
12  arises years before disease onset, displays interpatient autoantigen variability, and is associated
13 ap prediction in osseous regions and reduced interpatient bias variation in femur-adjacent VOIs.
14         Improved bioavailability and reduced interpatient biovariability are therefore desirable for
15 sivity in NF1, resulting in intrapatient and interpatient cNF tumor burden heterogeneity, that is, th
16                                      In this interpatient comparison, data support the use of THW in
17 rwent both standard and low-dose CT allowing interpatient comparison.
18                                              Interpatient comparisons were also made and showed that
19                                 Furthermore, interpatient differences in 5 gene variants (NRAS, HRAS,
20                                              Interpatient differences in both decay rates were signif
21                               Reflecting the interpatient differences in contrast enhancement, resect
22 deployment to elucidate the genomic basis of interpatient differences in drug response and disease ri
23                     This study helps explain interpatient differences in efficacy and safety followin
24  provide insights into mechanisms underlying interpatient differences in intracellular accumulation o
25 rovide new insight into the genomic basis of interpatient differences in intracellular TGN accumulati
26             This diagnostic study delineated interpatient differences in RAS variants present in thyr
27                                              Interpatient differences in RAS, BRAF V600E, and TERT pr
28 harmacology of drugs, potentially leading to interpatient differences in response.
29 w is to discuss genetic factors that lead to interpatient differences in the pharmacokinetics and pha
30                                          The interpatient differences in these variants were discrimi
31                               However, large interpatient disparities in the pharmacokinetics of TmAb
32                    Quantitative detection of interpatient disparities of RAS variants (ie, NRAS, HRAS
33                              Both intra- and interpatient diversification at the plasmid and transpos
34                                          The interpatient diversity of the clones from Botswana was h
35 ombinants were both remarkable for their low interpatient diversity, less than 1% for the full genome
36 llenged by high intratumor heterogeneity and interpatient diversity.
37 tients were treated with tipifarnib using an interpatient dose-escalation scheme.
38 fficacious, they are difficult to use due to interpatient dose-response variability and the risks of
39 get carboplatin AUC was 10 mg/ml x min, with interpatient escalation in increments of 25%.
40  showed that steady-state occurred by day 7, interpatient exposure was more variable than intrapatien
41 ear mixed model that is ideal to control for interpatient gene expression profile variation, such as
42                     Deep sequencing revealed interpatient gp350 sequence variation but conservation o
43                                   Intra- and interpatient group statistics were descriptive.
44 onclusion, our findings identify substantial interpatient heterogeneity and distinct patterns of dysr
45 me patients, we show that compaRe can reveal interpatient heterogeneity and recognizable phenotypic p
46                                 Cellular and interpatient heterogeneity and the involvement of differ
47 f CTCs has exposed dramatic intrapatient and interpatient heterogeneity and their evolution over time
48         We hypothesise that GARD will reveal interpatient heterogeneity associated with opportunities
49                                              Interpatient heterogeneity exists in tissue cell populat
50 ded to clarify the relevance of the observed interpatient heterogeneity in clonal constitution.
51 l thrombocythemia (ET) manifests substantial interpatient heterogeneity in rates of thrombosis, hemor
52                                              Interpatient heterogeneity in the absolute degree of tur
53 RET+ cell lines effectively recapitulate the interpatient heterogeneity observed in response to RET i
54 he proteome atlas highlights intertissue and interpatient heterogeneity of injected proteins with pot
55                      Stem cell assays reveal interpatient heterogeneity of JMML LSCs, which are prese
56 e-invasive and metastatic urothelial cancer (interpatient heterogeneity) probably contribute to varia
57 h they were derived, illustrating intra- and interpatient heterogeneity, and can be genetically modif
58  is cancer cell-intrinsic and independent of interpatient heterogeneity.
59 while exhibiting intrapatient similarity and interpatient heterogeneity.
60 r establishing a high degree of quantitative interpatient integral map pattern correspondence irrespe
61 associated with anxiety, it explained 24% of interpatient MCS variability.
62  a single strain the complete process of (i) interpatient microevolution, (ii) intrapatient respirato
63  dimensions are complementary, capture major interpatient molecular differences and are delimited by
64 lassification only accounts for up to 10% of interpatient molecular differences.
65                                      Whether interpatient pharmaco-kinetic differences in dexamethaso
66 ty was demonstrated but with high intra- and interpatient pharmacokinetic and pharmacodynamic variabi
67 oposide is feasible and dramatically reduces interpatient pharmacokinetic variability.
68                                OPTICAP is an interpatient protocol sequence randomized noninferiority
69   Emerging approaches such as multimodal and interpatient registration are discussed, alongside metri
70 hed (intrapatient) samples and in unmatched (interpatient) samples from rectal cancer patients after
71  microevolution both at the intrapatient and interpatient scenarios.
72 ional, misaligned movements and serves as an interpatient self-calibration index.
73                 DNA sequence analyses showed interpatient specific mutations (2 to 3 bp).
74 ncontrast cardiac MRI, facilitating detailed interpatient strain analysis and allowing precise tracki
75 kable variability and redundancy, intra- and interpatient, suggesting ongoing parallel adaptive diver
76 antigen-specific clones with both intra- and interpatient TCR similarities.
77                                              Interpatient transcriptional heterogeneity was evident,
78 licated by treatment-emergent resistance and interpatient transmission of cefiderocol-resistant A. ba
79 B typing demonstrated in vivo, in vitro, and interpatient transmission stability yet revealed that th
80 enhanced capacity for human infection and/or interpatient transmission.
81                                              Interpatient variabilities in genomic variants may refle
82                            Discrimination of interpatient variabilities in RAS in combination with BR
83           Analysis of variance revealed that interpatient variability (1.2-2.0x10(-3) mm2/sec) was si
84 ve the LLQ in most patients (93%), with wide interpatient variability (3.50-2,990 pg/mL).
85 seem to contribute significantly to the high interpatient variability (49%) in the clearance of this
86  the exposure profile of the drug showed low interpatient variability and a small peak:trough ratio o
87 piridol pharmacology, we observed unexpected interpatient variability and postinfusion peaks in appro
88 n of transporter substrates while decreasing interpatient variability and reversing tumor drug resist
89 ients using ultrafiltration to determine the interpatient variability and, therefore, whether individ
90            Reasons for its wide pretreatment interpatient variability are not well understood.
91  characteristic of Tac is the high intra and interpatient variability associated with its use.
92  studies of vesnarinone revealed significant interpatient variability at any given dose level.
93 d for adjacent biopsies, was larger than the interpatient variability for individuals with a history
94 e some pharmacological limitations including interpatient variability in antithrombotic effects in pa
95                             MCL showed large interpatient variability in basal levels, and elevated l
96 e was normalized to body-surface area (BSA), interpatient variability in Cl(S/F) was reduced from 20%
97                                              Interpatient variability in Cmax,ss and AUCtau,ss was es
98                                              Interpatient variability in community structure exceeded
99                                              Interpatient variability in HCY exposure at a given CY d
100 I) pharmacokinetic (PK) properties show high interpatient variability in hemophilia A patients.
101 e results suggest a strong genetic basis for interpatient variability in hyperbilirubinemia and amino
102     This study was conducted to test whether interpatient variability in neurocognitive outcomes can
103                             From evidence of interpatient variability in normal tissue sensitivity to
104                           The high degree of interpatient variability in parameter estimates suggests
105 ly fails even under perfect adherence due to interpatient variability in pharmacological parameters.
106 etion are important determinants of the wide interpatient variability in plasma free dobutamine and d
107                             There was marked interpatient variability in plasma PZA concentrations at
108                            There was a large interpatient variability in RBC MTXPG levels (median 35
109 a suggest that host factors may also predict interpatient variability in response to aromatase inhibi
110    Recognition that there is a great deal of interpatient variability in response to these antiplatel
111 been associated with a significant degree of interpatient variability in response to treatment.
112 ggesting activities potentially relevant for interpatient variability in response to treatment.
113                             There was marked interpatient variability in the degree of platelet aggre
114                            There was a large interpatient variability in the dosimetry parameters.
115                       This may contribute to interpatient variability in the risk of CsA-induced neph
116 nt with a narrow therapeutic index and large interpatient variability in the therapeutic dose.
117 nset of action, fewer interactions, and less interpatient variability in their antithrombotic effects
118 e limited by their calibration range and the interpatient variability in their dose-response curves.
119                                 To elucidate interpatient variability in thioguanine nucleotide (TGN)
120                              ML7710 captured interpatient variability in TPMAL uptake and prompted FG
121  administered monthly HBIg, intrapatient and interpatient variability in trough antibody to HBsAg (an
122 and TERT promoter variants can elucidate the interpatient variability in tumors and facilitate a defi
123  across 418 liver biopsies and evaluated the interpatient variability of 18 drug targets.
124 imicrobial pharmacokinetics, and significant interpatient variability of antimicrobial concentrations
125                  However, we show a striking interpatient variability of its deposition in this patie
126                                        Large interpatient variability of measurable immunosuppressant
127 r after transplantation explained 19% of the interpatient variability of PCS 3 months after transplan
128                                     However, interpatient variability of percentage of HbF (%HbF) res
129                   There was a high degree of interpatient variability of plasma alitretinoin concentr
130   Food and film coating apparently increased interpatient variability of the maximum observed plasma
131                         However, significant interpatient variability of the response to clopidogrel
132 nterleukin-4 receptor subunit alpha, with an interpatient variability producing heterogeneity in resp
133 e for body size or disease does not diminish interpatient variability sufficiently to obviate plasma
134 ay translate to less intestinal toxicity and interpatient variability than the SN-38 prodrugs thus fa
135                   There is also considerable interpatient variability that was not explained by the c
136 Vmax>pt overlapped between the 2 groups, and interpatient variability was greater for HER2+ than HER2
137                                       Marked interpatient variability was noted for which KIs were ef
138                                         Wide interpatient variability was noted in vorinostat disposi
139                                      A large interpatient variability was observed on clearance (coef
140 dren with first-dose PK studies, substantial interpatient variability was observed, plus a novel oral
141 A linear mixed-effects model controlling for interpatient variability was then used to assess differe
142           Lack of data reproducibility, high interpatient variability, and the absence of disease-dep
143 fferences in disease profiles are not due to interpatient variability, but rather, to unique disease
144 an those without, but because of significant interpatient variability, defining an effective general
145                          Despite significant interpatient variability, exposure to vandetanib increas
146 CD8(+) T lymphocyte response, despite marked interpatient variability, increased overall with STI.
147                        There was significant interpatient variability, which correlated with plasma c
148 mized for each patient indicated substantial interpatient variability.
149 and maximum plasma concentration with marked interpatient variability.
150  drug-drug interactions that may account for interpatient variability.
151  both radiopharmaceuticals with considerable interpatient variability.
152 3-14 d postimlifidase dose, with substantial interpatient variability.
153  durations of modern CT scanners, as well as interpatient variability.
154 ting in an inconclusive diagnosis because of interpatient variability.
155 anti-HLA antibodies, although with important interpatient variability.
156 heterogeneity and readily evident intra- and interpatient variability.
157           Organ dosimetry showed substantial interpatient variability.
158 years; IQR, -8.9% to 1.2%), indicating large interpatient variability.
159 min ranged from 1.2 to 59.0, with intra- and interpatient variability.
160 on in ARVD/C is progressive with substantial interpatient variability.
161 on, dose-proportional exposure, and moderate interpatient variability.
162  with increasing patient age, there is great interpatient variability.
163 um 57 mins), although there was considerable interpatient variation (20 to 175 mins with cisatracuriu
164                                              Interpatient variation across the entire CMV genome was
165 veiled that glycerophospholipids showed high interpatient variation and were strongly affected by pre
166 ths posttransplant but there was significant interpatient variation as to when peak levels occurred.
167      We demonstrate previously unappreciated interpatient variation in HIV protease processing effici
168  material, provides a possible mechanism for interpatient variation in host-stromal response to invad
169 AO as comodifiers explained up to 47% of the interpatient variation in ICARS progression.
170 based on body surface area results in marked interpatient variation in pharmacokinetics, toxic effect
171 or number, differences in receptor activity, interpatient variation in pharmacological dose-response
172                             There was marked interpatient variation in plasma concentrations of PZA.
173                                         Such interpatient variation in T-cell kinetics may be reflect
174                                   Intra- and interpatient variation of PZ ADCs was determined by mean
175                                The effect of interpatient variation on the assessment of prostate can
176 these paired comparisons, we can exclude the interpatient variation that is present in plasma samples
177                     PZ ADCs show significant interpatient variation, which has a substantial effect o
178 s greater than in HT29 cells but with marked interpatient variations and proficiently glucuronidated
179                                              Interpatient variations are relevant for prognosis and t
180 as used to determine the significance of the interpatient variations in ADCs.
181 ases promoter activity and may contribute to interpatient variations in hRFC expression and effects o
182                                              Interpatient variations in serum clearance rates were ob
183                                              Interpatient variations in serum clearance rates were ob
184 d stromal cells showed both intrapatient and interpatient variations, with no uniform distribution ov

 
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