ライフサイエンスコーパス: minocycline

1 reversed by anti-inflammatory treatment with minocycline.

2 come, and neuroprotective effect of the drug minocycline.

3 were resistant to levofloxacin, TMP-SMZ, and minocycline.

4 A total of 55 patients received minocycline.

5 bials, although only 16% were susceptible to minocycline.

6 sia in rats without CP, which was blocked by minocycline.

7 increasing concentrations of doxycycline or minocycline.

8 ctalkine-induced hyperalgesia was blocked by minocycline.

9 racotomy with either vehicle or 50 mg/kg/day minocycline.

10 in females, following neonatal incision with minocycline.

11 not observed for doxycycline monohydrate or minocycline.

12 proved therapeutics including diclofenac and minocycline.

13 les and EMMPRIN, and these were abrogated by minocycline.

14 can be prevented by the microglia inhibitor minocycline.

15 a antagonists (50 nl) (PACAP(6-38), 15 pmol; minocycline 10 mg/ml) microinjected bilaterally into RVL

16 s with fovea-involving DME who received oral minocycline 100 mg twice daily for 6 months.

17 NSCLC were randomly assigned to prophylactic minocycline (100 mg twice per day for 4 weeks), reactive

18 The minocycline 120 min post-sulfa (sulfa/mino+120) group ha

19 experimental sessions: once after 3 days of Minocycline 150 mg (twice daily), and once 3 days of pla

20 tency >365 days were nitrofurantoin (25%) or minocycline (17%).

21 10 mug/mouse, approximately 12 nmol), and by minocycline (2.25 mg/mouse, approximately 6.3 nmol).

22 18-year-old Japanese girl had received oral minocycline 200mg daily for treatment of acne vulgaris s

23 th the Etest method were 67.3% and 52.3% for minocycline, 21.5% and 18.7% for doxycycline, and 71% an

24 S and DMNV immunoreactivity was prevented by minocycline (25 mg kg(-1) /2 days during SH).

25 The minocycline 30 min post-sulfa (sulfa/mino+30) group was

26 The commercial antibiotics tetracycline (3), minocycline (4), chlortetracycline (5), oxytetracycline

27 following injury, animals were treated with minocycline (45 mg/kg intraperitoneal), tigecycline (7.5

28 reatments (67 received creatine, 66 received minocycline, 71 received coenzyme Q10, 71 received GPI-1

29 to all agents tested, with the exception of minocycline (79.1% susceptible) and colistin (98.8% susc

30 combinations of an anti-inflammatory agent (minocycline), a neurotrophic agent (LM11A-31), and physi

31 ence from recent animal studies suggest that minocycline, a broad-spectrum antibiotic capable of regu

32 investigated whether reprogramming NSCs with minocycline, a broadly used antibiotic also known to pos

33 Minocycline, a centrally-penetrant tetracycline antibiot

34 ed the safety and potential efficacy of oral minocycline, a drug capable of inhibiting microglial act

35 tion was inhibited in diabetics treated with minocycline, a drug known to inhibit early diabetic reti

36 Minocycline, a potent inhibitor of microglia activation,

37 Minocycline, a synthetic tetracycline, displays antitumo

38 ugs, such as indomethacin and ibuprofen, and minocycline, a tetracycline analog with neuroprotective

39 Minocycline, a tetracycline derivative, has potent antii

40 group, 80 patients) or pleural abrasion with minocycline (abrasion/minocycline group, 80 patients).

41 f the tetracycline class, and quantified the minocycline activity against contemporary (2007-2011) is

42 Minocycline administered prior to sulfa in jjs protects

43 revious 180 days to receive either 100 mg of minocycline, administered orally twice daily, or placebo

44 We investigated whether and how minocycline affects the expression of EMMPRIN on T cells

45 Administration of minocycline after SCI did not lead to significant behavi

46 Minocycline alone attenuated postinjury cortical lesion

47 B infections will help establish the role of minocycline alone or in combination with other antimicro

48 Minocycline also caused a significant increase in the ex

49 Minocycline also killed intracellular bacilli indirectly

50 Minocycline also reduced TNF-alpha-mediated NF-kappaB ac

51 Here we tested if minocycline also reversed vocalization deficits in these

52 halamus could be mitigated by treatment with minocycline, an anti-inflammatory agent capable of cross

53 In vivo treatment with minocycline, an inhibitor of microglia activation, incre

54 Oral treatment with minocycline, an inhibitor of microglial activation, atte

55 Administration of minocycline, an inhibitor of microglial activation, decr

56 The application of minocycline, an inhibitor of neuroinflammation, altered

57 ted Mueller-Hinton (MH) broth were 77.6% for minocycline and 29% for doxycycline, and 92.5% of isolat

58 usceptibility rates were 82.2% and 72.9% for minocycline and 34.6% and 34.6% for doxycycline, respect

59 of LM11A-31 effects by co-administration of minocycline and by the type of physical therapy applied

60 Although minocycline and doxorubicin have been cocrystallized wit

61 ist PACAP(6-38) or the microglia antagonists minocycline and doxycycline augmented sympathetic respon

62 PACAP(6-38) caused a 161% increase, whereas minocycline and doxycycline caused a 225% and 215% incre

63 g multiple sclerosis, which are exhibited by minocycline and evobrutinib, respectively.

64 al infusion of microglial activation blocker minocycline and IL-1beta antagonist IL-1RA attenuated CO

65 Prophylactic minocycline and reactive treatment are both acceptable o

66 Using catheters coated with minocycline and rifampin and implementing infection cont

67 Catheters coated with minocycline and rifampin are proven to decrease the rate

68 Catheters coated with minocycline and rifampin significantly decreased the inc

69 an association between catheters coated with minocycline and rifampin use and a decrease in central l

70 the study period, 9200 catheters coated with minocycline and rifampin were used hospitalwide over a t

71 valuated the effect of catheters coated with minocycline and rifampin with and without other infectio

72 WA-induced hyperalgesia was blocked by minocycline and SB203580 intrathecally.

73 eased IkappaBalpha expression was blocked by minocycline and SB203580.

74 As minocycline and tazarotene have distinct fluorescence li

75 be used to determine local distributions of minocycline and tazarotene within the skin.

76 l therapeutic efficacy of two tetracyclines, minocycline and the newer generation tigecycline, on fun

77 ng the combination of the topical antibiotic minocycline and the retinoid tazarotene to the pilosebac

78 ns, astrocytes, and microglia) to respond to minocycline and to modulate the inflammatory environment

79 ions that evaluated the role of doxycycline, minocycline, and azithromycin in OSD among adult patient

80 rugs nicotinamide (also called niacinamide), minocycline, and cyclosporine A exhibited a uniform prot

81 locking in vivo activation of microglia with minocycline, and depletion of microglia with a colony-st

82 s was investigated using microglial blocker, minocycline, and IL-1beta antagonist IL-1RA.

83 acter baumannii isolates were susceptible to minocycline, and susceptibility rates were highest in No

84 for amoxicillin-clavulanic acid, linezolid, minocycline, and tobramycin.

85 The in vivo effects of minocycline are also associated with reduced caspase-3 a

86 The anti-HIV effects of minocycline are mediated by altering the cellular enviro

87 c, our results provide a rationale for using minocycline as a therapeutic agent for treating ischemic

88 ion and may better inform the application of minocycline as an immunomodulatory agent.

89 In this pilot proof-of-concept study of DME, minocycline as primary treatment was associated with imp

90 Intrathecal minocycline at the time of adult injury selectively prev

91 Overall, minocycline attenuated the activation-induced elevation

92 In line with this, minocycline biased use of boundary- compared to landmark

93 Minocycline blocked allergen-specific IgE production in

94 ced increased NK1R expression was blocked by minocycline but not SB203580.

95 e results show a potentially broad effect of minocycline but that it may block IgE production in part

96 d attenuation of CD4(+) T cell activation by minocycline, but a specific mechanism has not been eluci

97 ve therapeutic downregulation in response to minocycline by means of noninvasive in vivo imaging.

98 ed microglial activation and its response to minocycline can be quantitatively imaged in the rat brai

99 administration of both antibiotics but only minocycline can decrease the extent of cell death in sel

100 model of asthma, a single administration of minocycline conferred excellent protection against ovalb

101 l T cell activation, and this was reduced by minocycline correspondent with decreased P-Akt levels.

102 The immunomodulatory antibiotic minocycline could be an effective, low-cost adjunctive t

103 We show here that minocycline delays neurodegeneration in ts1-infected mic

104 We conclude that minocycline delays retrovirus ts1-induced neurodegenerat

105 Moreover, minocycline demonstrated dose-dependent antiinflammatory

106 n independent protein abundance experiments, minocycline demonstrated dose-dependent inhibition of so

107 Minocycline-dependent alterations to M1/M2 gene expressi

108 Pharmacodynamic studies showed that minocycline depletes Wolbachia more effectively than dox

109 Minocycline displayed the highest susceptibility rate ov

110 ime profiles of 7 mg/kg/day human-equivalent minocycline dose achieved bacterial kill rates equivalen

111 cin, although all isolates were sensitive to minocycline, doxycycline, trimethoprim-sulfamethoxazole,

112 and it was not possible after treatment with minocycline due to lack of bacterial growth.

113 Treatment with minocycline during RSD prevented both microglia activati

114 VR, 1.96 +/- 0.33 (n = 10); and zymosan with minocycline DVR, 1.58 +/- 0.12 (n = 9).

115 ted and untreated WT control mice indicating minocycline effects were specific to vocalizations in th

116 Indeed, minocycline exerts antioxidant effects in vitro and in v

117 She had already discontinued oral minocycline five weeks before admission, because she mis

118 ve shown that treatment of Fmr1 KO mice with minocycline for 4weeks from birth can alleviate some beh

119 controls in adult Fmr1 KO mice treated with minocycline for four weeks from birth (P0-P28).

120 ptible isolates and the potential utility of minocycline for the treatment of many MDR A. baumannii i

121 icrobial Stewardship Program's evaluation of minocycline for the treatment of patients with multidrug

122 r the evaluation and use of intravenous (IV) minocycline for the treatment of these resistant organis

123 We administered minocycline for three days commencing one hour after inj

124 linics; 72 participants were assigned to the minocycline group and 70 to the placebo group.

125 Patients in the abrasion/minocycline group had a higher intensity of chest pain a

126 pleural abrasion with minocycline (abrasion/minocycline group, 80 patients).

127 61.0% in the placebo group and 33.4% in the minocycline group, a difference of 27.6 percentage point

128 group and 3 patients (3.8%) in the abrasion/minocycline group.

129 itive: 6/9 (67%) of patients who received IV minocycline had infections due to these organisms cured,

130 enesis, whereas treatment with imipramine or minocycline had minimal or no anti-depressive effects, r

131 These studies indicate that minocycline has a graded neuroprotective effect when adm

132 Minocycline has been shown to have neuroprotective effec

133 imicrobial susceptibility data suggests that minocycline has greater activity than other tetracycline

134 and in contrast to most older tetracyclines, minocycline has high activity against Acinetobacter spec

135 An intravenous formulation of minocycline has recently become available for clinical u

136 Thalidomide and minocycline have profound immunomodulatory actions in ad

137 valuates the neuroprotective capabilities of minocycline HCl (50 mg/kg) administered 30 or 120 min af

138 Minocycline HCl 1 mg microspheres were applied on biofil

139 Therapy with doxycycline hydrochloride and minocycline hydrochloride led to partial improvement in

140 to investigate the antimicrobial effects of minocycline hydrochloride microspheres versus infrared l

141 eaved by matrix metalloproteinase 8 (MMP-8), minocycline hydrochloride, bovine serum albumin, or an a

142 e to linezolid, tigecycline, and vancomycin; minocycline, imipenem, and meropenem were also highly ac

143 In summary, minocycline impaired human spatial memory performance, l

144 l action is the primary beneficial effect of minocycline in hypertension.

145 few reports of drug-induced lupus caused by minocycline in Japan.

146 which the limited treatment options include minocycline in the case of multidrug resistance.

147 ather than directly targeting virus, placing minocycline in the class of anticellular anti-HIV drugs.

148 uggest a possible novel therapeutic role for minocycline in the treatment of AD and related tauopathi

149 against resistant S. maltophilia The role of minocycline in the treatment of infections due to S. mal

150 zone of fetal rats were preconditioned with minocycline in vitro and transplanted into rat brains 6

151 Minocycline increased the activity of the NFAT kinase GS

152 Specifically, minocycline increased the fraction of microglia with res

153 on is insufficient, indicating a function of minocycline independent of apoptosis inhibition.

154 These findings provide a novel mechanism for minocycline induced suppression of CD4(+) T cell activat

155 Minocycline induced the expression of genes associated w

156 Additionally, preconditioning with minocycline induced the NSCs to release paracrine factor

157 econd case was that of a man in his 30s with minocycline-induced DIHS.

158 ase highlights the importance of considering minocycline-induced lupus.

159 IL4 neutralization dampens minocycline-induced M2 polarization and neuroprotection.

160 Minocycline-induced neuroprotection was abolished by tra

161 Minocycline induces Il4 expression and M2 polarization o

162 microglia than their male counterparts, and minocycline inhibition of microglia corrects the retinal

163 We examined the effects of minocycline (inhibitor of microglia) and fractalkine (mi

164 30 min after TBI, animals were treated with Minocycline (inhibitor of MMPs), or 2-Methoxyestradiol (

165 nt of literature reporting successful use of minocycline intravenous for treatment of serious MDR Aci

166 In addition, minocycline intravenous holds a US Food and Drug Adminis

167 Minocycline intravenous is active against many MDR strai

168 with the generally favorable tolerability of minocycline intravenous, support its use as a viable the

169 tember 2010 through March 2013) who received minocycline intravenously (IV) for a MDR-AB infection.

170 Minocycline is a semisynthetic tetracycline derivative w

171 Minocycline is a tetracycline antibiotic with immune-mod

172 Minocycline is a tetracycline family antibiotic that has

173 Minocycline is an "old-drug" with Food and Drug Administ

174 Minocycline is an effective therapy to modify neurogenic

175 Minocycline killed extracellular bacilli directly.

176 Minocycline, known for its anti-inflammatory and neuropr

177 the tetracycline antibiotics doxycycline and minocycline, known inhibitors of metalloproteases.

178 Microglial inhibition with oral minocycline may be a promising therapeutic strategy targ

179 These findings suggest that minocycline may be an effective treatment of core depres

180 nd in vivo models of AD to determine whether minocycline may have therapeutic efficacy against tau pa

181 P) activity in atherosclerotic plaques after minocycline (MC) intervention.

182 of the tet(X2) variants over a wide range of minocycline (MCN) concentrations.

183 Minocycline mediated a dose-dependent decrease in single

184 Accordingly, minocycline mediated Nlrp3 inflammasome inhibition and a

185 Minocycline microspheres (MMs) are being used to treat r

186 The cumulative action of minocycline microspheres on multispecies oral biofilms i

187 Minocycline (minimum inhibitory concentration that inhib

188 We previously reported that minocycline (MINO) co-treatment abrogates olanzapine (OL

189 For minocycline, minor error rates ranged from 14% to 37.4%.

190 chieved in 40/55 (73%) patients treated with minocycline monotherapy (n = 3) or in combination with a

191 The response rate to minocycline monotherapy or in combination for the treatm

192 Neither minocycline nor the TNF-alpha-neutralizing compound etan

193 n, levofloxacin, moxifloxacin, eravacycline, minocycline, omadacycline, polymyxin B, and tigecycline.

194 he extant literature examining the effect of minocycline on depressive-like behavior in rodent models

195 The overall effect of minocycline on depressive-like behavior was estimated us

196 However, the effects of minocycline on human memory have not previously been inv

197 The effect of minocycline on PARP may be indirect, as the drug failed

198 In this study, we investigated the effect of minocycline on the activity of three key transcription f

199 ore, administration of the immunosuppressant minocycline or an inhibitor of IL-1beta receptor signali

200 tial stress-induced microglial activation by minocycline or by transgenic interleukin-1 receptor anta

201 repeat protein (DARPin) complexes with bound minocycline or doxorubicin.

202 is study to determine whether treatment with minocycline or doxycycline, which are tetracycline deriv

203 The susceptibility of microorganisms to minocycline or infrared light was evaluated by a colony-

204 Treatment with minocycline or interfering with BDNF signaling restored

205 inhibited microglial function with systemic minocycline or intrathecal SB203580 at the time of neona

206 Administration of minocycline or placebo was continued until a diagnosis o

207 patients who were treated with prophylactic minocycline or reactive treatment.

208 ble effects on Wolbachia but synergized with minocycline or rifampicin (RIF) to deplete symbionts, bl

209 This increase was reversed by minocycline or SB203580 exposure.

210 rt by RGCs in mice systemically treated with minocycline or vehicle only.

211 the visceromotor response in rats exposed to minocycline or vehicle.

212 Mice treated with minocycline or wogonin, both of which limit infiltration

213 All secondary MRI outcomes favored minocycline over placebo at 6 months but not at 24 month

214 organisms, given potential advantages of IV minocycline over tigecycline and doxycycline.

215 show that the FDA-approved antibiotic drug, minocycline, partially corrects the pathological phenoty

216 Pleural abrasion with minocycline pleurodesis is as effective as apical pleure

217 Moreover, transplantation of the minocycline-preconditioned NSCs significantly attenuated

218 Minocycline preconditioning protected the grafted NSCs f

219 ore, in chronic angiotensin II-infused rats, minocycline prevented extravasation of BM-derived cells

220 In addition, minocycline prevents death of primary neurons when they

221 dy was designed to determine whether and how minocycline prevents paralysis and death in ts1-infected

222 iving attention of late, namely hydralazine, minocycline, propylthiouracil (PTU) and levamisole-adult

223 Hydralazine, minocycline, propylthiouracil and levamisole-adulterated

224 Minocycline protects against asthma independently of its

225 Here we show that minocycline protects against dNP in mouse models of type

226 Minocycline reduced conversion to multiple sclerosis in

227 Subgroup analyses revealed that minocycline reduced depressive-like behavior in diseased

228 Overall, minocycline reduced depressive-like behavior in rodents

229 Minocycline reduced microglial activation and improved R

230 This study demonstrates that minocycline reduces HIV replication and reactivation and

231 Finally, we demonstrate that the antibiotic minocycline reduces microglia-mediated synapse uptake in

232 mized, controlled trial to determine whether minocycline reduces the risk of conversion from a first

233 Minocycline reduces ubiquitination of the redox-sensitiv

234 an anti-inflammatory environment induced by minocycline reduces viral cytotoxicity during WNV infect

235 Although minocycline reduces virus titers in the CNS of infected

236 ycline exhibits superior PK in comparison to minocycline resulting in a 3-fold greater exposure in SC

237 gle-forming transgenic mice (htau line) with minocycline results in reduced levels of tau phosphoryla

238 Intrathecal injection of minocycline reversed and prevented the increase of nocif

239 nificant CRBSI reduction was associated with minocycline-rifampicin (RR, 0.29 [95% CI, .16-.52]) and

240 Current evidence suggests that the minocycline-rifampicin-impregnated CVC appears to be the

241 We also determined minocycline's capacity to act as a reducer of myocardial

242 However, minocycline's potential as an in vivo cardioprotector as

243 ere also assayed in rats given injections of minocycline, SB203580, or vehicle.

244 Our data demonstrate that minocycline selectively impairs NFAT-mediated transcript

245 ubsided spontaneously after the cessation of minocycline, she was considered to have drug-induced lup

246 Prophylactic treatment with minocycline significantly lengthened the time to the mos

247 Furthermore, against expectations, minocycline significantly reduced activity during memory

248 Minocycline stabilizes endogenous Nrf2 in kidneys of db/

249 Interestingly, the microglial inhibitor minocycline suppressed rCASP6 but not TNF-alpha-induced

250 , but only 34% were minocycline susceptible; minocycline susceptibility decreased significantly from

251 The essential agreement of minocycline susceptibility results (+/-1 log(2) MIC agre

252 breakpoints exist to guide interpretation of minocycline susceptibility results with Acinetobacter.

253 liably identified A. baumannii and predicted minocycline susceptibility results, which should help gu

254 rformance of A. baumannii identification and minocycline susceptibility testing by AXDX using 101 con

255 For minocycline susceptibility testing of carbapenem-resista

256 susceptibility was low (32%) in Africa while minocycline susceptibility was low in Asia-Pacific Rim (

257 , and vancomycin globally, but only 34% were minocycline susceptible; minocycline susceptibility decr

258 tibility other tetracyclines fails to detect minocycline-susceptible isolates and the potential utili

259 ore frequent among participants who received minocycline than among those who received placebo.

260 tiple sclerosis was significantly lower with minocycline than with placebo over 6 months but not over

261 ay for 10 days and given daily injections of minocycline, the p38 inhibitor SB203580, or saline.

262 lls are postulated to be a primary target in minocycline therapy.

263 broth microdilution methods) for testing of minocycline, tigecycline, and doxycycline against 107 ca

264 The ability of minocycline to be transported into cardiac cells, concen

265 a time- and temperature-dependent uptake of minocycline to levels that approximate those of normal m

266 et of subjects was treated systemically with minocycline to potentially alter microglial activation.

267 e microglial/macrophage activation inhibitor minocycline to the inflamed animals both lowered the lev

268 pancreatic cancer cells and synergized with minocycline to yield a robust mitochondria-mediated casp

269 Day 7 spleen transcripts from minocycline-treated EAE mice had a significantly lower M

270 g) did not significantly differ from that in minocycline-treated TBI mice (0.93 +/- 0.30 %ID/g, P = 0

271 ADP-ribose) immunoreactivity in the lungs of minocycline-treated/ovalbumin-challenged mice correlated

272 of IL-4, ex vivo, rescued IgE production by minocycline-treated/ovalbumin-stimulated B cells.

273 Minocycline treatment decreases cortical and periventric

274 In vivo minocycline treatment during EAE was used to address the

275 estingly, blocking microglia activation with minocycline treatment during PND 2-6 alcohol exposure am

276 symptoms, and that further investigation of minocycline treatment for clinically relevant depression

277 Blockade of inflammation by minocycline treatment immediately after the 6-OHDA admin

278 ust and relevant biomarkers of FXS, and that minocycline treatment is a promising avenue for treatmen

279 ed binding (P = 0.0001, 2-tailed t test) and minocycline treatment reduced zymosan-induced binding by

280 igations to examine the clinical efficacy of minocycline treatment regimens against lymphatic filaria

281 Minocycline treatment resulted in significant changes in

282 Minocycline treatment showed decreased NfL levels in the

283 In EAE-afflicted mice, minocycline treatment significantly reduced EMMPRIN leve

284 terestingly, neuron loss can be mitigated by minocycline treatment.

285 efficacy in a murine Brugia malayi model of minocycline versus doxycycline.

286 ibility.) Based in part on these results, IV minocycline was added to the formulary, primarily for th

287 Finally, minocycline was found to reduce both immobility-based an

288 howed that the combination of sabutoclax and minocycline was highly cytotoxic to pancreatic cancer ce

289 We found that minocycline was highly potent in laboratory strains of M

290 At all time points of survival assessment, minocycline was more effective (>2 log10 colony-forming

291 on of TNF-alpha-induced hyperexcitability by minocycline was overcome by coadministration of sIL-6R,

292 Telavancin, linezolid, tigecycline, and minocycline were active against >90% of VISA isolates, w

293 In contrast, C57BL/6 mice treated with minocycline, which affects monocytes/macrophages, microg

294 s significantly decreased in the presence of minocycline, which has antineuroinflammatory properties,

295 Intriguingly, the tetracycline antibiotic minocycline, which has been in clinical use for decades,

296 ; by an antibody to the IL-6 receptor; or by minocycline, which inhibits the microglia.

297 Thus, preconditioning with minocycline, which reprograms NSCs to tolerate oxidative

298 Taken together, we uncover a new function of minocycline, which stabilizes the redox-sensitive transc

299 PK/PD analysis predicts that minocycline would be expected to be 1.7 fold more effect

300 the rodent literature, we hypothesised that minocycline would selectively modulate hippocampal learn