ライフサイエンスコーパス: INH

1 INH may have a role in the management of latent multidru

2 INH was found to form covalent adducts with CYP2E1, CYP3

3 INH-R had a significant association with the combined ou

4 INH-R was found in 86 (26.7%) patients, MDR in 15 (4.7%)

5 INH/RIF coadministration was associated with limited cha

6 We found regulators that alter INH susceptibility when induced, several of which could

7 ed during 20.4 months after transplant among INH/RPT-treated recipients.

8 Long-acting nanoformulations of RIF and an INH derivative, pentenyl-INH (INHP), were prepared, and

9 icin monoresistance in 1 patient (0.3%), and INH-S + RIF-S in 220 (68.3%) patients.

10 The electroanalytical sensing of APAP and INH are possible with accessible linear ranges from 0.5

11 ere evaluated toward the sensing of APAP and INH in human serum, urine, saliva, and tablet samples.

12 ytic activity toward the sensing of APAP and INH with an enhanced analytical signal (voltammetric pea

13 e for the accurate determination of APAP and INH within human fluids and pharmaceutical formulations.

14 g a link between respiration homeostasis and INH sensitivity.

15 mited or no resistance to hydroperoxides and INH.

16 specificity for detection of MTB and RIF and INH drug resistance and may be an important tool for rap

17 pecificity for detection of MTB, and RIF and INH drug resistance and may be an important tool for rap

18 ipro to Hain V1 was demonstrated for RIF and INH resistance detection in isolates and sputum specimen

19 Patients receiving standard doses of RIF and INH, who are of the lower range of exposure distribution

20 ations associated with resistance to RMP and INH along with analysis for resistance to other first-li

21 ar and PHL DST results was 91.7% for RMP and INH collectively.

22 he simulated mechanism of action of RUTI and INH are in good alignment with the results coming from p

23 and discriminates between INH-sensitive and INH-resistant (S315T mutant KatG) TB.

24 combined effect between BCG vaccination and INH.

25 Anti-INH Abs were present in 8 sera; 11 had anti-cytochrome P

26 revious studies have failed to identify anti-INH antibodies (Abs).

27 compared mce3R-regulated genes with baseline INH transcriptional responses and implicated the gene ct

28 resistance mutations in isolates found to be INH resistant by DST and detection of mutations associat

29 acterial abundance and discriminates between INH-sensitive and INH-resistant (S315T mutant KatG) TB.

30 candidates for treating infections caused by INH resistant strains.

31 1 Abs, 14 had Abs against CYP2E1 modified by INH, 14 had anti-CYP3A4 antibodies, and 10 had anti-CYP2

32 n with icatibant was 8 and 11.5 h with pd-C1 INH.

33 C1-INH and C4 levels both increased.

34 C1-INH can also directly block leukocyte-endothelial cell a

35 C1-INH concentration and functional activity (C1-INHc+f ),

36 C1-INH contrasts with eculizumab and other distal inhibitor

37 C1-INH did not increase after resolution of the attack sugg

38 C1-INH functional activity was assessed by EIA.

39 C1-INH was effective for long-term prophylaxis and treatmen

40 C1-INH was well tolerated with no new safety signals identi

41 Delayed graft function developed in 1 C1-INH subject and 4 in the placebo.

42 erum concentrations and endogenous MASP-1/C1-INH complex levels in 128 HAE patients and 100 controls.

43 The levels of MASP-1 and MASP-1/C1-INH complexes are reduced in HAE patients compared with

44 Both MASP-1 and MASP-1/C1-INH complexes are related to the degree of complement C4

45 In conclusion, we show that MASP-1/C1-INH complexes circulate in normal human blood.

46 The level of MASP-1 and MASP-1/C1-INH complexes in HE patients correlated with the level o

47 MASP-1 levels and the quantity of MASP-1/C1-INH complexes might be associated with different paracli

48 tively high levels of pre-existing MASP-1/C1-INH complexes were observed in normal serum, and we foun

49 nor specific antibodies were reduced in 2 C1-INH treated patients tested, while immunoglobulin G DSA

50 We studied 258 C1-INH-HAE patients from 113 European families, and we expl

51 Pediatric patients should always carry a C1-INH-HAE information card and medicine for emergency use.

52 sma levels of C1-INH functional activity, C1-INH and C4 antigen levels during Week 4, and overall saf

53 D-dimer levels were associated with acute C1-INH-HAE attacks, particularly with submucosal involvemen

54 All neonates/infants with an affected C1-INH-HAE family member should be screened for C1-INH defi

55 levels of C1-INH functional activity and C1-INH antigen concentration, starting from 0.5h after firs

56 rse events (AEs)/serious AEs, C3, C4, and C1-INH levels were monitored and C1q+ HLA antibodies were a

57 the combination of antibody reduction and C1-INH may prove useful in prevention of AMR.

58 the complex formation between MASP-1 and C1-INH were significantly reduced in HAE patients compared

59 olin-3 (R = 0.2778; P = .0022), antigenic C1-INH (R = 0.3152; P = .0006), and C4 (R = 0.5307; P < .00

60 plasma was followed by detection of bound C1-INH.

61 ein expression induced by NO, bradykinin, C1-INH, or icatibant unlikely contribute to bradykinin-indu

62 olin-3, MASP-2, ficolin-3/MASP-2 complex, C1-INH, and C4, as well as the extent of ficolin-3-mediated

63 oups (3000 and 6000 IU) achieved constant C1-INH activity levels above 40% values, a threshold that w

64 Slightly decreased C1-INH activity and C4 concentration were observed in more

65 mprises HAE with C1-inhibitor deficiency (C1-INH-HAE) and HAE with normal C1-INH activity (nl-C1-INH-

66 angioedema with C1 inhibitor deficiency (C1-INH-HAE) have focused on adult patients.

67 1 esterase inhibitor (C1-INH) deficiency (C1-INH-HAE) includes therapy with exogenous C1INH.

68 angioedema with C1 inhibitor deficiency (C1-INH-HAE) is a rare inherited genetic disease characteriz

69 tary angioedema due to C1-INH deficiency (C1-INH-HAE) represent one of the oldest unsolved problems o

70 Plasma-derived C1-INH has been used to treat hereditary angioedema for mor

71 Plasma-derived C1-INH, recombinant C1-INH, and ecallantide are the only ag

72 cks normalized per month was lower during C1-INH treatment than during the 3 months prior (1.826 vs.

73 -HAE family member should be screened for C1-INH deficiency.

74 No abnormalities were found for C1-INH protein, C1q, alpha2-macroglobulin, antithrombin III

75 The Italian network for C1-INH-HAE (ITACA) created a registry including different f

76 AE recruited from the Italian Network for C1-INH-HAE (ITACA), we selected a large multiplex family wi

77 e-dependent increase in trough functional C1-INH activity was observed.

78 The level of functional C1-INH in all HAE types I and II plasma tested was less tha

79 Either method yields functional C1-INH levels in patients with HAE (types I and II) that ar

80 se in physiologically relevant functional C1-INH plasma levels.

81 the knowledge on the pathogenesis of HAE-C1-INH and for reconsidering the role of ECs as a possible

82 during attacks from 18 patients with HAE-C1-INH were compared with inter-attack samples of the same

83 by C1-inhibitor (C1-INH) deficiency (HAE-C1-INH) is a potentially life-threatening rare disease caus

84 deficiency of C1-inhibitor (C1-INH) (HAE-C1-INH).

85 Thirty-five patients with HAE-C1-INH, who have experienced severe attacks on 106 occasion

86 ctin pathway in the pathomechanism of HAE-C1-INH.

87 However, C1-INH spares the alternative pathway and the membrane atta

88 mized 1:1 to receive plasma-derived human C1-INH (20 IU/kg/dose) versus placebo intraoperatively, the

89 ngest in the PGD3 cohort and prolonged in C1-INH patients compared with the control group (29 [2-70]

90 ack PfMSP3.1 showed a marked reduction in C1-INH recruitment and increased C3b deposition on their su

91 ss than 100 and were treated with C1-INH (C1-INH-group).

92 ma due to the deficiency of C1-inhibitor (C1-INH) (HAE-C1-INH).

93 We studied the kinetics of C1-inhibitor (C1-INH) and other complement parameters in a self-limited e

94 edema (HAE) due to C1 esterase inhibitor (C1-INH) deficiency (C1-INH-HAE) includes therapy with exoge

95 angioedema (HAE) caused by C1-inhibitor (C1-INH) deficiency (HAE-C1-INH) is a potentially life-threa

96 hat application of C1-esterase-inhibitor (C1-INH) in LTX-recipients showing early signs of severe PGD

97 C1 esterase inhibitor (C1-INH) is a soluble regulator of complement activation tha

98 C1 inhibitor (C1-INH) is known to form complexes with the lectin compleme

99 C1 inhibitor (C1-INH) regulates several pathways which contribute to both

100 a functional deficiency of C1 inhibitor (C1-INH), leading to overproduction of bradykinin.

101 ansplantation is the use of C1 inhibitor (C1-INH), which blocks the first step in both the classical

102 C1 inhibitor (C1-INH, Berinert) inhibits the classical and lectin pathway

103 measured factor XIIa-C1-INH or kallikrein-C1-INH complexes, and the two assays were in close agreemen

104 further increased in patients with lower C1-INH functional activity.

105 reatment of C57BL/6 mice with PETN, L-NA, C1-INH or icatibant did not change B2R protein expression.

106 s of a cohort of Italian subjects with nl-C1-INH-HAE followed by ITACA to identify specific biomarker

107 A total of 105 nl-C1-INH-HAE patients were studied.

108 ) and HAE with normal C1-INH activity (nl-C1-INH-HAE), due to mutations in factor XII (FXII-HAE), pla

109 No C1-INH patient developed AMR during the study.

110 Hereditary angioedema (HAE) with normal C1-INH (HAEnCI) may be linked to specific mutations in the

111 ficiency (C1-INH-HAE) and HAE with normal C1-INH activity (nl-C1-INH-HAE), due to mutations in factor

112 hitherto unknown type of HAE with normal C1-INH and without mutation in the F12 gene.

113 Hereditary angioedema with normal C1-INH may be linked to specific mutations in the coagulati

114 HE patients correlated with the level of C1-INH (p = 0.0009 and p = 0.0047, respectively), the level

115 n, starting from 0.5h after first dose of C1-INH and lasting up to 72 hours.

116 -LP may deplete the innately low level of C1-INH and thus, it may contribute to the uncontrolled acti

117 ISA, Quidel Corp.) revealed the levels of C1-INH between 0 and 57% of normal (mean, 38%), and 42 samp

118 d enduring post-baseline plasma levels of C1-INH functional activity and C1-INH antigen concentration

119 The mean trough plasma levels of C1-INH functional activity, C1-INH and C4 antigen levels du

120 ability to detect known concentration of C1-INH in the plasma as a percent of normal.

121 Deficiency of C1-INH is associated with hereditary angioedema (HAE), an a

122 lso resulted in significant elevations of C1-INH levels, C3, C4, and reduced C1q+ HLA antibodies.

123 suggest significant beneficial effects of C1-INH with minimal toxicity.

124 rves were developed for quantification of C1-INH, serial dilutions of normal plasma were employed to

125 The symptoms of C1-INH-HAE often present in childhood.

126 ensus for the diagnosis and management of C1-INH-HAE patients was created.

127 gation of VEGFs and Angs as biomarkers of C1-INH-HAE severity.

128 rriage acts as an independent modifier of C1-INH-HAE severity.

129 sease caused by the decreased activity of C1-INH.

130 tered: 93% with icatibant and 59% with pd-C1-INH.

131 as abdominal pain is common in pediatric C1-INH-HAE, but also commonly occurs in the general pediatr

132 bitor l-nitroarginine (L-NA), plasma pool C1-INH, and the B2R antagonist icatibant.

133 Plasma-derived C1-INH, recombinant C1-INH, and ecallantide are the only agents licensed for th

134 stage malaria parasites, actively recruit C1-INH to their surfaces when exposed to human serum.

135 When bound to the merozoite surface, C1-INH retains its ability to complex with and inhibit C1s,

136 attack suggesting that factors other than C1-INH may be important in this process.

137 om animal and ex vivo models suggest that C1-INH ameliorates ischemia-reperfusion injury.

138 clinical studies and models suggest that C1-INH may decrease sensitization and donor-specific antibo

139 transplant recipients have suggested that C1-INH treatment may reduce IRI and delayed graft function,

140 The C1-INH also resulted in significant elevations of C1-INH le

141 The C1-INH appears safe in the posttransplant period.

142 evels also increased significantly in the C1-INH group compared to placebo.

143 One patient in the C1-INH group versus 2 patients in the placebo group develop

144 Although survival in the C1-INH treated patients was lower than in the remaining col

145 The C1-INH treatment may reduce ischemia-reperfusion injury.

146 The C1-INH trough levels increased with C1-INH treatment.

147 D scores were significantly higher in the C1-INH-group and PGD3-group as compared with the control gr

148 Thus, C1-INH may also be helpful in preserving function of establ

149 festation of hereditary angioedema due to C1-INH deficiency (C1-INH-HAE) represent one of the oldest

150 patient with hereditary angioedema due to C1-INH deficiency to better understand the pathomechanism o

151 ome was model-derived steady-state trough C1-INH functional activity.

152 andomized, placebo-controlled study using C1-INH in highly sensitized renal transplant recipients for

153 ratio less than 100 and were treated with C1-INH (C1-INH-group).

154 Studies with C1-INH in transplant recipients are limited, but have not r

155 ews clinical data and ongoing trials with C1-INH in transplant recipients, compares the results with

156 Treatment of PGD with C1-INH led to acceptable outcome.

157 The C1-INH trough levels increased with C1-INH treatment.

158 pecimens contributed by 139 patients with C1-INH-HAE at the annual control visits were studied retros

159 Patients with C1-INH-HAE experiencing more than 12 angioedema attacks per

160 g1, and Ang2 were higher in patients with C1-INH-HAE in remission than in healthy controls.

161 levels of VEGFs and Angs in patients with C1-INH-HAE may prompt the investigation of VEGFs and Angs a

162 ht healthy controls and 128 patients with C1-INH-HAE were studied.

163 and management of pediatric patients with C1-INH-HAE.

164 ations of VEGFs and Angs in patients with C1-INH-HAE.

165 riuria in the urinalysis of patients with C1-INH-HAE.

166 ment of acute attacks in 74 patients with C1-INH-HAE.

167 t in the OR were immediately treated with C1-INH.

168 tal score was shown during treatment with C1-INH.

169 rdless of whether we measured factor XIIa-C1-INH or kallikrein-C1-INH complexes, and the two assays w

170 Before the age of 1 year, C1-INH levels may be lower than in adults; therefore, it is

171 t INH induces an immune response that causes INH-induced liver injury.

172 refully selected SOT candidates, combination INH/RPT weekly given as directly observed therapy seems

173 To this day, INH remains a cornerstone of modern tuberculosis (TB) ch

174 enabled the discovery of the genes encoding INH resistance, namely, the activator (katG) and the tar

175 .1%/99.4%, 89.1%/99.4%, and 89.6%/100.0% for INH resistance detection.

176 DST results were 93.9% for RMP and 90.0% for INH.

177 MK, and KAN and the specificity was 100% for INH and FQ and 94% for AMK and KAN.

178 gents was 95.0% for RIF (132/139), 98.2% for INH (111/113), and 98.6% for EMB (141/143).

179 tinuation owing to side effects were 35% for INH, 21% for RIF, and 10% for RPT/INH.

180 ting at CDC were 97.4% for RMP and 92.5% for INH resistance.

181 4.4%/96.4%, 95.4%/98.8%, and 94.9%/97.6% for INH.

182 nce between molecular and phenotypic DST for INH and RMP for 285 isolates submitted as MTBC to CDC fr

183 the assay was 75% for FQs and 100% each for INH, AMK, and KAN and the specificity was 100% for INH a

184 tance and 97.3% and 70.9%, respectively, for INH resistance in new cases.

185 d 69.7%, 95.4%, and 86.8%, respectively, for INH resistance.

186 we found that C10 prevents the selection for INH-resistant mutants and restores INH sensitivity in ot

187 nt, bacterial subpopulations are similar for INH and RIF treatment: mostly intracellular with extrace

188 None of these Abs were detected in sera from INH-treated controls without significant liver injury.

189 soniazid [i.e., isonicotinic acid hydrazide (INH)].

190 val (HR, 0.34 [95% CI, .15-.76], P = .01) in INH-R TBM.

191 d a previously unknown role for this gene in INH susceptibility.

192 more, the small-molecule HSD17B12 inhibitor, INH-12, significantly reduces replication and infectious

193 years of age, 2,106 contacts (50%) initiated INH preventive therapy at enrollment.

194 ilic vehicle for the transport of its intact INH moiety into the mammalian cell and the mycobacterium

195 e complex interactions between intracellular INH, cell wall thickness, and the rate of cell wall synt

196 alysis purposely distinguishes intracellular INH concentration from the concentration in the plasma.

197 ions to predict the effects of intracellular INH on cell wall thickness and cell viability.

198 The intracellular INH concentration, however, depends on diffusion through

199 Isoniazid (INH) was the first synthesized drug that mediated bacter

200 Isoniazid (INH)-induced hepatotoxicity remains one of the most comm

201 resistance to rifampin (RMP) and isoniazid (INH) and in detecting multidrug-resistant tuberculosis (

202 d detection of rifampin (RIF) and isoniazid (INH) resistance.

203 ce to at least rifampin (RMP) and isoniazid (INH).

204 and susceptible to rifampicin and isoniazid (INH-S + RIF-S).

205 ess, and the frontline antibiotic isoniazid (INH).

206 n the presence of the antibiotics isoniazid (INH) and rifampicin (RIF), in an attempt to develop the

207 um tuberculosis (MTB), and detect isoniazid (INH) and rifampin (RIF) resistance.

208 ium tuberculosis (MTB) and detect isoniazid (INH) and rifampin (RIF) resistance.

209 DR-TB plus resistance to the drug isoniazid (INH) for point-of-care use.

210 first-line anti-tuberculosis drug isoniazid (INH).

211 the frontline antitubercular drug isoniazid (INH).

212 due to the antituberculosis drug isoniazid (INH).

213 ce to four first-line drugs [i.e. isoniazid (INH), ethambutol (EMB), rifampicin (RIF), pyrazinamide (

214 rifampin (RIF) (14/14), 90.0% for isoniazid (INH) (36/40), 70% for ethambutol (EMB) (7/10), and 89.1%

215 and 96.6%, respectively, and for isoniazid (INH) they were 70.6% and 99.1%.

216 esence of its common interference isoniazid (INH), which are both found in drug samples.

217 ed with LTBI were offered 9-month isoniazid (INH), 4-month rifampin (RIF), weekly rifapentine/isoniaz

218 rganization recommends the use of isoniazid (INH) alone or in combination with rifapentine to treat l

219 Twelve-week rifapentine (RPT)/isoniazid (INH) is effective for LTBI but clinical experience in RT

220 Here we show that Isoniazid (INH) treatment dramatically reduces Mycobacterium tuberc

221 We demonstrate that isoniazid (INH)-derived nanobiotics, alone or with additional encap

222 g susceptibility testing (DST) to isoniazid (INH), rifampin (RIF), moxifloxacin (MOX), ofloxacin (OFX

223 (PLWH) require TB treatment with isoniazid (INH) and rifampicin (RIF), which affect cytochrome P450

224 The granuloma is treated with isoniazid (INH), a drug that inhibits the synthesis of mycolic acid

225 2 y), and recently infected with isoniazid (INH)-resistant strains.

226 n major TB drugs (rifampin [RIF], isoniazid [INH], linezolid [LZD], moxifloxacin [MFX], clofazimine [

227 imarily attributable to the absence of known INH resistance mutations in isolates found to be INH res

228 05-0.66) compared with those exposed to mono-INH-resistant tuberculosis (adjusted hazard ratio, 0.80;

229 eated with either 12-week RPT/INH or 9-month INH from March 1, 2012, through February 28, 2014.

230 were started on 12-week RPT/INH and 9-month INH, respectively.

231 Taken together, the new INH derivatives are suitable for translation into clinic

232 nation significantly enhanced the ability of INH to control mycobacterial growth ex vivo.

233 ew portrays a detailed molecular analysis of INH killing and resistance mechanisms including persiste

234 In the case of INH, EMB, PZA and MDR-TB, DeepAMR achieved its best mean

235 und Abs present in sera of 15 of 19 cases of INH-induced liver failure.

236 Here we showed that new derivatives of INH (inhibitor for Nek2 and Hec1 binding) bind to Hec1 a

237 Sensitivity and specificity for detection of INH resistance was 82% (22/27 [63,92]) and 100% (205/205

238 Sensitivity and specificity for detection of INH resistance were 82% (22/27 [63-92%]) and 100% (205/2

239 This test may allow rapid detection of INH-sensitive TB.

240 iew describes the serendipitous discovery of INH, its effectiveness on TB patients, and early studies

241 Standard doses of INH (300 mg) and KAN (1,000 mg) did not reach therapeuti

242 The protective effect of INH was more extreme in contacts exposed to drug-sensiti

243 ction.Objectives: To evaluate the effects of INH preventive therapy on the contacts of patients with

244 together, our data indicate the efficacy of INH can be augmented following historical BCG vaccinatio

245 se in settings where rapid identification of INH resistance and clinically relevant NTM are prioritie

246 he activator (katG) and the target (inhA) of INH.

247 ants provided comprehensive understanding of INH mode of action and resistance mechanisms.

248 d the safety and tolerability of 12 weeks of INH/RPT given directly observed therapy in 17 consecutiv

249 l drug-action mechanism where the binding of INHs to Hec1 forms a virtual death-trap to trigger Nek2

250 ts and restores INH sensitivity in otherwise INH-resistant Mtb strains harboring mutations in the kat

251 comprised plasma-derived C1 inhibitor (pdC1-INH) for acute swelling attacks and progestins, tranexam

252 ections of plasma-derived C1-inhibitor (pdC1-INH) has been established as an effective treatment.

253 Compared with intravenous injection, pdC1-INH SC injection with CSL830 showed a lower peak-to-trou

254 Subcutaneous (SC) administration of pdC1-INH has not been studied in patients with HAE.

255 catibant-treated attacks and in 1.9% of pdC1-INH-treated attacks.

256 % were treated with approved therapies (pdC1-INH or icatibant), 15% were with tranexamic acid, and 35

257 Eleven women were treated with pdC1-INH for 143 facial attacks.

258 tions of RIF and an INH derivative, pentenyl-INH (INHP), were prepared, and their physicochemical pro

259 specific regulator, mce3R, which potentiated INH activity when induced.

260 encodes the enzyme that converts the prodrug INH to its active form.

261 licated the gene ctpD (Rv1469) as a putative INH effector.

262 ld or younger, only half this group received INH preventive therapy.Measurements and Main Results: Am

263 ne of the 76 household contacts who received INH preventive therapy compared with 3% (8 of 273) of th

264 Conclusions: Household contacts who received INH preventive therapy had a lower incidence of tubercul

265 defective Nek2 mutant, Nek2 R361L, resisted INH-induced Nek2 degradation.

266 ction for INH-resistant mutants and restores INH sensitivity in otherwise INH-resistant Mtb strains h

267 Overall microarray specificity for RIF, INH, and EMB combined was 97.2% (384/395).

268 tive and negative predictive values for RIF, INH, and EMB combined were 84.9% and 98.3%, respectively

269 Completion of RIF and RPT/INH for LTBI in an HCW population is more likely than IN

270 re 35% for INH, 21% for RIF, and 10% for RPT/INH.

271 pin (RIF), weekly rifapentine/isoniazid (RPT/INH) for 12 weeks, or no treatment.

272 pleted treatment with RIF (P < .0001) or RPT/INH (P < .0001) than INH.

273 de effects were lower among those taking RPT/INH.

274 cantly more frequent in the INH than the RPT/INH group (P = .0042).

275 nase elevations were not observed in the RPT/INH group, but occurred in 6 (5%) of the INH group.

276 %) and 110 (72%) were started on 12-week RPT/INH and 9-month INH, respectively.

277 Twelve-week RPT/INH appears to be an excellent choice for LTBI in RTC.

278 pliance rates were higher in the 12-week RPT/INH group (40 [93%] vs 52 [47%], P < 0.001) and (11/40 [

279 TC with LTBI treated with either 12-week RPT/INH or 9-month INH from March 1, 2012, through February

280 isoniazid resistant, rifampicin susceptible (INH-R), and susceptible to rifampicin and isoniazid (INH

281 RIF (P < .0001) or RPT/INH (P < .0001) than INH.

282 acterium avium, PCIH was more effective than INH at inhibiting bacterial growth in broth culture and

283 TBI in an HCW population is more likely than INH.

284 r TAM16 is approximately 100-fold lower than INH, suggesting that it can be developed as a new antitu

285 dissect Mtb persistence, we discovered that INH resistance is not absolute and can be reversed.

286 These data provide strong evidence that INH induces an immune response that causes INH-induced l

287 gh Peruvian national guidelines specify that INH preventive therapy should be provided to contacts ag

288 fects was significantly more frequent in the INH than the RPT/INH group (P = .0042).

289 RPT/INH group, but occurred in 6 (5%) of the INH group.

290 n, which is 3.5-fold longer than that of the INH-NAD adduct formed by the tuberculosis drug, isoniazi

291 o acids 408-422, immediately adjacent to the INH binding motif.

292 Subsequent binding of Nek2 to INH-bound Hec1 triggered proteasome-mediated Nek2 degrad

293 and eis genes responsible for resistance to INH, the fluoroquinolone (FQ) drugs, amikacin (AMK), and

294 ion (median RPL 0.61, range 0.21-2.4), while INH and KAN showed poor tissue penetration (median RPL 0

295 parameters of EFV400 without (PK1) and with INH/RIF following 4 (PK2) and 12 (PK3) weeks of coadmini

296 nonuclear cells (PBMC) were co-cultured with INH, with a similar trend during co-culture with RIF.

297 ads in culture, a property not observed with INH, which shares the isonicotinoyl hydrazide moiety wit

298 treatment improved survival in patients with INH-R TBM.

299 lly growing cultures of M. tuberculosis with INH reproducibly kills 99% to 99.9% of cells in 3 days.

300 eatment of mice with this kind of tumor with INHs significantly suppressed tumor growth without obvio