ライフサイエンスコーパス: co-treatment

1 ession at 3 hours also was 300% higher after CO treatment.

2 ; this interaction is superior after 24 h of CO treatment.

3 TGF-beta(2) treatment and inhibited by MG132 co-treatment.

4 d that stimulated by FGF-2 was observed with co-treatment.

5 lt + furosemide, but not with spironolactone co-treatment.

6 liver toxicity caused by bortezomib and LPS co-treatment.

7 ects, an effect markedly attenuated by L-NNA co-treatment.

8 ports continuing current recommendations for co-treatment.

9 eased by approximately 50% with beta-agonist co-treatment.

10 naling inhibitor and epidermal growth factor co-treatment.

11 tes and culture medium following lithium-VPA co-treatment.

12 oprotection induced by FGF-21 or lithium-VPA co-treatment.

13 ith or without 3 weeks prior and 3 weeks BF2 co-treatment.

14 in were significantly enhanced by LMB and IR co-treatment.

15 o IGF-IR was significantly attenuated by PRL co-treatment.

16 ular fumarate concentrations after metformin co-treatment.

17 the start of treatment; however, AI/estrogen co-treatment allowed for 90-100% survival and the mainte

18 e mice while pioglitazone and estradiol (E2) co-treatment ameliorated TFH cells and GC responses in m

19 er) undergoes structural rearrangement after CO treatment, and the observed changes help reconcile th

20 uroprotective when added as a pre-treatment, co-treatment, and even at 2 h post-insult.

21 /24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these incremental los

22 MK801 co-treatment completely blocked the shortening in respon

23 tic studies further revealed that all of the co-treatments containing ABT-869 resulted in decreased a

24 HHTx under short-course tacrolimus RESULTS: CO treatment (d0-28, 0-100) was remarkably effective in

25 OnM pretreatment or co-treatment does not inhibit IFN gamma responses.

26 , which induced DUSP1 expression, plus IL1B (co-treatment), DUSP1 expression was further enhanced.

27 d diseases (STDs) have recommended empirical co-treatment for chlamydia when patients are treated for

28 include once-daily dosing, simplification of co-treatment for tuberculosis, preservation of ritonavir

29 - 137 microg/24 h, respectively); furosemide co-treatment further increased (p < 0.05) urinary Ca2+ a

30 cytosolic NAD(+)/NADH ratio, whereas oleate co-treatment had the opposite effect on cellular redox.

31 inical trials testing Akt and EGFR inhibitor co-treatment in patients with elevated phospho-Akt level

32 urred in patients taking both ACEI and BB as co-treatment, in whom the decrease in LVIDd and increase

33 dition, FGF-21 knockdown reduced lithium-VPA co-treatment-induced Akt-1 activation and neuroprotectio

34 l gastric cancer xenograft mouse model, drug co-treatments led to increased mouse survival as well as

35 Histological analyses revealed that CO treatment markedly reduced platelet aggregation withi

36 Lithium-VPA co-treatment markedly prolonged lithium-induced Akt-1 ac

37 Taken together, these findings suggest that CO treatment may provide a therapeutic approach for TBI

38 tic testing for STDs have changed over time, co-treatment may no longer be needed as a clinical or pu

39 By contrast, CO treatment of the reduced enzyme converted nearly all

40 nic lymphocytic leukemia cells revealed that co-treatment of 1alpha,25-dihydroxyvitamin D3 plus inhib

41 eased Src activity, which was abrogated with co-treatment of 2',5'-DOA.

42 Furthermore, co-treatment of AhR-deficient cells that expressed AhRY9

43 metformin induced PIM-2 kinase activity and co-treatment of ALL cells with a PIM-1/2 kinase inhibito

44 4HPR-induced apoptosis was unaffected by co-treatment of both cell lines with equimolar RAR antag

45 Co-treatment of cells with SMV (1 microM) inhibited Ang

46 Importantly, co-treatment of cells with the reactive carbonyl MGO and

47 Interestingly, co-treatment of corticostriatal slices with NR2A antagon

48 Co-treatment of cry1 seedlings with Ca-prohexadione plus

49 Co-treatment of cultures with the cathepsin B inhibitors

50 Co-treatment of DNA with Cr(VI)/Asc and mannitol, a Cr(V

51 h the peptide iRGD, as well as the effect of co-treatment of DOX and iRGD on tumor weight and cell de

52 bited differential expression in response to co-treatment of dsRNA and virus.

53 Drug sensitivity was restored with co-treatment of either HDIs or an IGF-1R inhibitor, in c

54 Co-treatment of estrogen-exposed HOSE, OCa, and MCF-7 ce

55 In contrast, we found that co-treatment of IL-10, a predominantly anti-inflammatory

56 Furthermore, co-treatment of MCF-7 cells with the PFKFB3 inhibitor an

57 Co-treatment of melanoma cell lines with WNT3A-condition

58 Further, co-treatment of microglia with CD40L and anti-CD45 antib

59 Furthermore, co-treatment of monocytes with ATRA and P. acnes inhibit

60 In addition, co-treatment of NGFDPC12 cells undergoing lipotoxicity w

61 Co-treatment of PDAC cells with lumican and gemcitabine

62 Co-treatment of phenformin enhances the effect of anti-P

63 Moreover, co-treatment of PL with NF-kappaB inhibitor phenylarsine

64 Notably, co-treatment of PL with p50 mutant plasmid (C62S) partia

65 Inhibition of ErbB4/EGFR with erlotinib co-treatment of podocytes suppressed this signaling.

66 Importantly, co-treatment of RA with TPA or TGF-beta further stimulat

67 In addition, co-treatment of RAR-beta(2)-positive cells with BPDE and

68 of IGF1R-beta and PDGFR-beta are reversed by co-treatment of the cells with a HA antagonist.

69 However, co-treatment of these cultures with any of the five diff

70 Our results show that co-treatment of TRAIL-resistant cancer cells with TRAIL

71 The effect of vorinostat co-treatment on the development of resistance to other c

72 hase inhibitor N(G)-nitro-L-arginine (L-NNA) co-treatment or scrambled C-peptide.

73 rcome by low concentrations of estrogen in a co-treatment paradigm with high ICI levels indicating th

74 en was added at the same time as the AI in a co-treatment paradigm, normal developmental appearance o

75 ulated by both clade B and C gp120, and METH co-treatment potentiated these effects.

76 Co-treatment promotes myelination in OLP-neuron co-cultu

77 ed by caspase-7 and PARP cleavage, and IGF-I co-treatment protected against this response.

78 Additionally, IL-10 co-treatment protected skeletal muscle from IL-6 and lip

79 CO treatment reduced IL-1beta and iNOS peak expression b

80 Oleate co-treatment restored most fluxes to their control level

81 nclude that chronic lumacaftor and ivacaftor co-treatment restores stability in a small subpopulation

82 After CO treatment, significant changes are observed in the EX

83 n the absence of radiation exposure, and LPS co-treatment significantly affected their radiation resp

84 Importantly, co-treatment strongly activates both signaling pathways,

85 er, race, etiology, NYHA classification, and co-treatment therapy.

86 The ability of lurasidone co-treatment to prevent the PCP-induced NOR deficit was

87 PT/5-FU co-treatment was more effective in Caco-2 cells.

88 and the effects of estrogen were observed by co-treatment with 17beta-estradiol (E2).

89 Co-treatment with a caspase inhibitor did not prevent th

90 This effect was mimicked by co-treatment with a growth factor (aFGF, bFGF or BDNF; b

91 Co-treatment with a peroxisome proliferator-activated re

92 the change in expression could be blocked by co-treatment with a specific PPARgamma antagonist.

93 apoptosis, effects that could be reversed by co-treatment with a specific PPARgamma antagonist.

94 Co-treatment with a tyrosine phosphatase inhibitor (sodi

95 istant to paclitaxel and are resensitized by co-treatment with ABT-737, a BH3-mimetic small molecule

96 Co-treatment with actinomycin D reduced the MQ induction

97 Co-treatment with AGN193109 prevents these responses.

98 In contrast, E(2) co-treatment with AI (E(2)+AI) rescued a significant num

99 in keratinocytes that is further enhanced by co-treatment with all-trans retinoic acid.

100 optosis in fetal rhombencephalic neurons and co-treatment with alpha-lipoic acid (LA) or one of sever

101 Therefore, we examined whether co-treatment with an inhibitor of excitotoxicity would a

102 This was not diminished by co-treatment with an inhibitor of polyamine oxidase, sug

103 Co-treatment with an ultra-low-dose (0.1 ng/kg, s.c.) of

104 ive action of VIP on gp120 was attenuated by co-treatment with anti-MIP-1alpha.

105 Co-treatment with anti-transferrin receptor antibody and

106 oconstriction was symmetrically regulated by co-treatment with AT1R agonist and antagonist.

107 Moreover, co-treatment with ATM and vincristine (VCR), a microtubu

108 QP2 localization to the apical membrane, but co-treatment with ATP internalized AQP2.

109 response, which was partially protected via co-treatment with beta-mercaptoethanol, resulting in red

110 Mechanistically, we found that co-treatment with BI2536 and metformin induced p53-depen

111 Co-treatment with BMP15 and FGF8 promoted glycolysis and

112 Co-treatment with both hormones caused a gel shift great

113 It was abrogated by co-treatment with both inhibitors, suggesting that H11-t

114 Co-treatment with calpain inhibitors resulted in preserv

115 er reduction of photoreceptor cell demise by co-treatment with calpastatin and salubrinal suggests co

116 Co-treatment with cAMP promoted/restored nuclear localiz

117 rboplatin enriches for CA125-negative cells, co-treatment with carboplatin and birinapant eliminates

118 Co-treatment with CcnE1-siRNA once a week was sufficient

119 Co-treatment with compound C attenuated PPARalpha activa

120 Moreover, co-treatment with CQ and zinc/copper chloride led to dec

121 ation and hsp72 transcription was blocked by co-treatment with cycloheximide.

122 s with various forms of viral immunogens and co-treatment with cytokines and chemokines is being used

123 proteins and receptors and was inhibited by co-treatment with Dickkopf-related protein-1, an extrace

124 activity against such tumors is augmented by co-treatment with differentiation-inducing agents such a

125 of intracellular thiols by diethylmaleate or co-treatment with dithiothreitol decreased the accumulat

126 tosis alone, they can often be sensitized by co-treatment with DNA-damaging agents such as etoposide.

127 is present at the Cyp1a1 enhancer only after co-treatment with E2 and TCDD, in MCF-7 cells.

128 oth overexpression of catalase as well as by co-treatment with Ebselen.

129 ontaneous OM which was partially reversed by co-treatment with either 100 nM E2 or G-1.

130 rs, BMP4-induced cell death was prevented by co-treatment with either neurotrophin-3 (NT-3) or nerve

131 These phenotypes are alleviated by co-treatment with either of two different chemical chape

132 The extent of apoptosis is increased by co-treatment with either the protein synthesis inhibitor

133 Co-treatment with ER antagonists ICI 182,780 or 4-hydrox

134 Moreover, co-treatment with ETO and NAC inhibits ETO-induced necro

135 otic effect could be partly prevented by the co-treatment with exogenous OPG.

136 FTI-276 and K-Ras processing is resistant to co-treatment with FTI-276 and GGTI-297.

137 bited receptor tyrosine phosphorylation, and co-treatment with FTI-277 had no additional effect.

138 ese responses were significantly enhanced by co-treatment with GABA.

139 Moreover, co-treatment with GGOH significantly (15-fold) attenuate

140 s observed to block MAPK activation by PDGF, co-treatment with GGOH, but not FOH, restored its activa

141 cked PDGF receptor tyrosine phosphorylation, co-treatment with GGOH, but not FOH, reversed the lovast

142 nd 78 +/- 6%, both of which were reversed by co-treatment with GGPP but not FPP.

143 -hexose cell content which was suppressed by co-treatment with glycogen synthase kinase 3 inhibitor S

144 Furthermore, co-treatment with H7 and the proteosome inhibitor LLnL p

145 t vincristine markedly decreased CAT levels; co-treatment with HGF and CNTF (but not either factor al

146 genic MAPK signaling increased ETC activity, co-treatment with HKL ablated this response and vastly e

147 sufficient to phenocopy cry1 seedlings, but co-treatment with IAA plus GA4 produced cry1-like growth

148 tment with the antiprogestin but enhanced by co-treatment with ICI.

149 Intriguingly, PRL co-treatment with IGF-I augments IGF-I receptor (IGF-IR)

150 This effect of TGF-beta1 was prevented by co-treatment with IGFBP-3-neutralizing antibodies or IGF

151 Co-treatment with IL-17A synergistically enhanced up-reg

152 Telomerase activation was countered by co-treatment with Imetelstat (GRN163L), a potent telomer

153 Co-treatment with inhibitors of autophagy results in mar

154 pression of XIAP and Bcl-xl was prevented by co-treatment with ipsapirone.

155 Co-treatment with kelatorphan stabilizes putative endoge

156 Co-treatment with L-mevalonate or GGPP, but not FPP or L

157 RNA was selectively and markedly elevated by co-treatment with lithium and VPA in primary rat brain n

158 n collagen synthesis, which was abrogated by co-treatment with losartan (an AT-1R antagonist), wortma

159 ase in PI3K activity, which was abolished by co-treatment with losartan or 2',5'-dideoxyadenosine (2'

160 GGOH co-treatment with lovastatin enhances inhibition of onco

161 ory effects were significantly diminished by co-treatment with LTB4 at 0.1 nM.

162 Co-treatment with MA and mTBI further reduced this activ

163 Co-treatment with MA further reduced DOPAC/DA ratios in

164 Co-treatment with MA further reduced the DOPAC/DA ratio.

165 Co-treatment with maximal concentrations of either IGF-1

166 APP protein, soluble APP, and APLP2, whereas co-treatment with mecamylamine (an antagonist of nicotin

167 ed neuronal cell death that was prevented by co-treatment with MIP-1alpha, suggesting that this endog

168 antly increased MUC5AC-luc activity, whereas co-treatment with mithramycin A, a Sp1 inhibitor, abolis

169 resulting in unwanted side effects requiring co-treatment with muscarinic antagonists.

170 lation of MIP-1 alpha mRNA was suppressed by co-treatment with N-acetylcysteine, a synthetic antioxid

171 Co-treatment with NO donors did not prevent IkappaBalpha

172 Co-treatment with nonselective ER inhibitor or ERalpha-s

173 Moreover, co-treatment with oleate prevented the increase in ceram

174 Furthermore, co-treatment with phen and Abeta peptides results in mic

175 ncrease in PI3K activity was also blocked by co-treatment with PP2, an Src inhibitor, or AG1478, an e

176 of the NF-kappaB target IL-8 was blocked by co-treatment with PPARgamma agonists, and direct inhibit

177 In addition, co-treatment with PRDC antagonized the inhibitory effect

178 In contrast, co-treatment with proteasome inhibitors and castanosperm

179 oxide insult resulted in 85% cell death, but co-treatment with pyruvate dose-dependently attenuated c

180 , and it could be significantly inhibited by co-treatment with rapamycin.

181 r (PXR)-humanized mouse model, we found that co-treatment with RIF and INH causes accumulation of the

182 ors observed in situ, which was prevented by co-treatment with RU-486 or WIN55,212-2.

183 ptor protein levels, which were prevented by co-treatment with RU-486.

184 anslocation in the HTM, which was blocked by co-treatment with sFRP1.

185 Co-treatment with spironolactone, PDTC, or NAC attenuate

186 Co-treatment with sulfhydryl nucleophiles completely pre

187 Interestingly, co-treatment with TAM and TNF-alpha drastically decrease

188 The results show that co-treatment with TAM and TNF-alpha increases the MnSOD

189 rease in CAR association with the OARE after co-treatment with TCPOBOP and OA, indicating the indirec

190 5) M), induced apoptosis that was blocked by co-treatment with the antiprogestin but enhanced by co-t

191 tralizing this second mode of action through co-treatment with the beta-blocker propranolol, while le

192 In contrast, co-treatment with the classical GRP inducers thapsigargi

193 2F1-dependent dormancy is recapitulated by a co-treatment with the DNA-demethylating agent 5-Aza-C an

194 OR-P labeling was dose-dependent, blocked by co-treatment with the kappa antagonist norbinaltorphimin

195 Interestingly, co-treatment with the KMO inhibitor Ro 61-8048 reversed

196 ionophore-mediated increase, was blocked by co-treatment with the mitogen-activated protein (MAP) ki

197 o glutamate-induced excitotoxicity, and that co-treatment with the mood stabilizers lithium and valpr

198 Co-treatment with the nitric oxide (NO) donor L-arginine

199 In addition, in the face of NOS blockade, co-treatment with the NO donor sodium nitroprusside or t

200 AR phosphorylation was completely blocked by co-treatment with the PKC inhibitor, bisindolylmaleimide

201 ased c-Myc degradation, which was reduced by co-treatment with the proteasomal inhibitor, MG-132.

202 the replication forks and was attenuated by co-treatment with the proteasome inhibitor MG-132.

203 This degradation was abrogated by co-treatment with the proteasome inhibitor MG132.

204 Co-treatment with the protein phosphatase inhibitor okad

205 in WT vs. CD-WT mice, which was prevented by co-treatment with the reactive oxygen species scavenger

206 Co-treatment with the reactive oxygen species scavenger

207 Co-treatment with the receptor tyrosine kinase inhibitor

208 Co-treatment with the TrkB antagonist ANA-12 blocked HDA

209 nto the mechanism of liver injury induced by co-treatment with these compounds and may lead to their

210 nduced apoptotic cell shape changes, whereas co-treatment with this antibody plus V(+)H(+) reversed t

211 the promoters of MCP-1 and CINC-2beta during co-treatment with TNF-alpha and E2.

212 Co-treatment with TNFalpha and PMA did not result in a s

213 e site 311, which was effectively blocked by co-treatment with TSKI.

214 Co-treatment with tyramine and histamine was associated

215 Co-treatment with ultra-low-dose naltrexone or nor-binal

216 Co-treatment with XBP1 inhibitors reduced IL6 and IL8 pr

217 trations were equally protective and whether CO treatment would be effective in a large animal specie