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

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

5 ular fumarate concentrations after metformin co-treatment.

6 L-1beta, which was markedly amplified by TNF co-treatment.

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

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

9 ns after evaluation of confounders including co-treatment.

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

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

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

13 ports continuing current recommendations for co-treatment.

14 d with rifampin-containing tuberculosis (TB) co-treatment.

15 sensitivity to KCL that was prevented by HCQ co-treatment.

16 forming optimisation of HIV and tuberculosis co-treatment.

17 rphology, this was also abolished after BoxA co-treatment.

18 e to trametinib and were resensitized by JQ1 co-treatment.

19 naling inhibitor and epidermal growth factor co-treatment.

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

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

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

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

24 previously reported that minocycline (MINO) co-treatment abrogates olanzapine (OLZ)-induced hyperpha

25 Mechanistically, TNF-a and IFN-y co-treatment activated the JAK/STAT1/IRF1 axis, inducing

26 Mechanistically, TNF-alpha and IFN-gamma co-treatment activated the JAK/STAT1/IRF1 axis, inducing

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

28 The bergenin co-treatment also reduced isoniazid-induced immune impai

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

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

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

32 synergize with pharmacological and physical co-treatments, and should be increasingly integrated in

33 and dose adjustments or drug switches during co-treatment are commonly required.

34 /24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these incremental los

35 ory genes that was not aggravated by Abeta42 co-treatment but reversed by NL.

36 Mechanistically, we demonstrate that Bar co-treatment can effectively maintain the sensitivity of

37 MK801 co-treatment completely blocked the shortening in respon

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

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

40 crystalline, ~5 nm particles (Pd(NP)) during CO treatment, deactivating Pd(1)/TiO(2).

41 ents indicated that vactosertib+pomalidomide co-treatment decreased the viability of MM cell lines an

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

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

44 teine (NAC, 2.5 mM for 1 h) followed by METH co-treatment for 48 h rescued the cells completely from

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

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

47 - 137 microg/24 h, respectively); furosemide co-treatment further increased (p < 0.05) urinary Ca2+ a

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

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

50 In conclusion, dandelion/ATRA co-treatment, in addition to having strong cytotoxic eff

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

52 Simvastatin and TCDD (S + T) co-treatment increased hepatic AHR-battery gene expressi

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

54 However, HIV and tuberculosis co-treatment is challenging due to drug-drug interaction

55 In addition, the S + T co-treatment led to an increase in hepatic glycogen cont

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

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

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

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

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

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

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

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

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

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

66 Moreover, it was found that the co-treatment of BAY 11-7082 and TMZ significantly contri

67 Notably, co-treatment of bortezomib and SP1017 intensifies SP1017

68 4HPR-induced apoptosis was unaffected by co-treatment of both cell lines with equimolar RAR antag

69 In contrast, co-treatment of CBD-targeted cells with inhibitors of PI

70 ay with reversal of cell death observed with co-treatment of cells with an apoptosis inhibitor, Z-VAD

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

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

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

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

75 Co-treatment of cultures with the cathepsin B inhibitors

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

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

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

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

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

81 Additionally, co-treatment of HPA-12 and Crenolanib is effective in FL

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

83 Co-treatment of LPS along with IL-10-loaded exosomes, re

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

85 Co-treatment of Mcl-1-sensitive and Mcl-1 insensitive lu

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

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

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

89 Co-treatment of neuroblastoma cells with inhibitors of M

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

91 Finally, the co-treatment of Paclitaxel and fenofibric acid (fibrates

92 Co-treatment of PDAC cells with lumican and gemcitabine

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

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

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

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

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

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

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

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

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

102 Additionally, co-treatment of wild-type embryos with testosterone and

103 Co-treatment of y-aminobutyric acid receptor antagonist

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

105 riectomised mice, the osteogenic benefits of co-treatment on the trabecular bone were lower than load

106 sing antibodies or antagonists may provide a co-treatment opportunity for patients undergoing chemoth

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

108 ated with fucoxanthin and H(2)O(2) for 24 h (co-treatment) or pre-treated with fucoxanthin for 24 h f

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

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

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

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

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

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

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

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

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

118 more closely resembled those found upon 4-MU co-treatment resulted from MMP2/9 inhibition, suggesting

119 Co-treatment resulted in higher levels of Sch-B and 5-FU

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

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

122 The results revealed that the co-treatment significantly altered cell proliferation by

123 dentified several pathways where simvastatin co-treatment significantly impacted TCDD-induced changes

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

125 Cortical thickness was higher with co-treatment than in the mice treated with PTH alone.

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

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

128 Co-treatment was considered acceptable if > 80% of parti

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

130 Furthermore, co-treatment with 16 significantly improved the F508del-

131 Moreover, co-treatment with 17(18)-EpETE and 19(20)-EpDPA and the

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

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

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

135 Co-treatment with a peroxisome proliferator-activated re

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

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

138 Co-treatment with a tyrosine phosphatase inhibitor (sodi

139 In vivo co-treatment with AAV-miRzip-21 and AAV-miR-7 in mice be

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

141 d H1299 cells with leptin and decreased upon co-treatment with AChE and/or inhibitors targeting PKC,

142 Co-treatment with actinomycin D reduced the MQ induction

143 oligomers compared to the controls, however, co-treatment with AD therapeutics (Donepezil, Memantine,

144 This effect was enhanced by co-treatment with adenoviral vectors encoding SOX17.

145 B, IsdA and MntC vaccines can be overcome by co-treatment with adjuvants that promote IL-17A and IFN-

146 Co-treatment with AGN193109 prevents these responses.

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

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

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

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

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

152 undergoing endovascular thrombectomy without co-treatment with an intravenous thrombolytic agent.

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

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

155 Co-treatment with anti-transferrin receptor antibody and

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

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

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

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

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

161 Co-treatment with BMP15 and FGF8 promoted glycolysis and

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

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

164 Co-treatment with calpain inhibitors resulted in preserv

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

166 Co-treatment with cAMP promoted/restored nuclear localiz

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

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

169 o effect on HTT aggregate number, but a 72 h co-treatment with chloroquine (CQ) in GFP-72Q-expressing

170 Furthermore, co-treatment with chronic convallatoxin reduced morphine

171 lactate functions by regulating HDACs using co-treatment with CI-994, a brain-permeable class I HDAC

172 Co-treatment with compound C attenuated PPARalpha activa

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

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

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

176 Co-treatment with dexamethasone and cisplatin restores c

177 cts on placental gene expression compared to co-treatment with DHT and insulin.

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

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

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

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

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

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

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

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

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

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

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

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

190 Indeed, co-treatment with EWH prevented catalepsy, hippocampal o

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

192 Importantly, either co-treatment with FGF-receptor inhibitors or removal of

193 In wild-type mice, co-treatment with flutamide, an androgen receptor antago

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

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

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

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

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

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

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

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

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

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

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

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

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

207 Co-treatment with IGF-1 further elevated the levels of t

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

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

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

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

212 Co-treatment with inhibitors of autophagy results in mar

213 le ipatasertib resistance can be reversed by co-treatment with inhibitors of pathways including PIM s

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

215 Co-treatment with kelatorphan stabilizes putative endoge

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

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

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

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

220 GGOH co-treatment with lovastatin enhances inhibition of onco

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

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

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

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

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

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

227 These changes were specifically blocked by co-treatment with MINO.

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

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

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

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

232 Co-treatment with NO donors did not prevent IkappaBalpha

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

234 Co-treatment with novel nNOS inhibitors effectively alle

235 Co-treatment with OCA or INT-767 did not affect ACTA2 an

236 However, co-treatment with OIFE ameliorates D-gal-induced these i

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

238 tigate the use of ICRF193 in chemotherapy in co-treatment with other drugs.

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

240 loratory analysis indicated that vactosertib co-treatment with pomalidomide also reduced TGFbeta leve

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

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

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

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

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

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

247 Co-treatment with recombinant S100 calcium-binding prote

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

249 Co-treatment with RSV and insulin reduced the levels of

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

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

252 f murine neutrophils, which was prevented by co-treatment with S1P.

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

254 inocytes to TX100 were attenuated by pre- or co-treatment with SPD (100 mg/ml).

255 Co-treatment with specific UPR(ER) pathway inhibitors re

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

257 monosialotetrahexosylganglioside levels, and co-treatment with standard chemotherapeutics sensitized

258 Co-treatment with sulfhydryl nucleophiles completely pre

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

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

261 s was confirmed by TBK1 genetic knockdown or co-treatment with TBK1-specific inhibitor (MRT67307).

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

263 Co-treatment with testosterone was shown to have an anti

264 We observed that co-treatment with the anti-TB drug isoniazid and bergeni

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

266 Co-treatment with the BCL-2-specific inhibitor venetocla

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

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

269 2F1-dependent dormancy is recapitulated by a co-treatment with the DNA-demethylating agent 5-Aza-C an

270 Co-treatment with the entry inhibitor Myrcludex B ensure

271 Co-treatment with the GPR68 activator Ogerin or medium a

272 atment, and then reduced to <3 muM after the co-treatment with the herbal drug silymarin.

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

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

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

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

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

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

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

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

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

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

283 Co-treatment with the protein phosphatase inhibitor okad

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

285 Co-treatment with the reactive oxygen species scavenger

286 Co-treatment with the receptor tyrosine kinase inhibitor

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

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

289 In fact, like EPA/DHA, co-treatment with these metabolites prevented cytokines-

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

291 Co-treatment with TIMP-1, TIMP-3, mTC1, or mTC3 signific

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

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

294 Co-treatment with TSA and LPS enhanced pro-inflammatory

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

296 Co-treatment with tyramine and histamine was associated

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

298 However, co-treatment with wounding in addition to NbGLA1 inducti

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

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