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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 al administration of radiation and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) chemotherapy in three
5  to inhibit MGMT and to potentiate 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in a MGMT-positive hum
6 Low concentrations of diamide plus 1,3-bis(2 chloroethyl)-1-nitrosourea (BCNU) increased intracellula
7 tentiate the antitumor efficacy of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is being tested in cli
8     The bifunctional DNA alkylator 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is cytotoxic primarily
9 ion of eNOS, by exposure to either 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or glutathione reducta
10 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
11 onal cycles of chemotherapy using 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) resulted in similar in
12 ter resistance to cell killing by 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) than overexpression of
13 ured with buthionine sulfoximine and 1,3-bis(chloroethyl)-1-nitrosourea (BCNU) to inhibit glutathione
14 th adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an incre
15 stance to the cytotoxic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a CNU commonly used f
16  study, we examined the effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a commonly used CNU,
17 rly hematopoietic progenitors from 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a stem cell toxin, an
18 agenic effects of temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), and no further sensit
19 -disulfide oxidoreductase enzymes (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), arsenite, and phenyla
20        The chemotherapeutic agents 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), carboplatin, and camp
21 ucts and compromise its integrity (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, H(2)O(2) a
22                In combination with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), the prodrugs were not
23  and to the chloroethylating agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with and without AGT
24 in of safety than the nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
25 re > 10-fold resistant to the CENU 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
26 ncluding melphalan, cisplatin, and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
27 sferase (AGT) and are sensitive to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
28 ctive in enhancing cell killing by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
29 ro, 2,4-dinitrobenzene (CDNB); or 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU).
30 mbucil, melphalan, and carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)] weakly induced lucife
31 -benzylguanine (O6-BG, 20 microM) or 1,3-bis(chloroethyl)-1-nitrosourea (BCNU, 100 microM), resulted
32 roencapsulation of antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU, Carmustine) into biode
33  transduction and O6-benzylguanine/1,3-bis(2-chloroethyl)-1-nitrosourea (BG/BCNU) treatment has been
34 n animals treated with carmustine (1,3-bis(2-chloroethyl)-1-nitrosourea 20 mg/kg/week, i.v. x 2; diff
35  effects of chemotherapy [25 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea administered with a single i.
36 iving IL-2-transduced cells or 10% 1,3-bis(2-chloroethyl)-1-nitrosourea alone.
37  also protected HeLa cells against 1,3-bis(2-chloroethyl)-1-nitrosourea and methyl methanesulfonate c
38 e toxic and clastogenic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C (MMC), as mea
39 rapeutic alkylating agents, namely 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C, indicating t
40  cells and polymers containing 10% 1,3-bis(2-chloroethyl)-1-nitrosourea had significantly improved su
41 reatine:Pi and ATP:Pi ratios after 1,3-bis(2-chloroethyl)-1-nitrosourea treatment indicate improved b
42 oximine) or glutathione reductase (1,3-bis(2-chloroethyl)-1-nitrosourea) in the presence or absence o
43 ozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotec
44 ne in DNA with the antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea, a chemotherapeutic used to c
45 of BLMVECs with the GR inhibitor, 1,3 bis-(2 chloroethyl)-1-nitrosourea, abolished the inhibitory eff
46  had been treated with carmustine (1,3-bis(2-chloroethyl)-1-nitrosourea, or BCNU).
47 0 degrees C and after addition of 1,3-bis-(2-chloroethyl)-1-nitrosourea, there was effective S-thiola
48 -mediated tumor cell resistance to 1,3-bis(2-chloroethyl)-1-nitrosourea, we performed a novel dose es
49 ze human tumor cells to killing by 1,3-bis(2-chloroethyl)-1-nitrosourea, with O6-benzyl-3'-O-(gamma-f
50 lling by the combination of BG and 1,3-bis(2-chloroethyl)-1-nitrosourea.
51 tance to the combination of BG and 1,3-bis(2-chloroethyl)-1-nitrosourea.
52 kyl N-nitrosourea-type drugs, e.g. 1,3-bis(2-chloroethyl)-1-nitrosourea.
53 ne or in combination with 13 mg/m2 1,3-bis(2-chloroethyl)-1-nitrosourea.
54  with 0.5, 1, or 2 x LD10 doses of 1,3-bis(2-chloroethyl)-1-nitrosourea.
55 therapeutic drugs temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea.
56 lating agents, such as carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chlor
57 ere treated with the alkylator agent 1,3-bis-chloroethyl-1-nitrosourea.
58 of glutathione reductase (GR) with 1,3-bis[2-chloroethyl]-1-nitrosourea or transfection of macrophage
59 cells as compared with 19 exhibited by 4-[(2-chloroethyl)(2-mesyloxyethyl)amino]benzoyl-l-glutamic ac
60 ity differential than the published N-[4-[(2-chloroethyl)(2-mesyloxyethyl)amino]benzoyl]-l-glutamic a
61  of this class, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)- 2(-)[[2-chloroethyl)-amino]carbonyl]hydraz
62  of this class, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-(methylamino)carbonylhydrazine (101M).
63  another agent, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[(4-nitrobenzyloxy)carbonyl]hy drazine (P
64 ty to sensitize 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[(methylamino)carbonyl]hydrazine (laromus
65 f these agents, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[[1-(4-nitrophenyl)ethoxy]carb onyl]hydra
66 cumulation of a liposome formulation of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), an effec
67 r response to the chemotherapeutic drug 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea in vitro.
68 ethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea; CCNU], and stre
69 and presence of sublethal nitrosourea ([1-(2-chloroethyl)-3-cyclohexyl-l-nitrosourea]; CCNU) concentr
70 -(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU), an alkylating antitum
71  without affecting [3H](+)-7-OH-DPAT (D3); N-chloroethyl-7-OH-DPATs blocked both radioligands in Acc
72 bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adducts are fully converted into interstrand
73 ted esters provides CNTs functionalized with chloroethyl, allyl, and propargyl groups, which can furt
74 race impurities from the synthesis of tris(2-chloroethyl)amine (HN3) that point to the reagent and th
75 g PGP (N-p- inverted question markN,N-bis (2-chloroethyl)amino inverted question markphenoxycarbonyl-
76  higher than that of sarcolysin [(L-3-[bis(2-chloroethyl)amino]-L-phenylalanine] against all leukemia
77   ID50 and ID90 values for L-prolyl-L-m-[bis(chloroethyl)amino]-phenylalanyl-L-norvaline ethyl ester
78 a-glutamyl-alpha-amino-beta-[[[2-[[bis[bis(2-chloroethyl)amino]ph osp horyl]oxy]ethyl]sulfonyl]propio
79                       [3,5-Difluoro-4-[bis(2-chloroethyl)amino]phenyl]carbamoyl-l-glutamic acid gave
80  coupling of two key intermediates: 4-[bis(2-chloroethyl)-amino]-L-phenylalanine ethyl ester trifluor
81 s(methylsulfonyl)-1-(2-chloroethyl)- 2(-)[[2-chloroethyl)-amino]carbonyl]hydrazine, was further evalu
82 ompounds consist of 4-(3-aminopropyl)-N,N-(2-chloroethyl)-aniline linked to 2-(4'-hydroxyphenyl)-3-me
83 is (chloromethyl)-propane-1,3-diyltetrakis(2-chloroethyl) bisphosphate (V6)).
84 -bis(chloromethyl)propane-1,3-diyltetrakis(2-chloroethyl) bisphosphate, known as V6, is a flame retar
85  this N-substituent could be cleaved using 1-chloroethyl chloroformate.
86 -32 by S-(2-chloroethyl)glutathione and S-(2-chloroethyl)cysteine, in peptides 1-24 and 45-58, was si
87                                            N-chloroethyl derivatives of 7-hydroxy-1,2,3,4-tetrahydron
88 Dichloroborane adducts of monoglyme and beta-chloroethyl ether also showed high reactivity, even at r
89             Dioxane, ethyl acetate, and beta-chloroethyl ether form relatively stable boron trichlori
90                           Monoglyme and beta-chloroethyl ether give stable dichloroborane adducts req
91 ether, dioxane, anisole, ethyl acetate, beta-chloroethyl ether, and monoglyme, were examined as prosp
92                    Mass spectra for xenon, 2-chloroethyl ethyl sulfide (CEES), and octane were acquir
93 r the oxidation of a mustard gas analogue, 2-chloroethyl ethyl sulfide (CEES), in the presence of an
94  photooxidation of a mustard-gas simulant, 2-chloroethyl ethyl sulfide (CEES), is studied using a por
95  oxidation of the sulfur mustard simulant, 2-chloroethyl ethyl sulfide (CEES).
96  for binding the sulfur mustard surrogate, 2-chloroethyl ethyl sulfide (CEES).
97                          The hydrolysis of 2-chloroethyl ethyl sulfide has been examined in an effort
98 dditional products in the disappearance of 2-chloroethyl ethyl sulfide with k3 in particular causing
99 nethiol) and one S-type vesicant simulant (2-chloroethyl ethyl sulfide) were found in each case (samp
100 xidation (O(2) oxidation of the thioether, 2-chloroethyl ethyl sulfide, CEES) led to the discovery th
101             Detection of the CWA simulants 2-chloroethyl ethyl sulfide, triethyl phosphate, and dimet
102 CEES to the comparatively nontoxic product 2-chloroethyl ethyl sulfoxide (CEESO) without formation of
103 ES was transformed selectively to nontoxic 2-chloroethyl ethyl sulfoxide and vinyl ethyl sulfoxide us
104           A compound (Alchemix) with the bis-chloroethyl functionality confined to one side chain alk
105  by thioredoxins alkylated at Cys-32 by S-(2-chloroethyl)glutathione and S-(2-chloroethyl)cysteine, i
106  mutations seen in other organisms with S-(2-chloroethyl)glutathione or ethylene dibromide.
107                    The synthetic analog S-(2-chloroethyl)glutathione was used to produce DNA damage;
108 -based assays accompanied replacement of the chloroethyl group with unhalogenated substituents.
109 (aminocarbonyl)-1,2-bis(methylsulfonyl)-1-(2-chloroethyl)hydr azi nes were synthesized and primarily
110 ylating species 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)hydrazine (90CE) after bioreductive activati
111 yloxycarbonyl)-1, 2-bis(methylsulfonyl)-1-(2-chloroethyl)hydrazines (4, 6, and 7) were synthesized an
112                                        The 2-chloroethyl moiety on selected dithiazoles was also modi
113 ell-line panel at the NCI, indicate that the chloroethyl moiety plays a major role in the enhanced ac
114 wley rats were administered 50 mg/kg i.p. N-(chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) or were
115  NE in the spinal cord dorsal horn with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
116 inistered the noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
117 males with the noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
118  by cortical NA denervation with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride] a
119 rats and in rats pretreated with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], a neurotoxin t
120 tau transgenic mice with the neurotoxin N-(2-chloroethyl)-N-ethyl-bromobenzylamine (DSP-4) starting a
121  both O6-benzylguanine (O6BG) and N,N'-bis(2-chloroethyl)-N-nitroso-urea (BCNU) stably increased the
122 en a single dose of 35 mg/m(2) of N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU), which was otherwise i
123  and are sensitive to killing by N,N'-bis (2-chloroethyl)-N-nitrosourea (BCNU).
124  synthesis, complicates the use of N,N-bis(2-chloroethyl)-N-nitrosourea as a GR inhibitor.
125 (DBT-FG) sensitized the tumors to N,N'-bis(2-chloroethyl)-N-nitrosourea chemotherapy, as measured by
126  reports of various GR inhibitors, N,N-bis(2-chloroethyl)-N-nitrosourea, an anticancer drug with IC(5
127 olar range, it is more potent than N,N-bis(2-chloroethyl)-N-nitrosourea, which is currently the most
128  such alkylating chemotherapeutic drugs as 2-chloroethyl-N-nitrosourea (CNU) derivatives is countered
129 nes and alkylating antitumor drugs such as 2-chloroethyl-N-nitrosourea (CNU).
130 MT caused increased cellular resistance to 2-chloroethyl-N-nitrosourea suggests a therapeutic signifi
131 on induced by alkylating agents, including 2-chloroethyl-N-nitrosourea-based antitumor drugs.
132 in (SAP) +/- intraperitoneal injection of N-[chloroethyl]-N-ethyl-2-bromobenzylamine (DSP-4) (noradre
133 -nitrobenzyl ester (9) and carbamic acid, (2-chloroethyl)nitroso-2,3,4, 6-tetra-O-acetyl-1-alpha,beta
134              One compound, carbamic acid, (2-chloroethyl)nitroso-4-acetoxybenzyl ester (3), was selec
135 rementioned compound, both carbamic acid, (2-chloroethyl)nitroso-4-nitrobenzyl ester (9) and carbamic
136                                 Seven new (2-chloroethyl)nitrosocarbamates have been synthesized as p
137 er treatment, a time interval in which bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adduc
138 ic effects of the antitumor agents 1,3-bis(2-chloroethyl)-nitrosourea (BCNU) and temozolomide were st
139 ismatched-BALB/c model followed by N,N-bis(2-chloroethyl)-nitrosourea (BCNU) treatment to enhance don
140 rstrand cross-linking reaction of N,N'-bis(2-chloroethyl)-nitrosourea (BCNU) were investigated using
141 link induction and cytotoxicity of 1,3-bis(2-chloroethyl)-nitrosourea (BCNU).
142 he 5-member exocyclic ring and are formed by chloroethyl nitrosoureas, which are used in cancer thera
143 ide] into the homobenzylic C-Cl bond of 4-(2-chloroethyl)phenol 1.
144 nt (e.g., t(1/2) (HD) approximately 18 s, (2-chloroethyl phenyl sulfide, C(6)H(5)SCH(2)CH(2)Cl) appro
145                           Reactions of alpha-chloroethyl phenyl sulfone (14) and ethyl 2-chloropropio
146                                    Fmoc-4-(1-chloroethyl)-phenylalanine (5) was synthesized in four s
147                                 While tris-2-chloroethyl phosphate, tris(1-chloro-2-propyl)phosphate
148 loro-isopropyl) phosphate (TDCIPP) and bis(2-chloroethyl) phosphate (BCEP)-tris(2-chloroethyl) phosph
149                         Furthermore, tris (2-chloroethyl) phosphate (TCEP), a known carcinogen, was f
150 ris(2-butoxyethyl) phosphate (TBOEP), tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
151 e analyzed for three halogenated OPs (tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
152                    These OPEs include tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
153 or exposure pathway for SigmaTCPP and tris(2-chloroethyl) phosphate (TCEP), while participants had hi
154 d bis(2-chloroethyl) phosphate (BCEP)-tris(2-chloroethyl) phosphate (TCEP).
155 loroisopropyl) phosphate (TCIPP), and tris(2-chloroethyl) phosphate (TCEP).
156 hloro-2-propyl)phosphate (TDCIPP) and tris(2-chloroethyl)phosphate (TCEP).
157 propyl)phosphate (TCPP or TCIPP), and tris(2-chloroethyl)phosphate (TCEP).
158 hosphate (TDCIPP; max: 3150 ng/L) and tris(2-chloroethyl)phosphate (TCEP; max: 8450 ng/L).
159 to 150 pg/m3, and tributyl phosphate, tris(2-chloroethyl)phosphate, tris(1-chloro-2-propyl)phosphate,
160 pha-amino-beta(2-ethyl-N,N,N', N'-tetrakis(2-chloroethyl)phosphorodiamidate)-sulfonyl-propionyl-( R)-
161 ct with DABCO in hot PhCl to give N-{4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazol-5-ylidene
162 )methanes with DABCO failed to give {4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazol-5-ylidene
163 n-retrocycloaddition strategies from 4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazole-5-thione
164 gallamine (M2), and 4-4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (4-DAMP mustard; M
165 ) receptor inhibitor, 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (4-DAMP; 10(-5) M)
166 3 receptor antagonist 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride had no effect.
167                                       Six (2-chloroethyl)porphyrins were synthesized from a common di
168 gave 5-substituted 3-(chloromethyl)- or 3-(2-chloroethyl)pyrazoles.
169 D, bis(2-chlororethyl) sulfide) and a range (chloroethyl) sulfide simulants of variable lipophilicity
170 exposure to the DNA-damaging compound bis-(2-chloroethyl) sulfide.
171  toxic chemical warfare agent mustard (bis(2-chloroethyl)sulfide) in the environment and during its d
172 face or within the droplet core, a range of (chloroethyl) sulfides, including HD, spanning some 7 ord
173 he A1/A2 purinergic receptor blocker 7-(beta-chloroethyl) theophylline (CET; given at 5 x 10-6 M and
174  receptor affinity-enhancing effects of 7-(2-chloroethyl) vs 7-methyl were comparable to the known en
175 ance affinity over hydrogen, except for 7-(2-chloroethyl), which enhanced the affinity of theophyllin

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