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1 arrest in response to exposure to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) alone; however, 70-80%
2 e 5-day cycle (1omega) of low-dose 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and a second group rec
3 esponse to the chemotherapy agents 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cis-diamminedichlo
4 ating-agent-induced methylation by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) at the O(6) position o
5 al administration of radiation and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) chemotherapy in three
6 to inhibit MGMT and to potentiate 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in a MGMT-positive hum
7 Low concentrations of diamide plus 1,3-bis(2 chloroethyl)-1-nitrosourea (BCNU) increased intracellula
8 tentiate the antitumor efficacy of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is being tested in cli
10 ion of eNOS, by exposure to either 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or glutathione reducta
11 tion of 30 mg/kg 6-BG and 10 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or with 40 mg/kg BCNU
12 onal cycles of chemotherapy using 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) resulted in similar in
13 ter resistance to cell killing by 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) than overexpression of
14 ured with buthionine sulfoximine and 1,3-bis(chloroethyl)-1-nitrosourea (BCNU) to inhibit glutathione
15 th adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an incre
16 stance to the cytotoxic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a CNU commonly used f
17 study, we examined the effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a commonly used CNU,
18 rly hematopoietic progenitors from 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a stem cell toxin, an
19 agenic effects of temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), and no further sensit
20 -disulfide oxidoreductase enzymes (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), arsenite, and phenyla
22 ucts and compromise its integrity (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, H(2)O(2) a
24 and to the chloroethylating agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with and without AGT
31 mbucil, melphalan, and carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)] weakly induced lucife
32 -benzylguanine (O6-BG, 20 microM) or 1,3-bis(chloroethyl)-1-nitrosourea (BCNU, 100 microM), resulted
33 roencapsulation of antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU, Carmustine) into biode
34 transduction and O6-benzylguanine/1,3-bis(2-chloroethyl)-1-nitrosourea (BG/BCNU) treatment has been
35 n animals treated with carmustine (1,3-bis(2-chloroethyl)-1-nitrosourea 20 mg/kg/week, i.v. x 2; diff
36 effects of chemotherapy [25 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea administered with a single i.
38 also protected HeLa cells against 1,3-bis(2-chloroethyl)-1-nitrosourea and methyl methanesulfonate c
39 e toxic and clastogenic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C (MMC), as mea
40 rapeutic alkylating agents, namely 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C, indicating t
41 cells and polymers containing 10% 1,3-bis(2-chloroethyl)-1-nitrosourea had significantly improved su
42 reatine:Pi and ATP:Pi ratios after 1,3-bis(2-chloroethyl)-1-nitrosourea treatment indicate improved b
43 oximine) or glutathione reductase (1,3-bis(2-chloroethyl)-1-nitrosourea) in the presence or absence o
44 ozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotec
45 ne in DNA with the antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea, a chemotherapeutic used to c
46 of BLMVECs with the GR inhibitor, 1,3 bis-(2 chloroethyl)-1-nitrosourea, abolished the inhibitory eff
48 0 degrees C and after addition of 1,3-bis-(2-chloroethyl)-1-nitrosourea, there was effective S-thiola
49 -mediated tumor cell resistance to 1,3-bis(2-chloroethyl)-1-nitrosourea, we performed a novel dose es
50 ze human tumor cells to killing by 1,3-bis(2-chloroethyl)-1-nitrosourea, with O6-benzyl-3'-O-(gamma-f
57 lating agents, such as carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chlor
59 of glutathione reductase (GR) with 1,3-bis[2-chloroethyl]-1-nitrosourea or transfection of macrophage
60 cells as compared with 19 exhibited by 4-[(2-chloroethyl)(2-mesyloxyethyl)amino]benzoyl-l-glutamic ac
61 ity differential than the published N-[4-[(2-chloroethyl)(2-mesyloxyethyl)amino]benzoyl]-l-glutamic a
62 of this class, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)- 2(-)[[2-chloroethyl)-amino]carbonyl]hydraz
63 of this class, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-(methylamino)carbonylhydrazine (101M).
64 another agent, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[(4-nitrobenzyloxy)carbonyl]hy drazine (P
65 ty to sensitize 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[(methylamino)carbonyl]hydrazine (laromus
66 f these agents, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[[1-(4-nitrophenyl)ethoxy]carb onyl]hydra
67 cumulation of a liposome formulation of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), an effec
68 motherapy regimen between procarbazine, 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), and vinc
70 ethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea; CCNU], and stre
71 and presence of sublethal nitrosourea ([1-(2-chloroethyl)-3-cyclohexyl-l-nitrosourea]; CCNU) concentr
72 -(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU), an alkylating antitum
73 without affecting [3H](+)-7-OH-DPAT (D3); N-chloroethyl-7-OH-DPATs blocked both radioligands in Acc
74 bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adducts are fully converted into interstrand
75 ted esters provides CNTs functionalized with chloroethyl, allyl, and propargyl groups, which can furt
76 race impurities from the synthesis of tris(2-chloroethyl)amine (HN3) that point to the reagent and th
77 trophiles such as N-acylimidazoles and bis(2-chloroethyl)amines, covalent screening enabled the surpr
78 g PGP (N-p- inverted question markN,N-bis (2-chloroethyl)amino inverted question markphenoxycarbonyl-
79 higher than that of sarcolysin [(L-3-[bis(2-chloroethyl)amino]-L-phenylalanine] against all leukemia
80 ID50 and ID90 values for L-prolyl-L-m-[bis(chloroethyl)amino]-phenylalanyl-L-norvaline ethyl ester
81 a-glutamyl-alpha-amino-beta-[[[2-[[bis[bis(2-chloroethyl)amino]ph osp horyl]oxy]ethyl]sulfonyl]propio
83 coupling of two key intermediates: 4-[bis(2-chloroethyl)-amino]-L-phenylalanine ethyl ester trifluor
84 s(methylsulfonyl)-1-(2-chloroethyl)- 2(-)[[2-chloroethyl)-amino]carbonyl]hydrazine, was further evalu
86 th induced proximity; however, probes with N-chloroethyl aniline were more reactive and more specific
87 ompounds consist of 4-(3-aminopropyl)-N,N-(2-chloroethyl)-aniline linked to 2-(4'-hydroxyphenyl)-3-me
88 We converted PVC and styrene in up to 89% (1-chloroethyl)benzene in less than 1 h of white light irra
89 tothermally recycled styrene achieved 84% (1-chloroethyl)benzene under white LED light in 1 h, and co
90 S plastics via photothermal conversion to (1-chloroethyl)benzene, a commodity chemical with excellent
92 -bis(chloromethyl)propane-1,3-diyltetrakis(2-chloroethyl) bisphosphate, known as V6, is a flame retar
94 -32 by S-(2-chloroethyl)glutathione and S-(2-chloroethyl)cysteine, in peptides 1-24 and 45-58, was si
96 Dichloroborane adducts of monoglyme and beta-chloroethyl ether also showed high reactivity, even at r
99 ether, dioxane, anisole, ethyl acetate, beta-chloroethyl ether, and monoglyme, were examined as prosp
100 xyphenylsulfone (D-8) (<=230 ng/g ww), bis(2-chloroethyl)ether-4,4'-dihydroxydiphenyl sulfone monomer
101 d sulfur mustard and its chemical simulant 2-chloroethyl ethyl sulfide (CEES) with half-lives less th
103 r the oxidation of a mustard gas analogue, 2-chloroethyl ethyl sulfide (CEES), in the presence of an
104 photooxidation of a mustard-gas simulant, 2-chloroethyl ethyl sulfide (CEES), is studied using a por
109 lytically active for the photooxidation of 2-chloroethyl ethyl sulfide (CEES, a chemical warfare simu
111 d the adsorption behaviors of n-hexane and 2-chloroethyl ethyl sulfide to explore the structure-prope
112 dditional products in the disappearance of 2-chloroethyl ethyl sulfide with k3 in particular causing
113 nethiol) and one S-type vesicant simulant (2-chloroethyl ethyl sulfide) were found in each case (samp
114 xidation (O(2) oxidation of the thioether, 2-chloroethyl ethyl sulfide, CEES) led to the discovery th
116 CEES to the comparatively nontoxic product 2-chloroethyl ethyl sulfoxide (CEESO) without formation of
117 ES was transformed selectively to nontoxic 2-chloroethyl ethyl sulfoxide and vinyl ethyl sulfoxide us
119 by thioredoxins alkylated at Cys-32 by S-(2-chloroethyl)glutathione and S-(2-chloroethyl)cysteine, i
124 (aminocarbonyl)-1,2-bis(methylsulfonyl)-1-(2-chloroethyl)hydr azi nes were synthesized and primarily
125 ylating species 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)hydrazine (90CE) after bioreductive activati
126 yloxycarbonyl)-1, 2-bis(methylsulfonyl)-1-(2-chloroethyl)hydrazines (4, 6, and 7) were synthesized an
127 ed by agents such as lomustine and the N3-(2-chloroethyl)imidazotetrazine mitozolomide rapidly evolve
129 ell-line panel at the NCI, indicate that the chloroethyl moiety plays a major role in the enhanced ac
130 wley rats were administered 50 mg/kg i.p. N-(chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) or were
131 NE in the spinal cord dorsal horn with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
132 inistered the noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
133 males with the noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
134 by cortical NA denervation with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride] a
135 rats and in rats pretreated with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], a neurotoxin t
136 tau transgenic mice with the neurotoxin N-(2-chloroethyl)-N-ethyl-bromobenzylamine (DSP-4) starting a
137 both O6-benzylguanine (O6BG) and N,N'-bis(2-chloroethyl)-N-nitroso-urea (BCNU) stably increased the
138 en a single dose of 35 mg/m(2) of N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU), which was otherwise i
141 (DBT-FG) sensitized the tumors to N,N'-bis(2-chloroethyl)-N-nitrosourea chemotherapy, as measured by
142 reports of various GR inhibitors, N,N-bis(2-chloroethyl)-N-nitrosourea, an anticancer drug with IC(5
143 olar range, it is more potent than N,N-bis(2-chloroethyl)-N-nitrosourea, which is currently the most
144 such alkylating chemotherapeutic drugs as 2-chloroethyl-N-nitrosourea (CNU) derivatives is countered
146 MT caused increased cellular resistance to 2-chloroethyl-N-nitrosourea suggests a therapeutic signifi
148 in (SAP) +/- intraperitoneal injection of N-[chloroethyl]-N-ethyl-2-bromobenzylamine (DSP-4) (noradre
149 -nitrobenzyl ester (9) and carbamic acid, (2-chloroethyl)nitroso-2,3,4, 6-tetra-O-acetyl-1-alpha,beta
151 rementioned compound, both carbamic acid, (2-chloroethyl)nitroso-4-nitrobenzyl ester (9) and carbamic
153 er treatment, a time interval in which bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adduc
154 ic effects of the antitumor agents 1,3-bis(2-chloroethyl)-nitrosourea (BCNU) and temozolomide were st
155 ismatched-BALB/c model followed by N,N-bis(2-chloroethyl)-nitrosourea (BCNU) treatment to enhance don
156 rstrand cross-linking reaction of N,N'-bis(2-chloroethyl)-nitrosourea (BCNU) were investigated using
158 he 5-member exocyclic ring and are formed by chloroethyl nitrosoureas, which are used in cancer thera
160 nt (e.g., t(1/2) (HD) approximately 18 s, (2-chloroethyl phenyl sulfide, C(6)H(5)SCH(2)CH(2)Cl) appro
164 loro-isopropyl) phosphate (TDCIPP) and bis(2-chloroethyl) phosphate (BCEP)-tris(2-chloroethyl) phosph
165 ations of nine urinary OPE biomarkers: bis(2-chloroethyl) phosphate (BCEtp), bis(1-chloro-2-propyl) p
166 ng/g) had higher concentrations than tris(2-chloroethyl) phosphate (GM: 1608 ng/g) and triphenyl pho
170 ris(2-butoxyethyl) phosphate (TBOEP), tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
171 e analyzed for three halogenated OPs (tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
172 One mattress contained high levels of tris(2-chloroethyl) phosphate (TCEP), which has been prohibited
173 or exposure pathway for SigmaTCPP and tris(2-chloroethyl) phosphate (TCEP), while participants had hi
181 phosphate or TCIPP (303 ng m(-3)) and tris(2-chloroethyl)phosphate or TCEP (139 ng m(-3)), which are
182 to 150 pg/m3, and tributyl phosphate, tris(2-chloroethyl)phosphate, tris(1-chloro-2-propyl)phosphate,
185 pha-amino-beta(2-ethyl-N,N,N', N'-tetrakis(2-chloroethyl)phosphorodiamidate)-sulfonyl-propionyl-( R)-
186 )methanes with DABCO failed to give {4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazol-5-ylidene
187 ct with DABCO in hot PhCl to give N-{4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazol-5-ylidene
188 n-retrocycloaddition strategies from 4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazole-5-thione
189 gallamine (M2), and 4-4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (4-DAMP mustard; M
190 ) receptor inhibitor, 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (4-DAMP; 10(-5) M)
191 3 receptor antagonist 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride had no effect.
194 D, bis(2-chlororethyl) sulfide) and a range (chloroethyl) sulfide simulants of variable lipophilicity
196 toxic chemical warfare agent mustard (bis(2-chloroethyl)sulfide) in the environment and during its d
197 face or within the droplet core, a range of (chloroethyl) sulfides, including HD, spanning some 7 ord
198 he A1/A2 purinergic receptor blocker 7-(beta-chloroethyl) theophylline (CET; given at 5 x 10-6 M and
199 receptor affinity-enhancing effects of 7-(2-chloroethyl) vs 7-methyl were comparable to the known en
200 ance affinity over hydrogen, except for 7-(2-chloroethyl), which enhanced the affinity of theophyllin