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1 sition to parasitism can be modeled in vitro by stimulating infective larvae with a low molecular wei

2 By stimulating neurons with a submaximal agonist concent

3 ic conditions, and they could not be rescued by stimulating platelets with a PAR4 receptor agonist or

4 FasL expression is induced by stimulating T cells with a combination of phorbol est

5 By stimulating the retina with a bar that appears, stays

6 ment of activity propagation can be produced by stimulating the thalamus with a short, high-frequency

7 By stimulating corneal angiogenesis with an alkali burn

8 ion that are even higher than those achieved by stimulating cells with analogous concentrations of C5

9 By stimulating cells with anisomycin or UV light, JNK1 b

10 (active or inactive) and 15 normal subjects by stimulating once with anti-CD3, anti-CD28, and IL-2.

11 ated rafts to the site of T cell:APC contact by stimulating T cells with APCs that express the CD48 l

12 By stimulating PdCMs selectively with blue light, we wer

13 se in atrial CNTF receptor mRNA was enhanced by stimulating muscarinic receptors with carbachol in ov

14 Hl-like cells, which were generated in vitro by stimulating syngeneic splenocytes with donor alloanti

15 ke populations, which are generated in vitro by stimulating syngeneic splenocytes with donor alloanti

16 ced NO production was significantly enhanced by stimulating the cells with IFN gamma.

17 otein (Abeta), usually demonstrated in vitro by stimulating microglia with micromolar concentrations

18 d S-nitroso-N-acetylpenicillamine (SNAP), or by stimulating cells with multiple cytokines and lipopol

19 vage of fractalkine can be markedly enhanced by stimulating cells with phorbol 12-myristate 13-acetat

20 intracellular free Ca2+ with thapsigargin or by stimulating PKC with PMA.

21 erization and thereby autoactivation of Pyk2 by stimulating its interaction with PSD-95.

22 T-cell lines established by stimulating lymphocytes with recombinant RAP-1 protei

23 RAGE signaling was examined by stimulating chondrocytes with S100A4 and monitoring f

24 RAGE signaling was evaluated by stimulating chondrocytes with S100B and HMGB-1 and an

25 This promotes Sec2p function by stimulating its interaction with Sec15p.

26 E stimulation, but MMP-9 release was induced by stimulating monocytes with supernatants from activate

27 s defect in differentiation can be corrected by stimulating cells with the PPARgamma agonist rosiglit

28 Receptor function was assessed by stimulating Th2 cells with the CRTh2-specific agonist

29 By stimulating DCs with two distinct activation signals,

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