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1                                       Finally, our findings may explain a past clinical observation of a GABAA-R PAM redu
2 y of current drug susceptibility testing methodologies, and may explain an important proportion of false-negative resista
3 ven when patients are hemodialyzed with a catheter instead, may explain at least two thirds of the mortality benefit obse
4 sulin-mediated GU in multiple insulin-sensitive tissues and may explain, at least in part, the increased risk of type 2 d
5    Failure to account for fluctuation-dependent coexistence may explain deviations from the expected negative diversity-e
6 gomeric states of the Marburg and Ebola virus VP35 proteins may explain differences between them in polymerase function a
7 tained DM deactivation, characterizes successful ageing and may explain differential ageing trajectories across cognitive
8 vo reported antitumor effects, and possible mechanisms that may explain discrepancies between bioavailability and bioeffi
9                Accordingly, variation in initial conditions may explain divergent population responses to infection that
10          The models fit global patterns of isotope data and may explain features such as the DUPAL anomaly and long-stand
11 e microenvironments co-exist within a single individual and may explain in part the heterogeneous fates of metastatic les
12                                              These findings may explain, in part, observations from in vivo experiments t
13 ch has begun to probe the key psychological attributes that may explain it.
14 antly incorporated but also readily excised from RNA, which may explain its limited efficacy in vivo.
15 fferentiated induction of detoxification enzymes by 2,5-DCB may explain its lower phytotoxicity compared to 4'-OH-2,5-DCB
16 s, EMC is a transmembrane domain insertase, a function that may explain its widely pleiotropic membrane-associated phenot
17                               Such an atrial cardiomyopathy may explain many cases of embolic stroke of undetermined sour
18                          Shifts in the commensal microbiota may explain observed variations in giardiasis between hosts w
19                                                        This may explain our findings of increased lymph node invasion and
20          We discuss additional hypothetical mechanisms that may explain our paradoxical findings.
21   One hypothesis is that increasing childhood obesity rates may explain part of this increase, but, as T1D is rare, inter
22                            In contrast, redundant solutions may explain positive feedback, perhaps indicative of the impo
23 nd fibrosis with concomitant apoptosis of LX-2 cells, which may explain some potential mechanisms of liver damage observe
24                                             These responses may explain the association of Parkinson's disease with speci
25 ression variation between the two parental genotypes, which may explain the contrasting growth habits.
26                                 Here we report results that may explain the decreased efficiency of HDAC inhibition in EO
27 nhibition of CK5+ cell expansion through RAR/PR cross talk, may explain the efficacy of retinoids in prevention of some b
28 s deprived hazard-resistance entitlements of herders, which may explain the elevated effects of political pressures on li
29                                             This difference may explain the enhanced induction of Abs when targeting Ag t
30 rapies is comparable across all p53-deficient genotypes and may explain the high incidence of p53 loss of heterozygosity
31        The elevated levels of this proinflammatory cytokine may explain the increased incidence and progression of inflam
32 ere measured in the derivatized mixtures formed by ELW1 and may explain the increased toxicity of the ELW1 metabolites mi
33 mong DHA, APOE genotype, and stage of AD pathologic changes may explain the mixed results of DHA supplementation reported
34  a monomer that does not display quaternary epitopes, which may explain the modest success with soluble recombinant E (sR
35 egulation of methyltransferase DNMT3b and deacetylase SIRT1 may explain the observed p66(Shc)-related epigenetic changes.
36             Common underlying pathophysiological mechanisms may explain the risk of developing epilepsy following inciden
37 ross, and identify a putative HECT E3 ubiquitin ligase that may explain the variance.
38  in gastric fluid due to their structural differences which may explain their different toxicological profiles.
39 cretion of tumor-promoting factors by HNSCC-associated CAFs may explain their role in malignant development.
40                                       Behavioral mechanisms may explain these associations, such as the withdrawal of old
41                                            This versatility may explain why a variety of organisms have extensively explo
42                                    Taken together, our data may explain why colonization of superantigen-producing S. aur
43 he brain should be considered with regards to human use and may explain why fatigue, headaches and nervousness have been
44 hese data uncover a direct role for RANK in lung cancer and may explain why female sex hormones accelerate lung cancer de
45 olism of glutamine and related analogs by GDH in the L cell may explain why GLP-1 secretion, but not that of insulin, is
46  mechanism of killing for cationic, amphipathic AMPs, which may explain why most AMPs require micromolar concentrations f
47                                                Our findings may explain why osteogenesis imperfecta-causing mutations in
48                                           These differences may explain why pediatric cancer patients have a higher risk
49                                                        This may explain why TBI patients are more vulnerable to cognitive
50 abilities and suggest a potential underlying mechanism that may explain why variability quenching occurs.

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