1 We next address the pollution-based cardiotoxic mechanisms fi
2 We next adopted a 2-bottle choice procedure, whereby the rewa
3 To evaluate whether centrosome clustering was occurring,
we next analysed the number of centrioles revealing centriole
4 We next analyzed selected Arabidopsis mutants, and discovered
5 We next asked how aging and functional self-assembly influenc
6 Exploiting the coprophagic behavior of mice,
we next co-housed ob/ob and lean mice to investigate if the g
7 We next compared functional connectivity profiles of the SN a
8 al, and clinical measures of internal and external validity.
We next compared the AP molecular endotypes with previous des
9 Using partial information decomposition,
we next compute the intercellular gene-gene information flow
10 We next conduct a systematic review of the literature to asse
11 We next conducted a high-throughput virtual screen against th
12 We next convened a group of experts and stakeholders (n = 16)
13 We next cross-link the yeast proteasome, identifying 3,893 un
14 We next demonstrate that co-culturing human NPCs with rodent
15 We next demonstrate that the dominant super-enhancer modulate
16 We next determined downstream targets of YAP/TAZ in the poste
17 We next determined the exact location of the saccade-related
18 We next discuss current treatment paradigms for pancreatic ca
19 We next discuss how these studies can advance human health in
20 We next examined patient skin, colon, and blood during acute
21 We next examined the impact of inhibiting DRN-projecting LHb
22 We next examined the role of Hopx in AML by using the MN1 ove
23 We next exploited the differences and homologies in the pepti
24 We next expressed highly specialized nanobodies that target c
25 We next found that astrocytes are neuroprotective to seeded a
26 We next found that the AKT Ser/Thr kinase (AKT) inhibitor MK2
27 We next fused anti-GFP nanobodies to the receptors of Dpp, a
28 We next generated all iPSC-LBs by incubating individual cell
29 downstream target of dopamine D1-receptor (D1R) signaling,
we next generated mice with specific deletion of cacna1c from
30 We next identify a novel autocrine signaling axis in OCCC cel
31 We next induced severe disruption of circadian rhythms by exp
32 We next investigated how EPA improved murine hyperinsulinemia
33 ymptoms, and because they seem to precede traumatic events,
we next investigated the relationship between NTRK2 methylati
34 We next investigated their relatedness to cDC1 and cDC2 and d
35 We next isolated a subset of sensory neurons by sorting DRG n
36 We next leveraged a mass spectrometry metabolite profiling pl
37 We next optimized one of these NPs so that its stability is r
38 We next performed global transcriptome analysis of different
39 We next probed effects on human cardiomyocyte contractility.
40 We next report an MS1 automatized suspect screening workflow
41 s to ICAM1, an essential adhesin and virulence determinant,
we next showed that T4P-directed antibody blockade significan
42 We next showed that treatment with antibodies targeting TIGIT
43 We next tested a separate cohort of cases from University of
44 We next use novel multiple feature selection tools in Fmr1-KO
45 We next used 5 ms optical activation of Channelrhodopsin 2-ex
46 We next used immunofluorescence microscopy imaging, flow cyto
47 We next used MSU-42011 to treat established tumors in a clini
48 We next used single and double mutants to test whether mutati
49 gait, and as ChI loss has been associated with falls in PD,
we next used this task, as well as a previously established t
50 We next validated the specificity of this model to study empa