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1                                              AITC directly binds to multiple cysteine residues of the
2                                              AITC induced concentration-dependent dilation of pressur
3                                              AITC induced mitochondrion-mediated apoptosis, as shown
4                                              AITC is widely used experimentally as an inducer of acut
5                                              AITC turned out to be the best stimulus because the coug
6                                              AITC-induced dilation was attenuated by disruption of th
7                                              AITC-induced dilation was insensitive to nitric oxide sy
8                                              AITC-induced smooth muscle cell hyperpolarization was bl
9 caused by c-Jun N-terminal kinase (JNK), and AITC activates JNK.
10 ted based on their structural properties and AITC molecular characteristics.
11 lth promoting compounds such as sinigrin and AITC demonstrates that besides extending shelf life and
12 within 24h while the content of sinigrin and AITC increased post irradiation and thereafter remained
13 1 is a locus for cross-sensitization between AITC and acidosis in nociceptive neurons.
14              Inhibition of caspase-9 blocked AITC-induced apoptosis.
15  in G(1) phase by hydroxyurea abrogated both AITC-induced mitotic arrest and Bcl-2 phosphorylation.
16 the mechanism underlying TRPV1 activation by AITC remains unknown.
17                            Mitotic arrest by AITC was associated with increased ubiquitination and de
18 reover, we found that apoptosis induction by AITC depended entirely on mitotic arrest and was mediate
19 o partially supported activation of TRPA1 by AITC.
20  responses to the algesic markers capsaicin, AITC and alpha, beta-methylene ATP.
21  HC subjects and the increased threshold for AITC after capsaicin treatment in patients with IR demon
22                      The lower threshold for AITC based on NMPs in patients with IR compared with HC
23                                 Furthermore, AITC acts in a membrane-delimited manner and induces a s
24  as either type I (menthol-like) or type II (AITC-like), and provide a kinetic model that faithfully
25 e strong correlation between the increase in AITC threshold in patients with IR and symptom reduction
26 dly rectifying K(+) channels, also inhibited AITC-induced dilation.
27  allicin (garlic), and allyl isothiocyanate (AITC) (mustard oil).
28 a solution model using allyl isothiocyanate (AITC) and also determines the bioaccessibility and bioav
29 s similar to equimolar allyl isothiocyanate (AITC) in the nominal absence of calcium, suggesting a di
30 unted for the enhanced allyl isothiocyanate (AITC) in the volatile oils of the irradiated vegetable.
31 ed release of volatile allyl isothiocyanate (AITC) molecules.
32                        Allyl isothiocyanate (AITC) occurs in many commonly consumed cruciferous veget
33 d (13)C NMR spectra of allyl isothiocyanate (AITC) were measured, and the exchange dynamics were stud
34 luding cinnamaldehyde, allyl isothiocyanate (AITC), and 4-hydroxynonenal, increased [Ca(2+)](i) in my
35 gent chemicals such as allyl isothiocyanate (AITC), cinnamaldehyde, and allicin, produce nociceptive
36          The effect of allyl isothiocyanate (AITC), in combination with low temperature (10 degrees C
37                        Allyl isothiocyanate (AITC; aka, mustard oil) is a powerful irritant produced
38 the chemical irritants allyl isothiocyanate (AITC; also known as mustard oil) or capsaicin.
39  component of mustard, allyl-isothiocyanate (AITC), activates the extreme cold receptor transient rec
40 cin (TRPV1 agonist) or allyl-isothiocyanate (AITC, TRPA1 agonist) elicited responses in only 16% and
41 ing or small intestinal transit, but luminal AITC inhibited colonic transit via TRPA1.
42 ith vehicle, 1 mg norepinephrine/kg, or 5 mg AITC/kg.
43 ersal eating monitor in a test meal.In mice, AITC administration induced a 32% increase in energy exp
44       An optimum concentration of 0.05muL/mL AITC was found to be effective in maintaining the microb
45 udy was to evaluate the potential of mustard AITC to induce thermogenesis (primary outcome) and alter
46 essibility for both mycotoxins and mycotoxin-AITC conjugates, with duodenal fractions representing 63
47                            Administration of AITC by gavage did not alter gastric emptying or small i
48 structural flexibility of every conformer of AITC, the analysis provides a general explanation for th
49 or the cross-sensitization of the effects of AITC and low pH.
50                              The efficacy of AITC in extending the shelf life of minimally processed
51 27 demonstrated dose-dependent inhibition of AITC-induced flinching in rats, validating its utility a
52 nel as mediator of the algesic properties of AITC.
53  external stimulus to trigger the release of AITC molecules encapsulated in MOFs.
54                  In contrast, the release of AITC molecules from all these MOFs was triggered under h
55                    The conformation space of AITC contains three minima, Cs-M1 and enantiomers M2 and
56 reshold for evoking changes in NMPs based on AITC was significantly lower for patients with IR compar
57   Overexpression of a Bcl-2 mutant prevented AITC from inducing apoptosis.
58 that these MOFs could encapsulate and retain AITC molecules within their pores under low (30-35%) rel
59 large region of the potential energy surface AITC(gamma,epsilon,...) with 120 degrees < gamma < 180 d
60             Here we show that, surprisingly, AITC-induced activation of TRPV1 does not require intera
61                     These data indicate that AITC acts through reversible interactions with the capsa
62 tic analysis of channel gating revealed that AITC acts by destabilizing the closed channel, whereas m
63                            Here we show that AITC (allyl isothiocyanate; mustard oil) and menthol rep
64                           Here, we show that AITC arrests human bladder cancer cells in mitosis and a
65                       We further showed that AITC-induced Bcl-2 phosphorylation was caused by c-Jun N
66 ese MOFs, indicating that development of the AITC-MOFs delivering system is technically feasible.
67 pothesis that water vapors could trigger the AITC release from these MOFs, indicating that developmen
68  increased the threshold for the response to AITC at 4 and 12 weeks compared with placebo (P = .0406
69 sensitive to TRPV1 (capsaicin) and/or TRPA1 (AITC) agonists.
70 lability of reaction products (alpha-ZOL/ZEA-AITC) were lower than 42.13%, but significantly higher t
71 icity and estrogenic effect of alpha-ZOL/ZEA-AITC.

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