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