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1 ne or cromolyn), or a neurokinin antagonist (spantide).
2                    B6 mice were treated with spantide, and after infection, slit lamp examination; cl
3                        An NK(1)R antagonist, Spantide I (Span), conjugated to cholestanol (Span-Chol)
4 P (SP), were treated with the SP antagonist, Spantide I (with/without Mphi depletion), resulting in e
5                                              Spantide I and siRNA knockdown of SP abolished the promo
6               Subconjunctival inoculation of spantide I during the clinical phase of HSK resulted in
7  major receptor (NK1-R) using the antagonist spantide I in susceptible mice infected with Pseudomonas
8                                         With Spantide I present, MCN1 no longer elicited the gastric
9 P (SP) binding to neurokinin 1 receptor with spantide I prevents Pseudomonas aeruginosa-induced corne
10 , we used the tachykinin receptor antagonist Spantide I to eliminate the actions of CabTRP Ia.
11 n in vitro and blockade of SP signaling with spantide I, an antagonist of SP receptor Neurokinin-1, s
12               Subconjunctival inoculation of spantide I, SP receptor antagonist, was carried out duri
13 eu10]-substance P(7-11) and a SP antagonist, spantide I.
14 ropeptides in vitro, but was not affected by spantide I. mRNA for neurokinin-1-receptor-1 (NK-1R) was
15 ned delivery of two anti-inflammatory drugs, spantide II (SP) and ketoprofen (KP) on the skin permeat
16                                              Spantide II (SP) and ketoprofen (KP) were used as model
17           The SP receptor (SPR) antagonists, spantide II and RP-67,580, block both the initiation of
18                         Mice pretreated with spantide II and then orally inoculated developed advance
19  nonsubstance P receptor-mediated effects of spantide II on macrophages.
20                               Treatment with spantide II significantly reduced early Salmonella-induc
21 ent of mice with the substance P antagonist, spantide II, before oral inoculation with Salmonella.
22 ptibility to salmonellosis was not due to 1) spantide II-induced alterations in the uptake of this pa
23 ake of this pathogen from the gut, 2) global spantide II-mediated immune suppression, or 3) nonsubsta
24 sting a mechanism for the reduced ability of spantide II-treated mice to resist this pathogen.
25                            The SP antagonist Spantide provides a novel approach to reduce type 1 and
26                                              Spantide treatment of B6 mice significantly decreased th
27                                              Spantide treatment of Mphis reduced IL-1beta after LPS+S
28 otein) also were significantly reduced after spantide treatment.
29 as TGF-beta mRNA levels were unchanged after spantide treatment.