1 amine signaling and CRY levels are typically high at night,
this may explain why a chronic increase in levels of these mo
2 This may explain why,
after withdrawal of chronic glucocortic
3 this may explain why alpha-tryptase is not stored in secretor
4 This may explain why arrhythmia-prone patients with structura
5 This may explain why arrhythmogenic right-ventricular dysplas
6 This may explain why,
at least in one E. coli strain, the abu
7 This may explain why bats look for prey on flat surfaces like
8 ure of human HMGR is different from that of bacterial HMGR;
this may explain why binding of HMGR inhibitors to bacterial
9 This may explain why BLIP binds to SHV-1 beta-lactamase with
10 This may explain why Bmr has evolved the way it did, that is,
11 This may explain why both the immediate effects and after-eff
12 tic nature of smoking could be a cause of elevated ADP, and
this may explain why cardiovascular patients who smoke benefi
13 This may explain why centrosomes are such dominant sites of M
14 This may explain why certain high-degree proteins are not sig
15 This may explain why ClnR-4 shows a slight growth defect in v
16 This may explain why daunorubicin appeared to inhibit the bin
17 This may explain why F. nucleatum is often found in mixed inf
18 This may explain why GEP, by itself, can replace the IGF-IR f
19 atocytes hampers efficient innate control of HBV infection;
this may explain why HBV has adapted to specifically replicat
20 This may explain why Hcm1 mutants show 10-fold elevated rates
21 This may explain why Levy-like behaviour seems to be widespre
22 This may explain why most introduced species either fail to e
23 This may explain why nucleotide motif preferences are very si
24 This may explain why Pax6(-/-) optic vesicles are inefficient
25 This may explain why phenylglyoxal labeling of Arg155 inactiv
26 This may explain why PKA activity is required for Ca2+-stimul
27 This may explain why plants retain hundreds of expressed Y-li
28 This may explain why primate sociality seems to be so differe
29 influenza HA and nonstructural protein 1 proteins; further,
this may explain why rapid antigenic drift and a broad host r
30 This may explain why seemingly several peptides with very dif
31 This may explain why self-imposed tickle [3 and 4] or constan
32 rate oscillations much more easily than ER networks do, and
this may explain why SF networks are more evolvable than ER n
33 This may explain why some HF patients have better responses n
34 to prolate ellipsoids (rod-like) reduces sinking speed, and
this may explain why some nonmotile genera are rod-like.
35 This may explain why strabismic patients who are not diplopic
36 This may explain why such a diverse range of foragers have mo
37 This may explain why TBI patients are more vulnerable to cogn
38 This may explain why Th17 cells develop within an ongoing Th2
39 This may explain why the 10(4)-fold attenuated cleavage effic
40 This may explain why the [formula in text] motif is rarely ob
41 This may explain why the cdkn1b gene is rarely inactivated in
42 This may explain why the deterioration of various rhythmic pr
43 ynamically influence the anti-FMDV immune response and that
this may explain why the early immune response to FMDV has ev
44 This may explain why the incidence of ALS-PDC among the Chamo
45 Because increased Akt activity promotes survival,
this may explain why the level of apoptosis was increased in
46 ort is the rate-limiting step in microsomal G6P metabolism,
this may explain why the treated G6pc(-/-) mice could sustain
47 This may explain why transport of divalent cationic drugs by