コーパス検索結果 ( right1)
通し番号をクリックするとPubMedの該当ページを表示します
1 We demonstrate that TE-derived CTCF binding divergence may explain a large fraction of variable loops.
2 Glycogen content reduction from healthy to tumor tissue may explain AMPK switching from tumor suppressor to activator
3 s portraying these trends, and describe the mechanisms that may explain an increased risk of premature HF in South Asians
4 and the affection of the rod pathway through the AII cells may explain and be partially responsible for the reduced cont
5 ies directly in the path of the cleavage furrow, this delay may explain, at least in part, the delay in cytokinesis itsel
6 on via cell death across disparate but linked brain regions may explain how stereotyped patterns of neurodegeneration ari
8 against age-related erosion of the epigenetic landscape and may explain interspecific variation in lifespan.
9 al and functional components of PA2G4 and consider how they may explain its crucial role in the malignant phenotype.
10 induce key components of its gene expression program, which may explain its lack of efficacy in clinical settings.
12 relative shear wave speed, suggesting that variable gearing may explain muscle weakness after stroke.
13 dependent, MHC class II disparity with naive T cells, which may explain organ- and strain-specific differences in spontan
14 ationale for genomic retention of certain miRNA operons and may explain preferential evolutionary emergence of miRNA oper
15 of clinical symptoms, genetic factors, and medication that may explain progressive brain changes in BD.
16 Further, PPP and joint hyperextensibility may explain some of the nonimmunologically-mediated joint pro
18 PTEN antigen with concurrent increase in Akt activity which may explain the aberrant cell survival, proliferation and inv
19 sustained sensitivity and nociception without joint damage may explain the clinical disconnect in which symptomatic join
20 Alterations in these biological pathways may explain the considerable comorbidity between depression a
21 etence of floral organs to respond to fertilization signals may explain the different abilities of floral organs to form
22 Increased storage and release of mechanical energy may explain the enhanced bactericidal action of these nanopil
23 Q accelerated early factor Xa and thrombin formation, which may explain the higher OS activity based on a kinetic bias be
24 y in conduction are already present during sinus rhythm and may explain the higher vulnerability to atrial fibrillation o
25 ereffects are not uniform throughout cortical layers, which may explain the incomplete cDCS clinical efficacy.
26 two different backbone conformations within the same fibril may explain the increased aggregation propensity of S20G, and
27 ng, traumatic brain injury or other pathological mechanisms may explain the increased risk for developing proteinopathies
29 nfected bone marrow-derived DCs and purified MLN DCs, which may explain the mechanism underlying the impairment of DCs in
30 mal movements vary with the surrounding environments, which may explain the observation that animals often switch their m
31 The need to regulate these structures may explain the parallel expansion of the number of Nek famil
32 y be higher than previously anticipated, and integrated DNA may explain the persistence of high HBsAg serum levels in pat
34 We outline the mechanism for this effect and argue that it may explain the propensity for atrial arrhythmias in HF.
35 ntral interface to Pol31-Pol32, and this strategic location may explain the regulation of the oxidation state on Pol delt
36 etabolic rates and much larger hatchlings in most nautilids may explain the selective extinction of ammonoids as a conseq
37 Kpi(+) K. pneumoniae and indicate that the presence of Kpi may explain the success of the ST-15 clone.
38 in mesenteric arteries but not in pulmonary arteries, which may explain TRPV4(EC) -IK/SK channel coupling in mesenteric a
39 esource-rational cognition that accounts for these benefits may explain unexpected and seemingly irrational thought patte
42 ns at distinct levels of the perceptual-inference hierarchy may explain why hallucinations and delusions tend to cluster
43 ess and aid in stress adaptation, and this stress tolerance may explain why many cancers aberrantly express MAGEs Here, w
44 s of the P-TEFb subunit cyclin T1 than primary cells, which may explain why many LRAs are functional in model systems but
45 nt for why an insulin granule is selected for secretion and may explain why newly synthesized insulin is preferentially s
46 y low estimated inhibition levels at median exposure levels may explain why no relationship between exposure to TTR-bindi
47 Here we propose that Gestalt theory may explain why rodent islet architecture has historically be
48 al an important species difference in OCN regulation, which may explain why serum concentrations of OCN are higher in mou
49 the existence of mutually exclusive competing interactions, may explain why some proteins are dynamic while others are ri