1 We next used 5 ms optical activation of Channelrhodopsin 2-ex
2 naptic inputs to several classes of post-synaptic partners,
we next used a fluorescent reporter for synaptic contacts to
3 We next used a hamster model of amebic liver abscess to deter
4 We next used a microfluidics approach to profile the receptor
5 To assess the role of ELR(+) CXC chemokines in RCC,
we next used a model of syngeneic RCC (i.e., RENCA) in BALB/c
6 We next used a modified CR model (MCR) to examine disease inc
7 hese effects were mediated by a direct effect on Th2 cells,
we next used a murine adoptive transfer model of Th1- and Th2
8 We next used a natural translational elongation stall to show
9 We next used alpha-conotoxinMII and mecamylamine to understan
10 We next used an oligonucleotide-mediated mismatch ligation as
11 We next used an orthotopic rat model to evaluate the role of
12 We next used anterograde labeling to determine whether the CS
13 We next used antisense oligonucleotides directed against CREB
14 We next used atomic force microscopy to independently assess
15 We next used blocking antibodies to CD36 and SR-BI to demonst
16 We next used chromogenic in situ hybridization (CISH) to dire
17 We next used deuterium-labeled lutein and zeaxanthin as dieta
18 We next used fMRI to define the functional impact of elevated
19 We next used immunofluorescence microscopy imaging, flow cyto
20 leukin-1alpha are major mediators of cutaneous inflammation
we next used immunohistochemistry to determine whether the pe
21 We next used in vivo two-photon imaging from individual neuro
22 We next used laser-capture microdissection and quantitative p
23 We next used mice with lox-P modified alleles of either the g
24 We next used microarrays to follow replication throughout the
25 We next used MSU-42011 to treat established tumors in a clini
26 To investigate this further,
we next used NMDAR-subunit-specific antagonists.
27 To minimize washout of cytosolic constituents,
we next used nystatin perforated patch, but did not find any
28 We next used nystatin to selectively permeabilize the basolat
29 We next used optogenetic silencing to confirm the direct invo
30 TrkB in D2+ neurons increases their neuronal excitability,
we next used optogenetic tools to control selectively the fir
31 ervate overlapping populations of ventral pallidal neurons,
we next used optogenetics to examine whether changes in synap
32 We next used partner preference testing to determine whether
33 We next used PIMiM to jointly analyze a number of different t
34 We next used pre-pubertal hormone treatment to model early pu
35 We next used recombinant bacmids expressing WT or DN VPS4 pro
36 We next used RNA interference to generate stable knockdown of
37 In male and female rats,
we next used RNA sequencing to characterize LBN-induced trans
38 We next used single and double mutants to test whether mutati
39 We next used SLC gene-modified DCs as a treatment of establis
40 We next used stimulation and recording techniques in forelimb
41 We next used the human retinal pigment epithelial cell line R
42 To test the recombinogenic systems,
we next used the overlapping BACs to construct a full-length
43 We next used these sites as a map to evaluate the structural
44 We next used these three cell lines and their parental cells
45 We next used this model to address the role of transplanted c
46 We next used this predictor to discover these subgroups withi
47 gait, and as ChI loss has been associated with falls in PD,
we next used this task, as well as a previously established t
48 We next used transcranial direct current stimulation to discr
49 We next used viral adaptation and a set of Vif mutants to ide
50 We next used Wet-SEEC to image slime secretion, a poorly defi