ライフサイエンスコーパス: we were unable to

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

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

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

4 Due to high heterogeneity of the quantitative data, we were unable to conduct a meta-analysis; instead, we presen

5 Finally, we were unable to confirm previously described effects of par

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

7 T2D was increased after 27 of 32 AIds but we were unable to control for factors such as obesity and smo

8 pported by previous studies poses an intriguing hypothesis, we were unable to converge toward their conclusions in a mult

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 this group of neonates undergoing complex cardiac surgery, we were unable to demonstrate a difference in the incidence o

13 Given the prespecified noninferiority margin of 24%, we were unable to demonstrate noninferiority of antibiotic tr

14 ern blotting and enzyme linked immunosorbent assay (ELISA), we were unable to detect a difference in the level or kinetic

15 Using a nearly identical treatment regimen, we were unable to detect any evidence of drug efficacy despit

16 wn to be protective against virus infections in Drosophila--we were unable to detect any relationship between the presenc

17 ent relationships with effect sizes in clinical trials, and we were unable to detect dose-response relationships.

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

19 We have also received some hard lessons when we were unable to detect replicable genes of large effect siz

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

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

22 ded studies that reported only the current prevalence or if we were unable to establish whether they described current or

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

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

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

26 n a large cohort of NHLBI-funded cardiovascular R01 grants, we were unable to find a monotonic association between better

27 aused by a combination of allosteric and steric mechanisms, we were unable to find clear evidence for the allosteric mech

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

29 CBCT has been shown to be a reliable tool for measurements, we were unable to find studies comparing the differences betw

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

31 One important limitation is that we were unable to fully account for time-varying factors.

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

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

34 However, we were unable to identify any statistical relationship betwe

35 d and 15 unvaccinated macaques were compared to each other, we were unable to identify any vaccine breakthrough signature

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

37 genes (ABCA1, APOB, APOE, LDLR, LIPA, and PCSK9); however, we were unable to identify obvious genetic etiologies in the

38 Therefore, we were unable to identify robust and replicable findings.

39 ough our murine T-ALL model relies on transduction of HSCs, we were unable to isolate Notch-activated HSCs to test for LS

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

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

42 loads without ART, including an elite suppressor from whom we were unable to recover virus by QVOA.

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

44 However, we were unable to replicate the association in GERA.

45 In the YFS cohort, we were unable to replicate the initial discovery signal, but

46 In this study, we were unable to replicate this association in either a whit

47 Within the limits of the final sample size, we were unable to show any benefit for the addition of budeso

48 two independently generated Sirt2-/- mouse strains, however we were unable to show that inhibiting or depleting SIRT2 pro

49 day [95% CI]: 0.67 [0.51-0.89]; p = 6.5 x 10(-3)), although we were unable to stratify by smoking history; genetically pr

50 dy weight loss at 24 hours predicted death by 48 hours, but we were unable to validate a specific amount of weight loss a