ライフサイエンスコーパス: naloxone

1 nontransport after reversal of overdose with naloxone.

2 s, which express npr-17, did not response to naloxone.

3 are facility after reversal of overdose with naloxone.

4 ith pertussis toxin or the opioid antagonist naloxone.

5 ncement when co-administration with low dose naloxone.

6 -2200 was prevented by pre-administration of naloxone.

7 dence counseling; all received buprenorphine-naloxone.

8 ith pertussis toxin or the opioid antagonist naloxone.

9 e 2 success rates while taking buprenorphine-naloxone.

10 rrolidin-1-yl)methyl)phenoxy)benzamide], and naloxone.

11 without concurrent exposure to valsartan or naloxone.

12 ycemia, and this inhibition was prevented by naloxone.

13 ot reversed by a saturating concentration of naloxone.

14 of office-based treatment with buprenorphine-naloxone.

15 need assisted ventilation, and occasionally naloxone.

16 indirectly involved in analgesia produced by naloxone.

17 ex than lactic acid alone in the presence of naloxone.

18 eptibility to precipitation of withdrawal by naloxone.

19 ing negative-affective states in response to naloxone.

20 e independently more likely to be prescribed naloxone.

21 ) compared with patients who did not receive naloxone.

22 receiving long-term opioids were prescribed naloxone.

23 as rapidly reversed by the opioid antagonist naloxone.

24 n G carriers is blocked by pretreatment with naloxone.

25 kg) preceded by either saline (Sal-Nalb) or naloxone 0.4 mg (Nalox-Nalb).

26 nous administration of the opioid antagonist naloxone (0.15 mg/kg bolus + 0.1 mg/kg/h infusion) or sa

27 Pretreatment with naloxone (1 mg/kg, intravenously) resulted in a uniform

28 Pretreatment with naloxone (1 mg/kg, intravenously) resulted in a uniform

29 , the nonspecific opioid receptor antagonist naloxone (1 mum) enhanced MF transmission but there was

30 e preferential mu-opioid receptor antagonist naloxone (1, 10, or 30 mg/kg), decreased selective aggre

31 ults in remarkably similar rapid blocking of naloxone (10 microg/kg)-precipitated withdrawal hyperalg

32 esia is evoked by injection of a low dose of naloxone (10 microg/kg, s.c.) in naive mice after acute

33 ific effect blocked by the opioid antagonist naloxone (10 muM).

34 d-release naltrexone and 79 to buprenorphine-naloxone; 105 (66.0%) completed the trial.

35 ed twice, before and after administration of naloxone (16 mg intravenous; n = 9) and codeine (60 mg o

36 for 16 weeks (starting dose oxycodone 5 mg, naloxone 2.5 mg, twice daily).

37 al found that lower-concentration intranasal naloxone (2 mg/5 mL) was less effective than intramuscul

38 cacy between higher-concentration intranasal naloxone (2 mg/mL) and intramuscular naloxone, and 1 tri

39 Higher-concentration intranasal naloxone (2 mg/mL) seems to have efficacy similar to tha

40 s were pretreated with the opioid antagonist naloxone (3 mg/kg; intraperitoneally).

41 injury, the effects of the opioid antagonist naloxone (3 mg/kg; IP) on retinal neuroprotection induce

42 pendent rats, the opioid receptor antagonist naloxone (30 microg/kg) increased heroin consumption and

43 ould be reversed by the mu-opioid antagonist naloxone 4 months after gene transfer (P < 0.001).

44 ither daily oral flexible dose buprenorphine-naloxone, 4 to 24 mg/d, or extended-release naltrexone h

45 is analgesia is blocked by pretreatment with naloxone, a mu-opioid antagonist.

46 Blockade of OGF-OGFr interactions with naloxone abolished the increased expression of p16 prote

47 nd postnatal mortality, was conferred by (+)-naloxone administration after intrauterine administratio

48 ized trials that compared different doses of naloxone, administration routes, or transport versus non

49 l cyclase superactivation in the presence of naloxone after long-term treatment with morphine, etorph

50 Injection of either Leu-Enk or naloxone alone significantly increased the testicular in

51 (+)-Naloxone also reduced opioid (remifentanil) self-adminis

52 Naloxone ameliorated the clinical progression and severi

53 emonstrated that the opioid receptor blocker naloxone ameliorates HAAF.

54 Microinjections of naloxone (an opioid receptor antagonist) into the mNTS (

55 Naloxone, an opioid antagonist, restores HPA axis respon

56 The role of naloxone, an opioid receptor antagonist, on microglial i

57 onian rats; this effect was fully blocked by naloxone, an opioid receptor antagonist.

58 loxone methiodide (a peripherally restricted naloxone analog) and by local administration at the infl

59 We report the assessment of (+)-naloxone and (+)-naltrexone on the acute dopaminergic ef

60 mental conditions, the TLR4 antagonists, (+)-naloxone and (+)-naltrexone, did not specifically block

61 ion was obtained at the highest doses of (+)-naloxone and (+)-naltrexone, those doses also attenuated

62 Naloxone and a combination of mu and delta opioid recept

63 Naloxone and baclofen significantly reduced the stimulat

64 withdrawal by the opioid receptor antagonist naloxone and by the selective kappa-opioid receptor subt

65 -dependent migration effect was inhibited by naloxone and confirmed to be mu-opioid receptor-dependen

66 Naloxone and morphine were synergistic in NY1DD mice, su

67 gesia was reversed by the opioid antagonists naloxone and naloxone methiodide (a peripherally restric

68 Recently, the (+)-enantiomers of naloxone and naltrexone, TLR4 antagonists, have been rep

69 and administration of the opioid antagonist naloxone and placebo saline.

70 n silico and biophysical data to support (+)-naloxone and remifentanil binding to TLR4/MD2.

71 e evaluated in other mice injected s.c. with naloxone and tested for precipitated withdrawal.

72 and both the nonselective opioid antagonist naloxone and the kappa-selective blocker norbinaltorphim

73 santness reductions between the meditation + naloxone and the meditation + saline groups.

74 time in opioid dose among those who received naloxone and those who did not (IRR, 1.03 [CI, 0.91 to 1

75 s, as indicated by its sensitivity to spinal naloxone and to the selective mu1-opioid receptor antago

76 ranasal naloxone (2 mg/mL) and intramuscular naloxone, and 1 trial found that lower-concentration int

77 l10 in fetal membranes was suppressed by (+)-naloxone, and cytokine expression in the placenta, and u

78 (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH(2)), naloxone, and naltrexone behave like partial agonists.

79 eraction with the opioid receptor antagonist naloxone, and two-way analgesic cross-tolerance with mor

80 Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH(2)) and naloxone, antagonists of mu-opioid receptors, blocked mu

81 Tapentadol and oxycodone-naloxone are found to exhibit better tolerability charac

82 sal dentate gyrus infusions of either APV or naloxone attenuated detection of a spatial change, where

83 This effect was blocked with naloxone before each mating session; thus, VTA dopamine

84 [(3)H]Naloxone binding in membranes of the thalamus showed no

85 Furthermore, [(3)H]naloxone binding indicated a lack of mu receptor downreg

86 DAMGO-stimulated [(35)S]GTPgammaS and [(3)H]naloxone binding reveals that the anatomical distributio

87 gonist, carboxynitroveratryl-naloxone (caged naloxone), blocked the current induced by a series of ag

88 nistration of the opioid receptor antagonist naloxone blocks acute CB1R-induced feeding.

89 Buprenorphine-naloxone (BUP) is an effective treatment of opioid depen

90 oid antagonist, and sublingual buprenorphine-naloxone (BUP-NX), a partial opioid agonist, are pharmac

91 of a subset of these genes was preserved by naloxone but not valsartan.

92 ocorticoid secretion, a failure prevented by naloxone but not valsartan.

93 /5 mL) was less effective than intramuscular naloxone but was associated with decreased risk for agit

94 this series was found to be more potent than naloxone but weaker than 1.

95 of a caged antagonist, carboxynitroveratryl-naloxone (caged naloxone), blocked the current induced b

96 Naloxone can be coprescribed to primary care patients pr

97 signaling with the novel TLR4 antagonist (+)-naloxone can suppress the inflammatory cascade of preter

98 Carboxynitroveratryl-naloxone (CNV-NLX), a caged analog of the competitive op

99 lar, middle cingulate cortices, and putamen; naloxone co-admistration reduced all connectivity to non

100 Tapentadol was followed by oxycodone-naloxone combination in providing better tolerability an

101 e use of buprenorphine and the buprenorphine-naloxone combination.

102 Dynorphin A (1-13), U69,593 and naloxone competitively inhibited [3H]diprenorphine bindi

103 atment of animals with the opioid antagonist naloxone, confirming opioid receptor-mediated analgesia.

104 Naloxone decreased the surface/intracellular ratio and s

105 In mice, (+)-naloxone did not decrease drinking-in-the-dark and only

106 Naloxone did not prevent the initial experience-induced

107 in 37% of iterations and the combination of naloxone distribution and linkage to addiction treatment

108 health benefit for a particular budget) were naloxone distribution combined with linkage to addiction

109 ge to addiction treatment (cost saving), and naloxone distribution combined with PrEP and linkage to

110 Naloxone distribution for lay administration.

111 Naloxone distribution increased costs by $53 (CI, $3 to

112 ctiveness ratio (ICER) of $323 per QALY, and naloxone distribution plus linkage to addiction treatmen

113 itional intervention, naloxone distribution, naloxone distribution plus linkage to addiction treatmen

114 atment, naloxone distribution plus PrEP, and naloxone distribution plus linkage to addiction treatmen

115 ibution plus linkage to addiction treatment, naloxone distribution plus PrEP, and naloxone distributi

116 ompared with no additional intervention, the naloxone distribution strategy yielded an incremental co

117 INTERPRETATION: Naloxone distribution through syringe service programmes

118 Naloxone distribution to heroin users is likely to reduc

119 Naloxone distribution was cost-effective in all determin

120 Combining naloxone distribution with linkage to addiction treatmen

121 tive strategies: no additional intervention, naloxone distribution, naloxone distribution plus linkag

122 A strategy that combines naloxone distribution, PrEP, and linkage to addiction tr

123 tic sensitivity analysis, the combination of naloxone distribution, PrEP, and linkage to addiction tr

124 s, 6% of overdose deaths were prevented with naloxone distribution; 1 death was prevented for every 2

125 Thus, OR blockade with naloxone during antecedent exercise prevents the develop

126 reward and memory in male rats treated with naloxone during mating experience, either systemically o

127 xone treatment; if tapered off buprenorphine-naloxone, even after 12 weeks of treatment, the likeliho

128 ptor antagonist, nor-binaltorphimine, blocks naloxone-evoked hyperalgesia in GM1-pretreated naive mic

129 Twelve-day-old pups given naloxone (Experiment 1A) or baclofen (Experiment 1B) bef

130 action was found to be higher with oxycodone-naloxone followed by fentanyl and tapentadol.

131 ve efficacy similar to that of intramuscular naloxone for reversal of opioid overdose, with no differ

132 e group was noninferior to the buprenorphine-naloxone group (difference, -0.1; with 95% CI, -0.2 to 0

133 gh 12, patients in the 12-week buprenorphine-naloxone group reported less opioid use (chi(2)(1) = 18.

134 Patients in the 12-week buprenorphine-naloxone group were prescribed up to 24 mg per day for 9

135 Drug development strategies involving naloxone have been initiated to reduce peripheral opioid

136 Both naloxone hydrochloride and naloxone methiodide treatment

137 Naloxone hydrochloride completely abolished morphine-ind

138 ve as daily buprenorphine hydrochloride with naloxone hydrochloride in maintaining abstinence from he

139 were studied during intravenous infusion of naloxone hydrochloride or naloxone methiodide.

140 In the NY1DD mice, naloxone (i.c.v.) possessed approximately 300-fold great

141 .) but not by the opioid receptor antagonist naloxone (i.p.).

142 randomized to receive intravenous saline or naloxone immediately before sham and real left DLPFC rTM

143 s of FeTMPyP(5+) were abrogated by intra-RVM naloxone, implicating potential interplay between PN and

144 Continuing treatment with buprenorphine-naloxone improved outcome compared with short-term detox

145 dogenous opioid peptide agonists released by naloxone in GM1-treated mice, so that analgesia is evoke

146 is based on the local antagonist activity of naloxone in intestinal opioid receptors and the negligib

147 naltrexone was as effective as buprenorphine-naloxone in maintaining short-term abstinence from heroi

148 and (3) injection of the TLR4 antagonist (+)-naloxone in mice.

149 less severe opioid withdrawal symptoms than naloxone in morphine-dependent mice.

150 Providing naloxone in primary care settings may have ancillary ben

151 In contrast to its effects on low singers, naloxone in the POM of high singers dose dependently dec

152 isomer of the opioid receptor antagonist (-)-naloxone, in infection-associated preterm birth.

153 Similar antagonism of naloxone-induced analgesia also was observed when NY1DD

154 c shell of morphine-dependent rats prevented naloxone-induced conditioned place aversions and decreas

155 tagonist of GluA2-lacking AMPARs, attenuated naloxone-induced decreases in sensitivity to brain stimu

156 Microarray analysis suggested naloxone-induced down-regulation of the CC chemokine rec

157 ctivation of CaMKII and CREB, and absence of naloxone-induced withdrawal jumping.

158 Naloxone infused into either the ventral pallidum or nuc

159 Conversely, naloxone infused into the basolateral amygdala blocked f

160 -min hyperinsulinemic-euglycemic clamps plus naloxone infusion (control); 2) two 90-min hyperinsuline

161 c clamps with exercise at 60% Vo(2max), plus naloxone infusion (N+); or 3) same protocol as in the N+

162 However, naloxone infusion failed to reverse meditation-induced a

163 detection of a spatial change, whereas only naloxone infusions disrupted novel object detection.

164 uated detection of a spatial change, whereas naloxone infusions into dorsal CA1 disrupted novel objec

165 Either APV or naloxone infusions into dorsal CA3 disrupted both spatia

166 rforant path plasticity can be attenuated by naloxone infusions.

167 ked opioid receptor activity in the POM with naloxone injections and found that this increased both s

168 These effects were naloxone insensitive and thus are not opioid receptor me

169 to demonstrate that direct administration of naloxone into the POM influences sexually motivated song

170 stered with a mu-opioid receptor antagonist, naloxone, invoked a supralinear enhancement of prolonged

171 Acute MWD induced place aversion occurs when naloxone is administered 24 h following a single exposur

172 Naloxone is effective for reversing opioid overdose, but

173 ibution; 1 death was prevented for every 227 naloxone kits distributed (95% CI, 71 to 716).

174 compared in opioid-dependent, buprenorphine-naloxone-maintained, human immunodeficiency virus (HIV)-

175 The present study suggests that naloxone may be clinically useful in the treatment of pa

176 istered to GM1-treated mice, we suggest that naloxone may evoke hyperalgesia by inducing release of e

177 ersed by the opioid antagonists naloxone and naloxone methiodide (a peripherally restricted naloxone

178 We studied whether naloxone methiodide alters abnormal motility pattern ind

179 d morphine-induced RPCs in all dogs, whereas naloxone methiodide converted morphine-induced RPCs to a

180 Naloxone methiodide may be useful to prevent the undesir

181 Both naloxone hydrochloride and naloxone methiodide treatment virtually abolished the em

182 ased endogenous opioid function, naloxone or naloxone methiodide was administered.

183 agonists naloxone or peripherally restricted naloxone methiodide were administered, and pain was asse

184 Thus, naloxone methiodide, which does not cross the BBB, antag

185 venous infusion of naloxone hydrochloride or naloxone methiodide.

186 Naloxone modulates microglia accumulation and activation

187 ration of the nonopioid, unnatural isomer of naloxone, (+)-naloxone (rats), or two independent geneti

188 The opioid antagonists naloxone/naltrexone are involved in improving learning a

189 In vitro prolonged naloxone/naltrexone exposure significantly increased syn

190 We investigated the effect of naloxone/naltrexone on hippocampal alpha-amino-3-hydroxy

191 To measure naloxone/naltrexone-regulated AMPAR trafficking, pHluori

192 ecipitated by subcutaneous administration of naloxone (NLX) (2 mg/kg).

193 ays for entry of the nonselective antagonist naloxone (NLX) from the water environment into the well-

194 Meanwhile, intrathecal pretreatment with naloxone, non-selective opioid receptor antagonist, did

195 the effect of nalbuphine or nalbuphine plus naloxone on activity in brain regions that may explain t

196 The authors evaluated the effects of naloxone on Ccl2(-/-)/Cx3cr1(-/-) (DKO) mice, a murine m

197 ephalin (Met-Enk), and the opioid antagonist naloxone on gonad development in the Eastern lubber gras

198 exone showed noninferiority to buprenorphine-naloxone on group proportion of total number of opioid-n

199 The potential therapeutic effects of naloxone on retinal degeneration, including AMD, warrant

200 comes were proportion of patients prescribed naloxone, opioid-related emergency department (ED) visit

201 Pretreatments with (+)-naloxone or (+)-naltrexone did not attenuate, and under

202 were randomized to 12 weeks of buprenorphine-naloxone or a 14-day taper (detox).

203 Blood ethanol levels were not affected by naloxone or baclofen (Experiment 2).

204 th the readily reversible opioid antagonists naloxone or buprenorphine before norBNI responded strong

205 gnificantly altered by the administration of naloxone or codeine.

206 The presence of antagonists (naloxone or CTAP) during chronic morphine treatment inhi

207 ult of increased endogenous opioid function, naloxone or naloxone methiodide was administered.

208 re given daily intraperitoneal injections of naloxone or PBS for 2 months.

209 postsurgery, the opioid receptor antagonists naloxone or peripherally restricted naloxone methiodide

210 prior treatment with the opiate antagonist l-naloxone or the constitutive NO synthase inhibitor N(G)-

211 d by pretreatment with the opioid antagonist naloxone or the Src kinase inhibitor 4-amino-5-(4-chloro

212 he mu antagonist pharmacophores (naltrexone, naloxone, or nalbuphine) at the other end.

213 esic efficacy of prolonged-release oxycodone-naloxone (OXN PR) in patients with Parkinson's disease a

214 show a decline in avoidance of the formerly naloxone-paired chamber with increasing numbers of extin

215 s and the negligible oral bioavailability of naloxone, particularly in a prolonged-release formulatio

216 5% CI = 38%-70%) vs 52 12-week buprenorphine-naloxone patients (23%; 95% CI = 11%-35%).

217 [CI] = 47%-75%) vs 58 12-week buprenorphine-naloxone patients (26%; 95% CI = 14%-38%).

218 5% CI = 35%-67%) vs 49 12-week buprenorphine-naloxone patients (43%; 95% CI = 29%-57%).

219 treatment vs 52 of 74 12-week buprenorphine-naloxone patients (70%; chi(2)(1) = 32.90, P < .001).

220 Here we reveal that the opioid antagonist naloxone possesses potent analgesic activity in two tran

221 ade of morphine binding to PAG TLR4 with (+)-naloxone potentiated morphine antinociception significan

222 Application of the opioid antagonist naloxone potentiates noxious peripheral input into the s

223 In addition, JZL184 or PF-3845 blocked naloxone-precipitated hypersecretion in morphine-depende

224 e exhibited a trend (P = 0.055) toward fewer naloxone-precipitated jumps compared with CB2KO mice.

225 y tying enhanced cAMP-driven GABA release to naloxone-precipitated morphine withdrawal in the VTA.

226 Following naloxone-precipitated morphine withdrawal, NE release an

227 s of morphine and the aversive components of naloxone-precipitated morphine withdrawal.

228 he basolateral amygdala, interfered with the naloxone-precipitated MWD induced place aversion.

229 fatty acid amide hydrolase (FAAH) attenuates naloxone-precipitated opioid withdrawal signs in mice vi

230 eir drug intake over time and exhibited both naloxone-precipitated somatic signs of opioid withdrawal

231 sufentanil vapor), LgA rats again developed naloxone-precipitated somatic signs of withdrawal and sp

232 OW-CPA through pairings of one chamber with naloxone-precipitated withdrawal and the other chamber w

233 Low-dose naloxone-precipitated withdrawal hyperalgesia is a relia

234 as used to induce dependence, as revealed by naloxone-precipitated withdrawal in saline or mismatch-p

235 overflow during acute morphine exposure and naloxone-precipitated withdrawal in two regions associat

236 Chronic morphine exposure and naloxone-precipitated withdrawal increase activity of sp

237 endence was evaluated by quantifying/scoring naloxone-precipitated withdrawal signs.

238 ncomitantly promotes analgesic tolerance and naloxone-precipitated withdrawal, whereas downregulation

239 d clinic staff were trained and supported in naloxone prescribing.

240 Patients who received a naloxone prescription had 47% fewer opioid-related ED vi

241 d with a reversal of this reprogramming, and naloxone preserves some responses to hypoglycemia by pre

242 Naloxone pretreatment largely abolished rTMS-induced ana

243 Naloxone pretreatment to nalbuphine produced changes in

244 and this protective response was reversed by naloxone pretreatment.

245 Treatment with (+)-naloxone prevented preterm delivery and alleviated fetal

246 Intravenous naloxone produced 50% and 44% decreases in the specific-

247 Furthermore, mindfulness meditation during naloxone produced significantly greater reductions in pa

248 nonopioid, unnatural isomer of naloxone, (+)-naloxone (rats), or two independent genetic knock-outs o

249 In addition, morphine and naloxone respectively stimulated and inhibited feeding i

250 lying the joint was transiently increased in naloxone-responsive mice.

251 d evoke a pressor reflex), endomorphin-2 and naloxone resulted in a significantly greater pressor res

252 The non-selective opioid antagonist, naloxone, returned the water content nearly back to orig

253 Pretreatment with naloxone reversed both the functional and structural ret

254 Inhibition of the PVN with naloxone reversed the EA-inhibition.

255 Naloxone reversed the morphine-induced suppression of TN

256 synaptic release of opioid peptides and to a naloxone-reversible hypoalgesic/antiallodynic phenotype.

257 mic administration of the opiate antagonist, naloxone, robustly increased LC discharge rate in a mann

258 To synthesize evidence on 1) the effects of naloxone route of administration and dosing for suspecte

259 Nontransport after reversal of overdose with naloxone seems to be associated with a low rate of serio

260 Co-administration/pretreatment of naloxone selectively blocked activity in pulvinar, pons

261 aracteristics of both analgesia and algesia; naloxone selectively blocks activity in areas associated

262 chronic pain, intra-RVM FeTMPyP(5+) produced naloxone-sensitive reversal of mechanical allodynia in r

263 The antiallodynic effect of TGF-beta1 was naloxone-sensitive.

264 ial pressure, and spinal fluid drainage with naloxone (SFDN).

265 Naloxone significantly reduces the progress of retinal l

266 ment (phase 1) included 2-week buprenorphine-naloxone stabilization, 2-week taper, and 8-week postmed

267 uction in paraplegia risk using hypothermia, naloxone, steroids, spinal fluid drainage, intercostal l

268 t buprenorphine or with either naltrexone or naloxone, structurally related MOR antagonists.

269 NX was daily self-administered buprenorphine-naloxone sublingual film (Suboxone; Indivior).

270 tment with either methadone or buprenorphine/naloxone (Suboxone) over a 24-week open-label clinical t

271 reversible by intrathecal administration of naloxone, suggesting an opioid-mediated mechanism; pharm

272 ferential mu-opioid receptor inverse agonist naloxone, suggesting the participation of mu-opioid rece

273 fter induction with sublingual buprenorphine-naloxone tablets, patients received either 4 buprenorphi

274 s 8 weeks after completing the buprenorphine-naloxone taper (phase 2, week 24) dropped to 8.6% (31 of

275 were more common while taking buprenorphine-naloxone than 8 weeks after taper (49.2% [177 of 360] vs

276 a-low doses of naloxone, the higher doses of naloxone that evoke hyperalgesia in GM1-treated mice can

277 rsed by treatment with the opiate antagonist naloxone, the beta-receptor agonist metaproterenol, or t

278 r signaling is blocked by ultra-low doses of naloxone, the higher doses of naloxone that evoke hypera

279 a novel small molecule TLR4 antagonist, (+)-naloxone, the non-opioid isomer of the opioid receptor a

280 analogue of 14,15-EET, the opioid antagonist naloxone, the thromboxane mimetic U46619, or the cannabi

281 When advised to offer naloxone to all patients receiving opioids, providers ma

282 C chemokine ligand 5 [CCL5 (RANTES)] enabled naloxone to produce analgesia similar to that observed i

283 in vitro or injection of the MOR antagonist naloxone to rats in vivo affords protection against isch

284 ina in DKO mice was significantly reduced in naloxone-treated animals compared with control untreated

285 nscripts and A2E were significantly lower in naloxone-treated DKO animals and cultured microglial cel

286 mes in phase 2 during extended buprenorphine-naloxone treatment (week 12), with no difference between

287 However, naloxone treatment attenuated the longer-term expression

288 the primary care, office-based buprenorphine-naloxone treatment of opioid dependence.

289 emia, but not after antecedent hypoglycemia; naloxone treatment prevented this failure.

290 Adherence to buprenorphine-naloxone treatment varied; increased adherence was assoc

291 d for rescue use of sublingual buprenorphine-naloxone treatment was exceeded.

292 ed phase 2: extended (12-week) buprenorphine-naloxone treatment, 4-week taper, and 8-week postmedicat

293 in nontransported patients after successful naloxone treatment.

294 ly to reduce opioid use during buprenorphine-naloxone treatment; if tapered off buprenorphine-naloxon

295 A B agonist (baclofen) or opioid antagonist (naloxone) treatments.

296 rio" where overdose was rarely witnessed and naloxone was rarely used, minimally effective, and expen

297 l symptoms following injections of 1.0 mg/kg naloxone were compared in active and inactive male and f

298 in the absence of morphine by administering naloxone with an alpha2 antagonist.

299 Surprisingly, co-injection of naloxone with either enkephalin enhanced the effect asso

300 demonstrate a significant interaction of (+)-naloxone with subjective effects of cocaine.