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1 However, to date, pharmacological agents have failed to achieve significant target engagement in vivo, poss
5 treatment failure (the proportion of women in which surgery failed to adequately resolve midline pain) and the frequency
6 acking Flvcr2 had altered expression of angiogenic factors, failed to adopt tip cell properties, and displayed reduced sp
7 enocarcinoma (HR, 0.18; 95% CI, 0.02-1.61), although the HR failed to attain statistical significance.
8 unately, proposed countermeasures against such attacks have failed to be effective, as they do not consider the utility o
10 her different degrees of severity in morbidity or mortality failed to be statistically significant because of survey desi
11 al ADPKD therapies with promising outcomes in animal models failed to be translated to human disease, our platform also i
12 directed medical therapies, imaging of myocardial viability failed to deliver effective guidance of coronary bypass surge
14 mC-dependent depletion of local fumarate, the DeltahemB SCV failed to elicit trained immunity and protection from a secon
15 t depletion of host T(conv) and host T(regs), donor T(regs) failed to engraft even with interleukin-2 (IL-2) support.
16 , in both groups, eszopiclone increased spindle density but failed to enhance sleep-dependent procedural memory consolida
20 -proficient extension produced regular CLPs in bacteria but failed to form stable nucleocapsids in hepatoma cells.
21 the disruption of a C(32-)A(38) cross-loop interaction but failed to fully explain the means by which s(2)C(32) restrict
22 ashout of these chronically exposed cells for up to 1 month failed to fully reverse the transcriptional and phenotypic ef
23 However, SD-Foxo1 actively repressed CD127 expression and failed to generate memory precursors and long-lived memory T
25 In alpha2delta-1 gene KO mice, treatment with FK506 failed to increase the frequency of NMDAR-mediated mEPSCs and
26 d that in insulin-resistant animals, portal vagal afferents failed to inhibit their spiking activity during glucose infus
27 MLAV VP24 differed from MARV VP24 in that it failed to interact with Keap1 or activate an antioxidant resp
28 high DFI (62.7 +/- 7.2% for IVF and 73.3 +/- 8.1% for ICSI) failed to litter after embryo transfer compared to embryos fr
30 xogenously provided competence stimulating peptide 1 (CSP1) failed to modulate the onset kinetics of competence developme
31 ite their intact cGAS sensing pathway, human CD4(+) T cells failed to mount a reverse transcriptase (RT) inhibitor-sensit
32 In the most extreme case, almost a third of observers failed to notice when less than 5% of the visual display was
33 entions targeting catabolic pathways have, however, largely failed to preserve muscle mass in cachexia, suggesting that o
34 thway that reduces synthesis of membrane proteins that have failed to properly assemble in the endoplasmic reticulum (ER)
35 strategies that have worked in rodent models of stroke have failed to provide protection in clinical trials.
36 r in PLDRH group than in the ODRH group (8% vs. 3%), but it failed to reach statistical significance (P = 0.167).
37 t gI could self-interact and that the rod-shaped structures failed to recognize glycoprotein E, the well-known binding pa
39 typical CYP monomer structure, isavuconazole-bound AcCYP51 failed to refold 74 N-terminal residues.
41 Exploratory analyses of the microbiome failed to reveal possible responder compared with nonresponde
43 However, Smoothened (SMO) inhibitors have failed to show clinical benefit in patients with cancers disp
44 tional T lymphocytes or recombination-activating gene (Rag) failed to show rescue of mutant colonization.
46 cytotoxicity and dendritic cell-induced proliferation, they failed to sufficiently regulate T cells stimulated by anti-CD
50 rA was highly expressed during pneumonia-derived sepsis but failed to turn off the competent state in mice.