ライフサイエンスコーパス: cyclo

1 4 marrow suppression after topotecan or topo-cyclo.

2 ne, oxytetracycline, erythromycin, spinosad, cyclo-1,3,5,7-tetramethylene tetranitrate (HMX), and cyc

3 ,3,5-trimethylenetrinitramine (RDX), tetryl, cyclo-1,3,5,7-tetramethylenetetranitrate (HMX), hexameth

4 3,5,7-tetramethylene tetranitrate (HMX), and cyclo-1,3,5-trimethylene trinitramine (RDX)).

5 then 2:1 adducts between the high explosive cyclo-1,3,5-trimethylene-2,4,6-trinitramine (RDX) and ha

6 lutions of three common military explosives: cyclo-1,3,5-trimethylene-2,4,6-trinitramine (RDX), nitro

7 f the commonly used secondary explosive RDX (cyclo-1,3,5-trimethylene-2,4,6-trinitramine).

8 tetranitrate (PETN), trinitrotoluene (TNT), cyclo-1,3,5-trimethylenetrinitramine (RDX), tetryl, cycl

9 Reported here is a new hybrid macrocycle, cyclo[1]furan[1]pyridine[4]pyrrole (1), that bears analo

10 anolone, (3alpha,5alpha,20E)-3-hydroxy-13,24-cyclo-18-norcholan-20-ene-21-carbonitrile, eltanolone, 5

11 ns including the stereoisomeric R and S 5',8-cyclo-2'-deoxyadenosine (cdA) and 5',8-cyclo-2'-deoxygua

12 8,5'-cyclo-2'-deoxyadenosine (cdA) and 8,5'-cyclo-2'-deoxygua

13 ry of DNA damage products including the 8,5'-cyclo-2'-deoxyadenosine (cdA) and 8,5'-cyclo-2'-deoxygua

14 rst evidence that both (5'R)- and (5'S)-5',8-cyclo-2'-deoxyadenosine (cdA) in a CAG repeat tract caus

15 -cyclo-2'-deoxyguanosine (cyclo-dG) and 8,5'-cyclo-2'-deoxyadenosine (cyclo-dA) in five different str

16 n human cells, the oxidative DNA lesion 8,5'-cyclo-2'-deoxyadenosine (CydA) induces prolonged stallin

17 n the significant accumulation of (5'R)-8,5'-cyclo-2'-deoxyadenosine (R-cdA) and (5'S)-8,5'-cyclo-2'-

18 clo-2'-deoxyadenosine (R-cdA) and (5'S)-8,5'-cyclo-2'-deoxyadenosine (S-cdA) in liver DNA of neil1(-/

19 ity of several enzymes to release (5'S)-8,5'-cyclo-2'-deoxyadenosine [(5'S)-cdA] from dinucleotides a

20 ure 8-hydroxy-2'-deoxyguanosine, (5'-S)-8,5'-cyclo-2'-deoxyadenosine, (5'-R)-8,5'-cyclo-2'-deoxyguano

21 5',8-cyclo-2'-deoxyadenosine (cdA) and 5',8-cyclo-2'-deoxyguanosine (cdG) pairs that have been detec

22 8,5'-cyclo-2'-deoxyadenosine (cdA) and 8,5'-cyclo-2'-deoxyguanosine (cdG) tandem lesions.

23 esions including (5'S) diastereomers of 8,5'-cyclo-2'-deoxyguanosine (cyclo-dG) and 8,5'-cyclo-2'-deo

24 do-5-formamido-2-iminohydantoin (d2Ih), 5',8-cyclo-2'-deoxyguanosine (cyclo-dG), and the free base gu

25 8,5'-cyclo-2'-deoxyadenosine (cdA) and 8,5'-cyclo-2'-deoxyguanosine generated in DNA by both endogen

26 The 8,5'-cyclo-2'-deoxyguanosine lesion (cdG) has been recently r

27 S)-8,5'-cyclo-2'-deoxyadenosine, (5'-R)-8,5'-cyclo-2'-deoxyguanosine, and (5'-S)-8,5'-cyclo-2'-deoxyg

28 ,5'-cyclo-2'-deoxyguanosine, and (5'-S)-8,5'-cyclo-2'-deoxyguanosine.

29 5',8-cyclo-2'-deoxypurines (cdPus) are common forms of oxidiz

30 nt an oxidative deamination to produce 3,5'- cyclo-2'-deoxyxanthosine (19), whereas 17 was hydrolyzed

31 action with malonyl dichloride to afford two cyclo-[2]-malonate tethers that were separated by column

32 hat the flexible tetraimidazolium macrocycle cyclo[2](2,6-bis(1H-imidazol-1-yl)pyridine)[2](1,4-dimet

33 previously reported mixed heterocycle system cyclo[2]pyridine[4]pyrrole (2) and cyclo[6]pyrrole 3, an

34 nctional properties of 1 and the octapeptide cyclo(3-14)H-Cys-Phe-Phe-Trp(8)-Lys-Thr-Phe-Cys-OH (soma

35 logical properties of astressin B analogues {cyclo(30-33)[D-Phe(12),Nle(21,38),C(alpha)MeLeu(27,40),G

36 t, a CRF2 receptor antagonist (astressin-2B [cyclo(31-34) [d-Phe11,His12,C alphaMeLeu13,39, Nle17, Gl

37 A series of cyclo-3beta-(4-aminophenyl)-2beta-tropanemethanol analog

38 Cyclo-3beta-(4-aminophenyl)-2beta-tropanemethanol pimeli

39 Cyclo-3beta-(4-aminophenyl)-2beta-tropanemethanol sebaci

40 The congener TIP peptide AP318 [Cyclo(4-aminobutanoic acid-GQRETPEGAEAKPWYD)] activated

41 Several 6- and 7-monosubstituted N3,5'-cyclo-4-(beta-d-ribofuranosyl)-vic-triazolo[4,5-b]pyridi

42 , respectively) than the lead compound N3,5'-cyclo-4-(beta-D-ribofuranosyl)-vic-triazolo[4,5-b]pyridi

43 anti-hepatitis C virus (HCV) agent, N(3),5'-cyclo-4-(beta-D-ribofuranosyl)-vic-triazolo[4,5-b]pyridi

44 with alternate bridging constraints such as cyclo (6-11), cyclo (6-12), and cyclo (7-11).

45 e bridging constraints such as cyclo (6-11), cyclo (6-12), and cyclo (7-11).

46 The quinquedentate macrocyclic ligand cyclo-6,6'-[1,9-(2,5,8-trithianonane)]-2,2'-bipyridine (

47 The crystal structure of a homologous cyclo[6]aramide reveals a disk-shaped, near-planar molec

48 Additionally, cyclo[6]aramides show unusual mesophase transitions from

49 Cyclo[6]aramides, a type of macrocycle with a hydrogen-b

50 The various forms of cyclo[6]pyridine[6]pyrrole are characterized by distinct

51 A large porphyrin analogue, cyclo[6]pyridine[6]pyrrole, containing no meso bridging

52 le system cyclo[2]pyridine[4]pyrrole (2) and cyclo[6]pyrrole 3, an all-pyrrole 22 pi-electron aromati

53 It was also found that cyclo[6]pyrrole bound to d(T(2)AG(3))(4) better than oct

54 ctaethylporphyrin, a finding rationalized by cyclo[6]pyrrole having a 2+ charge, while octaethylporph

55 ints such as cyclo (6-11), cyclo (6-12), and cyclo (7-11).

56 ys(12)]SRIF (31) (sst(1) IC(50) = 16 nM) and cyclo(7-12) Des-AA(1,2,5)-[Glu(7),d-Trp(8),IAmp(9),m-I-T

57 Cyclo(7-12)Des-AA(1,5)-[Tyr(2),Glu(7),d-Trp(8),IAmp(9),h

58 view was challenged by the isolation of 3',8-cyclo-7,8-dihydro-guanosine 5'-triphosphate (3',8-cH2GTP

59 e structure of this molecule to be (8S)-3',8-cyclo-7,8-dihydroguanosine 5'-triphosphate (3',8-cH2GTP)

60 system, consisting of an expanded porphyrin, cyclo[8]pyrrole (C8) and a pyrene carboxylate (Py) is ca

61 micros, which decays to the triplet state of cyclo[8]pyrrole, also an exceedingly long-lived species.

62 2-hydroxypropyl-beta-cyclodextrin (CYCLO), a modifier of cholesterol efflux from cellular m

63 ynthetase (PKS-NRPS) that makes and releases cyclo-acetoacetyl-L-tryptophan (cAATrp), the tetramic ac

64 peptide synthetase (PKS-NRPS) that generates cyclo-acetoacetyl-L-tryptophan (cAATrp).

65 These findings suggest that CYCLO acutely reverses the lysosomal transport defect se

66 enerated by copper-catalyzed [3 + 2] Huisgen cyclo-addition between an alkyne-functionalized C5-thymi

67 ro-2-nitrovinylbenzene, to trap the putative cyclo-addition intermediate, thereby demonstrating that

68 acyclic intermediate formed by a 1,3 dipolar cyclo-addition of prFMN with the alpha-beta double bond

69 MN can function as a dipole in a 1,3 dipolar cyclo-addition reaction as the initial step in a novel t

70 ol by attaching an azide fluorophore through cyclo-addition.

71 However, enzyme-catalyzed 1,3 dipolar cyclo-additions are unprecedented and other mechanisms a

72 e dose of 2-hydroxypropyl-beta-cyclodextrin (CYCLO) administered at 7 days of age immediately caused

73 The experimental spectrum for protonated cyclo AG compares very well with the theoretical spectra

74 rom the reaction of OH with a series of C10 (cyclo)alkanes, with 0-3 rings, in order to better unders

75 ylation of ketones to yield aryl benzyl and (cyclo)alkyl benzyl ketones with substitution patterns th

76 ldren who received topotecan, 76% after topo-cyclo, and 25% after paclitaxel.

77 Topotecan and topo-cyclo are active in children with NB, are well tolerated

78 n emission tomography (PET) and [(64)Cu]DOTA-cyclo-(Arg-Gly-Asp-dPhe-Lys) {[(64)Cu]DOTA-c(RGDfK)} can

79 (4:4)-As4)] (3a) and [(Cp'''Fe)2(mu,eta(4:4)-cyclo-As4)] (3b).

80 he expected complex [(Cp(Bn)Fe)2(mu,eta(4:4)-cyclo-As4)](+).

81 y, cyclic peptides derived from MTII, Ac-Nle-cyclo(Asp-His6-D-Phe7-Arg8-Trp-Lys)-NH2 (a pan-agonist a

82 They are exemplified by peptide 29, Ac-Nle-cyclo(Asp-Oic6-D-4,4'-Bip7-Pip8-Trp-Lys)-NH2 (Oic=octahy

83 identical withMo(N[(i)Pr]Ar)(3) leads to the cyclo-AsP(2) complex (OC)(5)W(cyclo-AsP(2))Mo(N[(i)Pr]Ar

84 ) leads to the cyclo-AsP(2) complex (OC)(5)W(cyclo-AsP(2))Mo(N[(i)Pr]Ar)(3).

85 cyclo[D-Asp(7),Lys(10)]- and cyclo[Asp (6),Lys(10)]N/OFQ(1-13)NH2 exhibit high affini

86 d synthesis of aryl and heteroaryl-annulated cyclo[b]carbazoles has been developed via SnCl4-mediated

87 The Cope rearrangement of cyclo-biphenalenyl 9 is studied by exploring its potenti

88 idence for lysosomal enhancing properties of CYCLO, but caution that prolonged interference with cell

89 based upon cationic [Rh(PCy(3))(2)](+) (Cy = cyclo-C(6)H(11)).

90 r is aromatic, and in partially hydrogenated cyclo-C18 derivatives with both radial and tangential pi

91 3b, C6H4-4-NEt23d; CR2 = adamantylidene 3c, cyclo-C3Ph23e).

92 C6H3N=CMe)2C5H3N; R = Et, (n)Bu, (i)Bu, CH2 (cyclo)C5H 9; 1-R), were synthesized either by direct alk

93 AP301 [Cyclo(CGQRETPEGAEAKPWYC)], a cyclic peptide comprising t

94 One of these peptides, cyclo-[(CH(2))(3)CO-Gly(1)-His(2)-D-Phe(3)-Arg(4)-D-Trp(

95 Here we report cyclo-CLLFVY, identified from a library of 3.2 million c

96 observed to react with 3-Mo to generate the cyclo-CP2 complex (AdCP2)Mo(N[(i)Pr]Ar)3.

97 d out to synthesize the cyclic model peptide cyclo(Cys-Thr-Abu-Gly-Gly-Ala-Arg-Pro-Asp-Phe): (i). sid

98 The Asp-Pro-Ala-Ala-Thr-Ala-Tyr-cyclo[Cys-Arg-DPhe-DPhe-Asn-Ala-Phe-Cys]-Tyr-A la-Arg-Ly

99 f N-methylated analogues of the stem peptide cyclo(d-Ala-Ala5 ); 2) selection of cyclic peptides with

100 en positions 5 and 8 yielded [N-benzylTyr(1),cyclo(d-Asp(5),Dap(8))]Dyn A-(1-11)NH(2) (zyklophin, 13)

101 (Dyn) A analogue zyklophin ([N-benzyl-Tyr(1)-cyclo(d-Asp(5),Dap(8))]dynorphin A(1-11)NH2) is a kappa

102 dynorphin A analogue [N(alpha)-benzylTyr(1),cyclo(D-Asp(5),Dap(8))]dynorphin A-(1-11)NH(2) (Dap = 2,

103 ane affinity of the decapeptide Gramicidin S cyclo(d-Phe-Pro-Val-Orn-Leu-)2 (GS).

104 s) for the important model cyclopentapeptide cyclo(D-Pro1-Ala2-Ala3-Ala4-Ala5) were performed in expl

105 template structures based on a library of 54 cyclo(-D-Ala-Ala(5)-) peptides with different N-methylat

106 Cyclo-(d-Pro-l-Pro-d-Pro-l-Pro) has been studied with de

107 Except for cyclo[d-Asp(2), Pro(3),Dap(5)]Dyn A-(1-11)NH(2), which w

108 s of Gly(3) by Ala, d-Ala, Trp, and d-Trp in cyclo[d-Asp(2),Dap(5)]Dyn A-(1-11)NH(2) and its linear c

109 Incorporation of d-Ala at position 3 of cyclo[d-Asp(2),Dap(5)]Dyn A-(1-11)NH(2) exhibited 2-fold

110 ous modifications were made in position 3 of cyclo[d-Asp(2),Dap(5)]Dyn A-(1-11)NH(2) that could influ

111 cyclo[d-Asp(2),Dap(5)]Dyn A-(1-13)NH(2) (Dap, 2,3-diamin

112 stitutions, most of the peptides (except for cyclo[d-Asp(2),Pro(3),Dap(5)]Dyn A-(1-11)NH(2) and [d-As

113 cyclo[d-Asp(2),Pro(3),Dap(5)]Dyn A-(1-11)NH(2) showed th

114 cyclo[D-Asp(7),Lys(10)]- and cyclo[Asp (6),Lys(10)]N/OFQ

115 ical constraints with penicillamines, 2 (Tyr-cyclo[d-Pen-Gly-Phe-Pen]-Pro-Leu-Trp-NH-[3',5'-(CF(3))(2

116 (cyclo-dG) and 8,5'-cyclo-2'-deoxyadenosine (cyclo-dA) in five different strains of Escherichia coli

117 roups, prior to the intramolecular oxidative cyclo-dehydrogenation.

118 Cryptophycins, naturally occurring cytotoxic cyclo-depsipeptides, have been modified by total synthes

119 cells with LR-disrupting agents methyl beta-cyclo dextrin (MbetaCD) or nystatin significantly inhibi

120 we also isolated significant amounts of 3,5'-cyclo-dG (16) and 2,5'-cyclo-dT (17), respectively.

121 astereomers of 8,5'-cyclo-2'-deoxyguanosine (cyclo-dG) and 8,5'-cyclo-2'-deoxyadenosine (cyclo-dA) in

122 antoin (d2Ih), 5',8-cyclo-2'-deoxyguanosine (cyclo-dG), and the free base guanine (Gua).

123 ared by the palladium-catalyzed ring-opening cyclo-dimerization of the three-membered heterocycle Re(

124 ed conversion of 2-C-methyl-D-erythritol-2,4-cyclo-diphosphate into (E)-1-hydroxy-2-methylbut-2-enyl-

125 the substrate, 2-C-methyl-D-erythritol-2, 4-cyclo-diphosphate.

126 of Me2PCl and TMSOTf to form the unexpected cyclo-diphosphino-1,2-diphosphonium salt [(Me2P)2(PtBu)2

127 The cyclo-diphosphinophosphonium salt [(PtBu)3Me][OTf] (2) h

128 cyclo[DKP-f3-RGD]-PTX 11 displayed sufficient stability

129 sized with the aim of using the tumor-homing cyclo[DKP-RGD] peptidomimetics for site-directed deliver

130 orms the biosynthetic step that provides the cyclo-DOPA moiety of all red betacyanins.

131 talamic acid condenses with imino compounds (cyclo-DOPA or its glucosyl derivatives), or amines and/o

132 A formation and its subsequent conversion to cyclo-DOPA, CYP76AD6 uniquely exhibits only tyrosine hyd

133 me P450 gene that catalyzes the formation of cyclo-DOPA.

134 Mice injected with Cyclo/Dox at ZT2 lost more body mass than mice injected

135 Cyclo/Dox injected at ZT2 increased the expression of se

136 within the liver responsible for converting Cyclo/Dox into their toxic metabolites increased among m

137 Mice were injected intravenously with Cyclo/Dox or the vehicle two hours after lights on (zeit

138 inistering cyclophosphamide and doxorubicin (Cyclo/Dox), a common treatment for breast cancer, to fem

139 icant amounts of 3,5'-cyclo-dG (16) and 2,5'-cyclo-dT (17), respectively.

140 Here, we investigated CYCLO effects on autophagy in wild-type mice and TgCRND8

141 f the alphavbeta6 integrin-selective peptide cyclo(FRGDLAFp(NMe)K) via click chemistry.

142 f the alphavbeta6 integrin-selective peptide cyclo(FRGDLAFp(NMe)K) via click chemistry.

143 The polyamide, cyclo-gamma-ImPyPy-gamma-PyPyPy-, binds to target DNA wi

144 d cyclic peptide with 6 amino acid residues, cyclo(Gln-Trp-Phe-Gly-Leu-Met), is confirmed not to adop

145 r new CI-4 derivatives, cyclo-(L-Arg-L-Pro), cyclo-(Gly-L-Pro), cyclo-(L-His-L-Pro), and cyclo-(L-Tyr

146 The structures reveal that the common cyclo-(Gly-Pro) substructure is sufficient for binding,

147 dimethyl-6-t-butyl-dimethyl-silyoxy-methyl-1-cyclo-hexanone to give a vinyl cyclohexanol derivative a

148 )-3,4-dichloro-N-methyl-N-[2-1-pyrrolidinyl)-cyclo-hexyl] benzeneacetamide (U50488) into the LC did n

149 (10)-methylenetetrahydrofolate dehydrogenase/cyclo hydrolase (FolD) is essential for growth in Trypan

150 Second, CYCLO impeded autophagosome-lysosome fusion as evidenced

151 otecan, and topotecan-cyclophosphamide (topo-cyclo) in newly diagnosed children with stage IV NB.

152 294002) and endothelin-A receptor antagonist cyclo(L-Leu-D-Trp-D-Asp-L-Pro-D-Val) (BQ123).

153 itro show that it can use the cyclodipeptide cyclo(l-Tyr-l-Tyr) (cYY) as a substrate.

154 structural analysis has revealed that CI-4 [cyclo-(L-Arg-D-Pro)] inhibits family 18 chitinases by mi

155 ion structures of four new CI-4 derivatives, cyclo-(L-Arg-L-Pro), cyclo-(Gly-L-Pro), cyclo-(L-His-L-P

156 ves, cyclo-(L-Arg-L-Pro), cyclo-(Gly-L-Pro), cyclo-(L-His-L-Pro), and cyclo-(L-Tyr-L-Pro), in complex

157 cyclo-(Gly-L-Pro), cyclo-(L-His-L-Pro), and cyclo-(L-Tyr-L-Pro), in complex with a family 18 chitina

158 jects with severe periodontitis (P2 and P3), cyclo (-leu-pro) and cyclo (-phe-pro) were significantly

159 strongly associated with 2 novel metabolites-cyclo (-leu-pro) and cyclo (-phe-pro)-at 21 d of biofilm

160 (MTHFS; also called 5-formyltetrahydrofolate cyclo-ligase; EC 6.3.3.2) activity responsible for the o

161 Novel hybrid cyclo[m]pyridine[n]pyrroles have been synthesized using

162 ing only 1,1'-disubstituted ferrocene units (cyclo[n], n = 5-7, 9).

163 lision cross section of each d(T(2)AG(3))(4)/cyclo[n]pyrrole complex.

164 tiparallel G-quadruplex arrangement and each cyclo[n]pyrrole externally stacked below the G-quartets

165 Nano-ESI-MS indicated that the smaller the cyclo[n]pyrrole, the more strongly it binds to the telom

166 a similar function, a series of diprotonated cyclo[n]pyrroles (where n = 6, 7, and 8) was each added

167 As a first step toward testing whether cyclo[n]pyrroles display a similar function, a series of

168 ) and (2) the overall size and charge of the cyclo[n]pyrroles play important roles in defining the bi

169 Diprotonated cyclo[n]pyrroles represent a set of expanded porphyrin a

170 When the cyclo[n]pyrroles were intercalated or nonspecifically bo

171 dominant binding mode for the interaction of cyclo[n]pyrroles with d(T(2)AG(3))(4) and (2) the overal

172 expanded compounds that are examined include cyclo[n]pyrroles, [22]pentaphyrins(1.1.1.1.1), sapphyrin

173 dy using the IgG binding cyclic depsipeptide cyclo[(Nalpha-Ac)-S(A)-RWHYFK-Lact-E] is presented to de

174 (CO)4] (4a) but instead lead to (bisNHC)Al(2-cyclo-OC4H7)[Fe(CO)4] (4) and (bisNHC)Al(2-cyclo-OC5H9)[

175 2-cyclo-OC4H7)[Fe(CO)4] (4) and (bisNHC)Al(2-cyclo-OC5H9)[Fe(CO)4] (5), respectively.

176 clopentadienyl, arene, cycloheptatrienyl and cyclo-octatetraenide complexes, cyclobutadienyl derivati

177 with uranium complexes of larger arenes and cyclo-octatetraenide, where delta-bonding dominates.

178 azide was then selectively derivatized with cyclo-octyne conjugates to various probes.

179 on thin-film gold electrodes deposited onto Cyclo Olefin Polymer (COP) substrates was fabricated for

180 d to an AS18 latex-coated surface-sulfonated cyclo-olefin polymer (COP) capillary column with an inne

181 Thermoplastics such as polystyrene (PS) and cyclo-olefin polymer (COP) have become common materials

182 ice was based on a disposable and single-use cyclo-olefin polymer (COP) microfluidic chip interfaced

183 three different materials (polystyrene (PS), cyclo-olefin polymer (COP), and PDMS).

184 the experiments establish that a step-growth cyclo-oligomerization process operates during CB[n] form

185 We identified two major actions of CYCLO on autophagy underlying amelioration of lysosomal

186 ophen interferes with the oxidation state of cyclo-oxygease.

187 Should selective cyclo-oxygenase (COX) 2 inhibitors be used?

188 and whether its effects are mediated through cyclo-oxygenase (COX) and prostaglandins (PG).

189 ed vasodilatation with nitric oxide (NO) and cyclo-oxygenase (COX) signalling pathways, microdialysis

190 Cyclo-oxygenase (COX), the enzyme responsible for conver

191 prostacyclin (PGI2) derived from adenoviral cyclo-oxygenase (COX)-1/prostacyclin synthase (PGIS) (Ad

192 Cyclo-oxygenase (COX)-2 selective inhibitors decrease up

193 Upper gastrointestinal safety of cyclo-oxygenase (COX)-2 selective inhibitors versus trad

194 inhibition of nitric oxide (NO) synthase or cyclo-oxygenase (COX).

195 Increased generation of cyclo-oxygenase (COX-1 and COX-2)-derived vasoconstricto

196 of nitric oxide synthase (NOS; with l-NAME), cyclo-oxygenase (COX; with indomethacin) and endothelium

197 Cyclo-oxygenase 2 (COX2)-selective inhibitors should red

198 The potential for cyclo-oxygenase 2 (COX2)-selective inhibitors to increas

199 appaBalpha and proinflammatory genes such as cyclo-oxygenase 2 and interleukin 8.

200 a-2 agonists, beta-blockers,corticosteroids, cyclo-oxygenase 2 inhibitors, and regional anesthetic bl

201 Current exposure to cyclo-oxygenase 2 selective and non-selective NSAIDs was

202 including overexpression of IL-6, IL-1beta, cyclo-oxygenase 2, M-CSF, and IDO.

203 nducible NO synthase, arginase-1, TNF-alpha, cyclo-oxygenase 2, vascular endothelial growth factor [V

204 , alternatively, the restoration of PTHrP or cyclo-oxygenase activity by the administration of PTH an

205 t acetaminophen is an effective inhibitor of cyclo-oxygenase activity in intact cells.

206 ise mechanism of action for acetaminophen on cyclo-oxygenase activity is debated.

207 ophen has no affinity for the active site of cyclo-oxygenase but instead blocks activity by reducing

208 xide synthase, soluble guanylate cyclase and cyclo-oxygenase but was blocked by 25 mm potassium.

209 shes bombesin-induced gastroprotection while cyclo-oxygenase inhibition partially reverses this effec

210 d reduced ET-induced vascular leakage with a cyclo-oxygenase inhibitor (indomethacin), agents that in

211 yet, undeveloped therapeutic window for the "cyclo-oxygenase inhibitor".

212 ed in the presence of high concentrations of cyclo-oxygenase inhibitor, aspirin.

213 administration of indomethacin or celecoxib (cyclo-oxygenase inhibitors), pyrilamine, aprepitant (a n

214 ls, and is independent of the release of NO, cyclo-oxygenase or cytochrome P450 products.

215 and substrate supply, and not the isoform of cyclo-oxygenase present, dictate the effects of NSAIDs o

216 Acetaminophen works by lowering cyclo-oxygenase products preferentially in the central n

217 vity by reducing the active oxidized form of cyclo-oxygenase to an inactive form.

218 e caused by the previous suggested effect on cyclo-oxygenase, as inhibition also was observed in the

219 phen selectively inhibits a distinct form of cyclo-oxygenase, cyclo-oxygenase-3.

220 , unco-ordinated-5H3 (unc5H3), doublecortin, cyclo-oxygenase, sonic hedgehog and Disrupted in schizop

221 man vessels and endothelial cells containing cyclo-oxygenase-1 (COX-1) without any detectable COX-2,

222 hacin or diclofenac, which also inhibit both cyclo-oxygenase-1 and cyclo-oxygenase-2, were unaffected

223 2 selective inhibitor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase-2 inhibitors ibuprofen

224 ripts of a limited number of genes including cyclo-oxygenase-2 (COX-2) and major histocompatibility c

225 ates parathyroid-related peptide (PTHrP) and cyclo-oxygenase-2 (COX-2) as possible factors underlying

226 ophosphatidic acid (LPA) lead to synergistic cyclo-oxygenase-2 (COX-2) expression, an enzyme strongly

227 -2), matrix metalloproteinase-9 (MMP-9), and cyclo-oxygenase-2 (COX-2) in the mammary gland.

228 Cyclo-oxygenase-2 (COX-2) selective inhibitors have been

229 of interleukin-8 (IL-8), IL-6, IL-1beta, and cyclo-oxygenase-2 (COX-2) were greatest in differentiate

230 Cyclo-oxygenase-2 (COX-2), an inducible enzyme important

231 SAIDs), particularly selective inhibitors of cyclo-oxygenase-2 (COX-2), is associated with an increas

232 expression of the pro-inflammatory mediator cyclo-oxygenase-2 (COX-2), providing a mechanism whereby

233 Here, we have used an in vitro model of cyclo-oxygenase-2 activity (A549 cells stimulated with I

234 uated by inhibiting the prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine re

235 tivity, and (iii) protein expression of ODC, cyclo-oxygenase-2 and nitric oxide synthase.

236 t of titres of lentiviral vectors expressing Cyclo-oxygenase-2 by 600-fold, and adenoviral vectors ex

237 Selective inhibition of cyclo-oxygenase-2 has been associated with an increased

238 over nonsteroidal anti-inflammatory drug and cyclo-oxygenase-2 inhibitor safety continues.

239 sessed the effect of 3-year treatment with a cyclo-oxygenase-2 inhibitor, rofecoxib (25 mg), on recur

240 tor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase-2 inhibitors ibuprofen and naproxen were

241 ear has led to a reassessment of the role of cyclo-oxygenase-2 inhibitors in osteoarthritis therapy a

242 c pain is typically treated with opioids and cyclo-oxygenase-2 inhibitors with well known side effect

243 of nonsteroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors.

244 Similarly the inhibitory effects of the cyclo-oxygenase-2 selective inhibitor rofecoxib or the m

245 some NSAIDs, including the newly introduced cyclo-oxygenase-2 selective inhibitor rofecoxib, owe par

246 Cyclo-oxygenase-2 selective inhibitors and non-selective

247 s of nonsteroidal anti-inflammatory drug and cyclo-oxygenase-2 therapy for individuals is covered.

248 Cyclo-oxygenase-2(-/-) mice had increased plasma levels

249 okeratin, high-molecular-weight cytokeratin, cyclo-oxygenase-2, EMA, HER2, matrix metalloproteinases

250 hich also inhibit both cyclo-oxygenase-1 and cyclo-oxygenase-2, were unaffected by t-butylOOH.

251 ious impact that select therapies (including cyclo-oxygenase-2-specific inhibitors) may have in terms

252 These observations dispel the notion that cyclo-oxygenase-3 is involved in the actions of acetamin

253 inhibits a distinct form of cyclo-oxygenase, cyclo-oxygenase-3.

254 In addition, nitric oxide and cyclo-oxygenase-derived byproducts are required for full

255 ory actions to effects on oxidation state of cyclo-oxygenase.

256 a 1-week high-salt (HS) diet on the role of cyclo-oxygenases (COX-1 and COX-2) and the vasoconstrict

257 ng terminals, but resistant to inhibition of cyclo-oxygenases.

258 Cyclo-P(3) complexes can be obtained when ancillary liga

259 ple bond]Nb(N[Np]Ar)3](-), 3-Nb, to give the cyclo-P3 complexes (P3)M(N[(i)Pr]Ar)3 and [(P3)Nb(N[Np]A

260 butylimido complexes to produce the bridging cyclo-P4 phosphide species {[(BDI)(N(t)Bu)M]2(mu-eta(3):

261 All prior examples of cyclo-P5 are stabilized by d-block metals, so 2 shows th

262 from uranium to the cyclo-P5 unit to give a cyclo-P5 charge state that approximates to a dianionic f

263 rger size and superior acceptor character of cyclo-P5 compared to cyclopentadienyl, the strongly redu

264 the unprecedented actinide inverted sandwich cyclo-P5 complex [{U(Tren(TIPS))}2(mu-eta(5):eta(5)-cycl

265 tabilized by d-block metals, so 2 shows that cyclo-P5 does not require d-block ions to be prepared.

266 Although cyclo-P5 is isolobal to cyclopentadienyl, which usually

267 ls three different coordination modes of the cyclo-P5 ligand including a novel pi-coordination.

268 ent with charge transfer from uranium to the cyclo-P5 unit to give a cyclo-P5 charge state that appro

269 5 complex [{U(Tren(TIPS))}2(mu-eta(5):eta(5)-cyclo-P5)] (2).

270 thiaspirane nuphar alkaloid from 3-methyl-2-cyclo-pentenone is reported.

271 iodontitis (P2 and P3), cyclo (-leu-pro) and cyclo (-phe-pro) were significantly associated with incr

272 ith 2 novel metabolites-cyclo (-leu-pro) and cyclo (-phe-pro)-at 21 d of biofilm overgrowth (P = 0.02

273 The cyclo(Phe-Pro) inhibition of CT and TCP production corre

274 In this work, we present evidence that cyclo(Phe-Pro) inhibits the production of the virulence

275 Cyclo(Phe-Pro) is a cyclic dipeptide produced by multipl

276 piro-ionenes are successfully synthesized in cyclo-polycondensations of tetrakis(bromomethyl)benzene

277 ) a one-pot reaction of phosphonium dimers ([cyclo-(PR2CH2CH(OH)(-))2][Br]2), KOtBu, FeBr2, and Ph2PC

278 the orally bioavailable somatostatin analog cyclo(-Pro-Phe-NMe-D-Trp-NMe-Lys-Thr-NMe-Phe-), and the

279 lo[R-G-D-f-N(Me)V] 1, and its parent peptide cyclo(R-G-D-f-V) 2, potent antagonists of the alphavbeta

280 ormed on the cyclic RGD-peptide Cilengitide, cyclo[R-G-D-f-N(Me)V] 1, and its parent peptide cyclo(R-

281 By 49 days of age, this single injection of CYCLO resulted in a reduction in whole-body C burden of

282 der of potency of GRGDNP > GRGDSP > GRGDTP = cyclo-RGD.

283 ptor-specific binding and cellular uptake of cyclo(RGDfC)-modified quantum dots via the alphavbeta3 i

284 knottin-RGD peptide instead of biotinylated cyclo[RGDfK] (as reported by Piras et al.), as integrin-

285 d alpha5beta1, while binding of biotinylated cyclo[RGDfK] was very weak and only detectable for alpha

286 ed peptides, that is: (i) linear GRGDS, (ii) cyclo[RGDfK], and (iii) the knottin-RGD itself for bindi

287 halasin D (to block actin polymerization) or cyclo(RGDfV) (to block vitronectin receptors) significan

288 Blocking studies with cyclo[RGDfV] inhibited the in vivo uptake of Cyp-GRD, su

289 d by coincubation with a cyclic RGD peptide (cyclo[RGDfV], f is d-phenylalanine) that binds ABI with

290 The synthetic cyclic hexapeptide cWFW (cyclo(RRRWFW)) has a rapid bactericidal activity against

291 Dipeptide cyclo[(S)-His-(S)-Phe] 1, first applied by Inoue et al.

292 and 0.075nmol)], and specific MC4-R agonist (cyclo [ss-Ala-His-D-Phe-Arg-Trp-Glu]-NH2; 0.024nmol) bot

293 First, CYCLO stimulated lysosomal proteolytic activity by incre

294 content rivalling or exceeding that of HMX (cyclo-tetramethylene tetranitramine, a commonly used con

295 ture of a unique series of dinuclear group 5 cyclo-tetraphosphide inverted sandwich complexes.

296 by comparative studies of the corresponding cyclo-tetraphosphorus cation in [(PtBu)4Me][OTf] (10), w

297 ay intracerebroventricular administration of CYCLO to 8-month-old TgCRND8 mice that exhibit moderatel

298 e synthesis are a microwave-mediated [2+2+2] cyclo-trimerization reaction to construct the central be

299 a[NV(N[(t)Bu]Ar)3] (Na[4]) to yield trimeric cyclo-triphosphane [PNV(N[(t)Bu]Ar)3]3 (3) with a core c

300 ualed 79 mg x d(-1) x kg(-1), treatment with CYCLO within 24 h increased C movement out of the E/L co