ライフサイエンスコーパス: we were unable to

1 Therefore, we were unable to accurately estimate the timing of each inva

2 In conclusion, we were unable to acquire the GDM phenotype in any of our exp

3 Because no events occurred during the study or follow-up, we were unable to assess the duration of response or progress

4 drogenase, a flavoprotein encoded by the gene lpdG Although we were unable to co-crystallize LpdG with an endogenous phen

5 udy include that we did not review grey literature and that we were unable to conduct moderation analyses for several pre

6 Despite individual patient data analysis from five RCTs, we were unable to confidently rule in nor rule out an Xpert M

7 However, we were unable to confirm that 3-MPA inhibited PEPCK-M enzyme

8 es with pharmacological and genetic loss-of-function tools, we were unable to confirm that KRAS-driven tumor lines requir

9 merase II occupancy of TNF targets such as IL8 and TNFAIP2, we were unable to correlate specific binding sequences for GR

10 In contrast to complex plant meristems, we were unable to correlate the plant morphogen auxin with bu

11 HSR is impaired in mouse models of Huntington's disease but we were unable to corroborate the general repression of trans

12 Because we were unable to define the site of the block in the infecti

13 e of those for whom radiotherapy is frequently recommended, we were unable to demonstrate any beneficial therapeutic effe

14 However, we were unable to demonstrate improved potency relative to th

15 With our sample size, we were unable to detect an interaction between stress echoca

16 Surprisingly, we were unable to detect any specific change in the expressio

17 a1-antitrypsin (AAT) deficiency, unlike the case for FENIB, we were unable to detect defects in calcium signalling.

18 ae were briefly reported to use sulfate for respiration but we were unable to detect DSR in these isolates.

19 domain; yet, consistent with results from previous studies, we were unable to detect GMD modification.

20 Moreover, in one elite controller, we were unable to detect intact proviral sequences despite an

21 Identification of QPSSSR has never been reported, and we were unable to detect it by traditional methods.

22 eep sequencing analyses performed with both Cpf1 nucleases, we were unable to detect off-target cleavage for more than ha

23 Surprisingly, using Western blot analysis, we were unable to detect the known isoforms of Myo18A, Myo18A

24 ved at less than 3% relative to the spiked control brains), we were unable to detect the other individual ABX in brain ho

25 d transport as well as known ThDP-dependent enzymes(4), and we were unable to detect thiamin or its derivatives in Bb cel

26 2%) were alive and out of care, and 203 (9%) were alive but we were unable to determine care status.

27 In this observational analysis, we were unable to determine the cause of the decline in malar

28 The main limitations of our study were that we were unable to determine why CA125 tests were performed an

29 However, data are limited, and we were unable to estimate NDI after GBS sepsis.

30 One limitation of our analyses is that we were unable to examine the characteristics of cases that w

31 despite employing multiple behavioral analysis approaches, we were unable to extend these findings to normal mice observ

32 nd faecal incontinence bothersome enough to seek treatment, we were unable to find evidence against the null hypotheses t

33 ) mice showed no overt changes in epithelial structure, and we were unable to find evidence for a role for keratinocyte S

34 patients with serial assessments of renal function and CI, we were unable to find within-subject associations between ch

35 not been reported previously in L. major, but unexpectedly, we were unable to generate fkp40(-)/afkp80(-) double mutants,

36 siological relevance of this discovery remained unclear, as we were unable to identify a functional adenylate cyclase in

37 e skin microbiota in patients hospitalized with cellulitis, we were unable to identify a typical cellulitis microbiota.

38 various inflammatory, immune and cancer-related processes, we were unable to identify any additional disease association

39 prevalence of injury was seen on postoperative imaging, and we were unable to identify any clinical risk factors for brai

40 However, we were unable to identify evidence for an association betwee

41 sters over time, the unexpected degree of variability meant we were unable to judge the benefit or harms of the intervent

42 One limitation to note is that we were unable to model for changes in multimorbidity during

43 However, we were unable to observe any form of dADG phosphate, implyin

44 Hence, despite using a variety of techniques, we were unable to obtain experimental evidence that would sup

45 Therefore, as we were unable to perform our planned statistical analysis, t

46 Therefore, we were unable to recommend minimum surgeon volume.

47 ce that high-risk patients had more to gain from treatment, we were unable to replicate any genotype-treatment interactio

48 Therefore, we were unable to replicate the "qM" component and its corres

49 Despite extensive efforts, we were unable to reproduce the finding that glutamate, AP5,

50 Additionally, while we were unable to verify the presence of synaptic Zn(2+) in t