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1 lylamino)phenyllithium (1), derived from N,N-diallyl-2-bromoaniline (2) by low-temperature lithium-br
2 ane mediated by BF(3).OEt(2), leading to 2,4-diallyl-2-methyl-6-aryltetrahydro-2H-pyran ring systems
3 substituted 3-(3-butenyl)cycloalkenes or 2,3-diallyl-5,6-dimethyl-1,4-hydroquinone diacetate (16) for
4 ed biphenyl, amine, and lactam moieties, 7,8-diallyl-5-benzyl-7,8-dihydrodibenzo[e,g][1,4]diazocin-6(
5 clopentyl-1,3-dipropylxanthine (CPX) and 1,3-diallyl-8-cyclohexylxanthine (DAX) are xanthine adenosin
6 ate (VMA), allyl methacrylate (AMA), and N,N-diallyl acrylamide (DAA) by Cs-ligated zirconocenium est
7 , 4-vinylbenzyl methacrylate (VBMA), and N,N-diallyl acrylamide (DAA).
8 es of N,N-dibenzylleucine enkephalin and N,N-diallyl[Aib(2),Aib(3)]leucine enkephalin (ICI-174, 864)
9                                     With N,N-diallyl amide substrates, tandem radical cyclizations ca
10 atalyst for the [2pi + 2pi] cycloaddition of diallyl amines as well as the hydrogenative cyclization
11                              In vivo the N,N-diallyl analogue exhibited weak antinociceptive activity
12         In comparison to previously reported diallyl- and dithioacetoxypropyl-substituted calix[4]are
13              By use of externally deuterated diallyl carbonate, we could probe, for the first time, t
14 nes was more resistant to garlic extract and diallyl compounds treatment than E. coli O157:H7.
15 infrared (FT-IR) spectroscopy indicated that diallyl constituents contributed more to the antimicrobi
16 hibited negligible agonist activity, and N,N-diallyl[D-Pro10]Dyn A-(1-11) showed weak antagonist acti
17  aptamers (apt), and positively charged poly diallyl dimethyl ammonium chloride (PDDA) was used.
18 nylpiridine-co-styrene) > HA > PDADMAC (poly diallyl-dimethyl-ammonium-chloride), correlating to pyre
19  sodium poly(styrene sulfonic acid) and poly(diallyl dimethylammonium chloride).
20 he major constituents diallyl trisulfide and diallyl disulfide (45.76 and 15.63%) than purple-skin cu
21 ylmercaptan (PM), dimethyl disulfide (DMDS), diallyl disulfide (DADS), propyl disulfide (PDS), and 2,
22  organosulfur compounds, such as allicin and diallyl disulfide (DADS), which account for their pungen
23 ptosis inducer than diallyl sulfide (DAS) or diallyl disulfide (DADS).
24                          Here we showed that diallyl disulfide and diallyl trisulfide can transfer al
25                                 In addition, diallyl disulfide was non-covalently bound.
26     The garlic derived compounds allicin and diallyl disulfide were bound covalently to the native an
27          The binding reaction of allicin and diallyl disulfide with beta-lactoglobulin and the influe
28  specific transporter stabilizing allicin or diallyl disulfide.
29  of non-covalent binding sites increased for diallyl disulfide.
30                     The target analytes were diallyl disulphide (DADS), diallyl sulphide (DAS), diall
31 2-dithiin (2-VD), diallyl sulphide (DAS) and diallyl disulphide (DADS).
32     E-to-Z isomerization of the product from diallyl ether was only <10(-6) times as fast as its form
33 lective inhibitor of CYP2E1 enzyme activity (diallyl ether).
34 -mediated cascade rearrangement reactions of diallyl ethers were developed leading to selective [2,3]
35  reactants, the synthesized monomer, terpene-diallyl maleate adduct, was prepared by D-A addition, hy
36 cs of complexes 1-3 with the olefins diethyl diallyl malonate (DEDAM), butyl vinyl ether (BuVE), 1-he
37 ompounds containing a disulfide or an active diallyl moiety.
38 y radical thiol-ene photo-cross-linking of a diallyl monomer bearing the N,O-acetal moiety with anoth
39                                              Diallyl monosulfide is inert with respect to this allyl
40 hand, diallyl sulfone, a known metabolite of diallyl monosulfide, alkylates both amines and thiols un
41                        The N,N-diCPM and N,N-diallyl peptides are lead compounds in the development o
42                  Stepwise pathways involving diallyl radicals are formed via two different C-C formin
43 xtract (25, 50, 75, 100, and 200 muL/ml) and diallyl sulfide (5, 10, and 20 muM) on Listeria monocyto
44 ificantly more potent apoptosis inducer than diallyl sulfide (DAS) or diallyl disulfide (DADS).
45     This synergistic toxicity was reduced by diallyl sulfide (DAS), an inhibitor of CYP2E1; Trolox ([
46 hyl ester, catalase, or the CYP2E1 inhibitor diallyl sulfide partially reversed the elevation of prot
47                                 Catalase and diallyl sulfide prevented basal and AA-induced messenger
48 ed carboxyl proxyl, and the CYP2E1 inhibitor diallyl sulfide prevented the loss of CcO activity and t
49  the presence of salicylate was prevented by diallyl sulfide, a CYP2E1 inhibitor, and by the antioxid
50 ced, and this was prevented by cyclosporine, diallyl sulfide, and Trolox.
51 ity was prevented by 4-methylpyrazole and by diallyl sulfide, inhibitors of CYP2E1.
52  cells with inhibitors, 4-methylpyrazole and diallyl sulfide.
53 h saline controls, and this was prevented by diallyl sulfide.
54 tion in the E47 cells, a reaction blocked by diallyl sulfide.
55                           On the other hand, diallyl sulfone, a known metabolite of diallyl monosulfi
56 d (Z)-ajoene, 2-vinyl-4H-1,2-dithiin (2-VD), diallyl sulphide (DAS) and diallyl disulphide (DADS).
57 get analytes were diallyl disulphide (DADS), diallyl sulphide (DAS), diallyl trisulphide (DATS), alli
58                                     Allicin (diallyl thiosulfinate) from garlic is a highly potent na
59 rlic-derived organosulfides (OSCs) including diallyl trisulfide (DATS) are highly effective in afford
60                  Administration of H2S donor diallyl trisulfide (DATS) or overexpression of CSE resto
61                We have shown previously that diallyl trisulfide (DATS), a constituent of processed ga
62 lar mechanism of cell cycle arrest caused by diallyl trisulfide (DATS), a garlic-derived cancer chemo
63                                              Diallyl trisulfide (DATS), a metabolic byproduct of garl
64  in G(2)-M phase cell cycle arrest caused by diallyl trisulfide (DATS), which is a highly promising a
65  show that p.o. gavage of garlic constituent diallyl trisulfide (DATS; 1 and 2 mg/day, thrice/week fo
66 a lower percentage of the major constituents diallyl trisulfide and diallyl disulfide (45.76 and 15.6
67    Here we showed that diallyl disulfide and diallyl trisulfide can transfer allyl side chains to low
68     Treatment with a hydrogen sulfide donor, diallyl trisulfide, prevented these changes.
69  checkpoint kinase 1-dependent mechanism for diallyl trisulfide-induced mitotic arrest in human prost
70 The lack of a role of checkpoint kinase 2 in diallyl trisulfide-induced phosphorylation of Cdc25C or
71                                          The diallyl trisulfide-induced Ser(216) phosphorylation of C
72 e arrest or Cdc25C phosphorylation caused by diallyl trisulfide.
73 l disulphide (DADS), diallyl sulphide (DAS), diallyl trisulphide (DATS), allicin, 3-vinyl-4H-1,3-dith
74 locked by the delta-selective antagonist N,N-diallyl-Tyr-Aib-Aib-Phe-Leu-OH (ICI 174,864).
75           Similar treatment with delta [N, N-diallyl-Tyr-Aib-Aib-Phe-Leu-OH (ICI 174,864)] or kappa [