ライフサイエンスコーパス: minocycline

1 A total of 55 patients received minocycline.

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

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

4 not observed for doxycycline monohydrate or minocycline.

5 increasing concentrations of doxycycline or minocycline.

6 ctalkine-induced hyperalgesia was blocked by minocycline.

7 proved therapeutics including diclofenac and minocycline.

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

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

10 can be prevented by the microglia inhibitor minocycline.

11 reversed by anti-inflammatory treatment with minocycline.

12 come, and neuroprotective effect of the drug minocycline.

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

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

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

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

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

18 10 mug/mouse, approximately 12 nmol), and by minocycline (2.25 mg/mouse, approximately 6.3 nmol).

19 echanical allodynia and hyperalgesia whereas minocycline (20.0 mg/kg) reduced taxol-induced mechanica

20 18-year-old Japanese girl had received oral minocycline 200mg daily for treatment of acne vulgaris s

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

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

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

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

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

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

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

28 10 g), (n=45), followed by administration of minocycline, 90 mg/kg (group 1: minocycline IP, n=15; gr

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

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

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

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

33 Minocycline, a synthetic tetracycline, displays antitumo

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

35 ted 6-week-old DBA/2J mice for 25 weeks with minocycline, a tetracycline derivative known to reduce m

36 Minocycline, a tetracycline derivative, has potent antii

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

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

39 MMP inhibitor capacities, it is likely that minocycline acts to limit myocardial ischemic injury via

40 Minocycline administered prior to sulfa in jjs protects

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

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

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

44 Minocycline alone attenuated postinjury cortical lesion

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

46 Minocycline also caused a significant increase in the ex

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

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

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

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

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

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

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

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

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

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

57 Although minocycline and doxorubicin have been cocrystallized wit

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

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

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

61 Minocycline and its analogues were tested in primary ret

62 Minocycline and methacycline were cytoprotective against

63 Neutrophils appear to accumulate minocycline and other tetracyclines through a mechanism

64 Prophylactic minocycline and reactive treatment are both acceptable o

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

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

67 Catheters coated with minocycline and rifampin significantly decreased the inc

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

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

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

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

72 eased IkappaBalpha expression was blocked by minocycline and SB203580.

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

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

75 Minocycline and/or NIM811 might be useful clinically in

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

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

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

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

80 s tested, with the exception of doxycycline, minocycline, and tigecycline.

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

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

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

84 eek 4, a lower proportion of patients in the minocycline arm reported moderate to severe itch than in

85 Patients in the minocycline arm trended toward lower frequency of modera

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

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

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

89 Intrathecal minocycline at the time of adult injury selectively prev

90 Overall, minocycline attenuated the activation-induced elevation

91 Minocycline blocked allergen-specific IgE production in

92 Minocycline blocked the MPT by decreasing mitochondrial

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

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

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

96 e-month-old mice were treated with saline or minocycline by intraperitoneal injection every other day

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 Minocycline-dependent alterations to M1/M2 gene expressi

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

107 ncubation in medium containing 10 micro g/ml minocycline, doxycycline, or tetracycline yielded steady

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

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

110 Treatment with minocycline during RSD prevented both microglia activati

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

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

113 In addition, minocycline exerted anti-inflammatory effects when admin

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

115 Minocycline exerts beneficial immune modulatory effects

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

117 rent drug administration schemes, the use of minocycline following contusive SCI requires further inv

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

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

125 gical adverse events were more common in the minocycline group than in the placebo group, but these e

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 Our finding that minocycline has a harmful effect on patients with ALS ha

133 Minocycline has been shown to have neuroprotective effec

134 Minocycline has been shown to have neuroprotective effec

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

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

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

138 Although positive effects with minocycline have been reported in several animal models

139 Thalidomide and minocycline have profound immunomodulatory actions in ad

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

141 Minocycline HCl 1 mg microspheres were applied on biofil

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

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

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

145 nism may underlie the pleiotropic effects of minocycline in CNS inflammatory disorders.

146 were randomly assigned to receive placebo or minocycline in escalating doses of up to 400 mg/day for

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

148 ents with ALS has implications for trials of minocycline in patients with other neurological disorder

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

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

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

152 Minocycline increased the activity of the NFAT kinase GS

153 Specifically, minocycline increased the fraction of microglia with res

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

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

156 Minocycline induced the expression of genes associated w

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

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

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

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

161 Minocycline-induced neuroprotection was abolished by tra

162 Minocycline induces Il4 expression and M2 polarization o

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

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

165 30 min after TBI, animals were treated with Minocycline (inhibitor of MMPs), or 2-Methoxyestradiol (

166 ght to elucidate the molecular mechanisms of minocycline inhibitory effects on MHC II expression in m

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

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

169 Minocycline intravenous is active against many MDR strai

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

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

172 istration of minocycline, 90 mg/kg (group 1: minocycline IP, n=15; group 2: minocycline IV, n=15; gro

173 Minocycline is a semisynthetic tetracycline derivative w

174 Minocycline is a tetracycline antibiotic with immune-mod

175 Minocycline is a tetracycline family antibiotic that has

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

177 Minocycline is an antibiotic now recognized to have anti

178 Minocycline is an effective therapy to modify neurogenic

179 Minocycline is highly lipophilic and has shown promise a

180 /kg (group 1: minocycline IP, n=15; group 2: minocycline IV, n=15; group 3: vehicle IP, n=8; group 4:

181 Minocycline, known for its anti-inflammatory and neuropr

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

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

184 Because of these properties, minocycline may be of benefit in reducing neuronal apopt

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

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

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

188 Minocycline mediated a dose-dependent decrease in single

189 Accordingly, minocycline mediated Nlrp3 inflammasome inhibition and a

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

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

192 Minocycline (minimum inhibitory concentration that inhib

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

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

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

196 eligible patients were randomly assigned to minocycline (n = 24) or placebo (n = 24).

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

198 ted the effect of the anti-inflammatory drug minocycline on Abeta accumulation, neuroinflammation, an

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

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

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

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

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

204 We found that treatment with either minocycline or doxycycline increased the median lifespan

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

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

207 Treatment with minocycline or interfering with BDNF signaling restored

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

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

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

211 This increase was reversed by minocycline or SB203580 exposure.

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

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

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

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

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

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

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

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

220 Minocycline preconditioning protected the grafted NSCs f

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

222 In primary cortical neurons, minocycline prevents beta-amyloid-induced neuronal death

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

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

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

226 Hydralazine, minocycline, propylthiouracil and levamisole-adulterated

227 Minocycline protects against asthma independently of its

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

229 Minocycline reduced microglial activation and improved R

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

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

232 Minocycline reduces ubiquitination of the redox-sensitiv

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

234 Although minocycline reduces virus titers in the CNS of infected

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

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

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

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

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

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

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

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

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

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

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

246 Minocycline significantly reduced infarct size (approxim

247 We found that minocycline significantly reduces neuronal apoptosis and

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

252 For minocycline susceptibility testing of carbapenem-resista

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 vident by significantly smaller abscesses in minocycline-treated mice.

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

269 aminin-alpha2 gene were placed into control, minocycline-treated, or doxycycline-treated groups.

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

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

272 Minocycline treatment decreases cortical and periventric

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

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

275 Beneficial effects of minocycline treatment included a significant improvement

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

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

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

279 Minocycline treatment resulted in significant changes in

280 Minocycline treatment showed decreased NfL levels in the

281 Finally, minocycline treatment significantly decoupled RGC axon l

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

283 ormational changes in tau are susceptible to minocycline treatment, but are not directly associated w

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

285 emical assays and cultured cardiac cells for minocycline uptake experiments.

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

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

288 Minocycline was also capable of protecting the brain par

289 Minocycline was concentrated approximately 24-fold in no

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

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

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

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

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

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

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

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

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

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

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