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2 progression toward autoimmune insulin deficiency in adults is probably due to a lower genetic load overall combined with
3 vative, XAC-X-BY630, revealed that the decrease in affinity is probably due to a significant increase in dissociation rat
4 re, the emergence of bone marrow failure in Fanconi anaemia is probably due to aldehyde-mediated genotoxicity restricted
5 This effect is sex- and oestrous cycle-dependent and is probably due to an oestrous cycle-dependent change in the
6 th predicted in vitro tropism of SIVrcm for macrophages and is probably due to expansion of coreceptor usage.
7 g a variety of blockers we determined that the augmentation is probably due to insertion of GABA(A)Rs into the synapse by
9 tidis pfs and luxS mutants is not due to quorum sensing but is probably due to metabolic imbalance and, in the case of pf
10 The smaller amount of the FMO protein in the mutant cell is probably due to the degradation of the apo-FMO protein at
11 fold selectivity of PAP-1 for Kv1.3 over other Kv1 channels is probably due to its preferential affinity to the C-type in
12 epancy between observed and expected nitrite concentrations is probably due to a combination of factors, including an inc
18 d H4K12 acetylation that occurs following acrolein exposure is probably due to the formation of acrolein-histone lysine a
19 yed temporal response between RLC phosphorylation and force is probably due to mechanical effects associated with elastic
20 di-GMP to form aggregates (as compared to that of c-di-GMP) is probably due to a higher activation barrier to convert fro
21 erence in Lisch nodule burden between light and dark irides is probably due to the photoprotective effects of pigmentatio
22 retains its native globular structure, so its activity loss is probably due to loss of specific toxin-receptor residue pa
23 This discrepancy with the earlier studies using microsomes is probably due to the known accessibility of microsomal carb
25 The increased severity of the Lama1 null mutant phenotype is probably due to the complete loss of the inner limiting me
30 association between high transcription and genome stability is probably due to a variety of factors including an enhanced
31 reduced in the nuclei of transfected cells, an effect that is probably due to a general defect in 3' RNA processing.
32 s markedly enhanced upon acetylation of K56, an effect that is probably due to increased conformational entropy of the al
33 re is large unexplained variability in cytokine levels that is probably due to genetic-environmental associations.
44 ha-Smooth Muscle Actin) upon treatment with TGF-beta1; this is probably due to intrinsic variability of cytokine concentr
45 ther than restricted developmental potential, however, this is probably due to a matter of timing.
46 antly reduced the N2 O production from these pathways; this is probably due to the observed reduction in the expression o
48 gulator, and the recalcitrancy to transformation in At vip2 is probably due to the combination of muted gene expression r
49 ron and manganese remain mainly between +II and +III, which is probably due to short residence time of these particles in
50 tead of isolated pathways, may overcome this problem, which is probably due to the extreme heterogeneity of human tumors.
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