1 We then asked developers to run their software on our data; m
2 We then asked how these single-orientation responses combine
3 We then asked if 5-HT-positive axons appose cholinergic neuro
4 We then asked if any of these compounds were present endogeno
5 We then asked if genes possibly modulate the effect of impati
6 We then asked subjects to estimate virtual-room size with eit
7 We then asked to what extent a linear combination of chemical
8 We then asked whether 17B1.3 prevents signaling by binding to
9 Since glycosylation can enhance the function of a compound,
we then asked whether adding a glucose makes aesculin activat
10 We then asked whether BIG1 phosphorylation altered its GEP ac
11 We then asked whether complexes of these glycoproteins could
12 We then asked whether food consumption during a hypothesized
13 We then asked whether gene transfer of viral IL-10 could decr
14 We then asked whether miR-3189 was expressed in clinical samp
15 specific markers of chondrocyte differentiation in culture,
we then asked whether PKA phosphorylation could modulate the
16 We then asked whether prolonged PSAP/IntA experience would ne
17 We then asked whether such CTL escape mutations had an impact
18 We then asked whether the aberrant tangential migration of GA
19 We then asked whether the CGRP promoter in the viral vector c
20 We then asked whether the connected neurons are presynaptic o
21 We then asked whether the differences between real and appare
22 We then asked whether the replication and the mitotic phenoty
23 We then asked whether the responses in these regions reflecte
24 We then asked whether the SR protein binding sites in these e
25 Using these models,
we then asked whether this vascular defect could be rescued b
26 Using a series of recombinant X genotypes,
we then asked whether X overexpression in hybrids is controll