ライフサイエンスコーパス: INH

1 INH acetylator genotypes were determined and urine teste

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

3 INH-ODN 2088 is a prototypic member of this class of INH

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

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

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

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

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

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

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

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

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

13 mited or no resistance to hydroperoxides and INH.

14 del, we found that co-treatment with RIF and INH causes accumulation of the endogenous hepatotoxin pr

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

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

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

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

19 an interaction between acetylator status and INH treatment with respect to ELISPOT results over time.

20 Two strip logic gates ("OR" and "INH") were designed in our paper and the combinatorial l

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

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

23 INH-ODN 2088 and G-modified INH-ODNs such as INH-ODN 24888, TLR7-induced TNF-alpha release and TLR7-

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

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

26 candidates for treating infections caused by INH resistant strains.

27 nal dendritic cells was equally inhibited by INH-ODN 2088 and G-modified INH-ODNs such as INH-ODN 248

28 1 Abs, 14 had Abs against CYP2E1 modified by INH, 14 had anti-CYP3A4 antibodies, and 10 had anti-CYP2

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

30 C1-INH and C4 levels both increased.

31 C1-INH concentrate is safe and effective for prophylaxis.

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

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

34 C1-INH functional activity was assessed by EIA.

35 C1-INH was removed from factor XII-deficient plasma by mean

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

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

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

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

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

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

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

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

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

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

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

47 ients with angioedema because of acquired C1-INH deficiency (AAE).

48 edema (HAE types I, II and III), acquired C1-INH deficiency, and angiotensin-converting enzyme inhibi

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

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

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

52 f plasma deficient in both factor XII and C1-INH led to conversion of prekallikrein to kallikrein and

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

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

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

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

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

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

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

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

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

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

63 1 esterase inhibitor (C1-INH) deficiency (C1-INH-HAE) includes therapy with exogenous C1INH.

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

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

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

67 -term prophylaxis if human plasma-derived C1-INH is not available.

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

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

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

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

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

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

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

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

76 s higher in patients with undiagnosed HAE-C1-INH (63 cases) than in patients with diagnosed HAE-C1-IN

77 ases) than in patients with diagnosed HAE-C1-INH (7 cases).

78 nts with and without the diagnosis of HAE-C1-INH and analyzed fatal laryngeal attacks.

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

80 he management of female patients with HAE-C1-INH is presented.

81 each case should be treated based on HAE-C1-INH symptoms during pregnancy and previous labors.

82 addressed include special features of HAE-C1-INH treatment in female patients, genetic counseling, in

83 ortality in patients with undiagnosed HAE-C1-INH underscores the need to identify these patients and

84 asphyxiated patients with undiagnosed HAE-C1-INH was on average approximately 31 years shorter than p

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

86 horter than patients with undiagnosed HAE-C1-INH who died of other causes.

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

88 edema due to C1 inhibitor deficiency (HAE-C1-INH) is characterized by relapsing skin swellings, abdom

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

90 ma caused by C1 inhibitor deficiency (HAE-C1-INH).

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

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

93 tetric events in female patients with HAE-C1-INH.

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

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

96 tibant, ecallantide, or recombinant human C1-INH (rhC1INH).

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

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

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

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

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

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

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

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

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

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

107 chiometric and inhibited by C1 inhibitor (C1-INH) or corn trypsin inhibitor.

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

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

110 E), caused by deficiency in C1-inhibitor (C1-INH), leads to unpredictable edema of subcutaneous tissu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Lack of C1-INH leads to overproduction of bradykinin, a potent vaso

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

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

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

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

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

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

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

133 Postoperative courses of C1-INH-treated recipients were compared with a subgroup of

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

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

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

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

138 atous attack, and the medicinal products (C1-INH concentrate, tranexamic acid, and danazol) administe

139 in 72 hours after LTX but did not receive C1-INH.

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

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

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

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

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

145 drugs administered for STP revealed that C1-INH concentrate (Berinert((R)) , CSL Behring, Marburg, G

146 These results indicate that C1-INH stabilizes the prekallikrein-HK complex to prevent H

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

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

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

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

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

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

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

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

155 urvival in the PGD3-cohort was 71.4%, the C1-INH-treated-group had a one-year-survival of 82.5%, the

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

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

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

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

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

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

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

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

164 s recommend preoperative prophylaxis with C1-INH or attenuated androgens in patients with HAE undergo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 .1%/99.4%, 89.1%/99.4%, and 89.6%/100.0% for INH resistance detection.

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

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

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

184 nd 82.6% for MGIT and by drugs was 92.2% for INH, 91.5% for RMP, 79.0% for EMB, and 97.5% for PZA.

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

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

187 4.4%/96.4%, 95.4%/98.8%, and 94.9%/97.6% for INH.

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

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

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

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

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

193 notypes were determined and urine tested for INH metabolites to confirm adherence.

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

195 y atresia and idiopathic neonatal hepatitis (INH).

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

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

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

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

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

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

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

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

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

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

206 therapy with rifampicin (RIF) and isoniazid (INH) used to treat tuberculosis in humans frequently cau

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

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

209 The MTBDRplus assay detected isoniazid (INH) resistance directly from the sputum specimen in 159

210 f M.tb. resistance to the TB drug isoniazid (INH) conferred by loss of a sigma factor, SigI.

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

212 the frontline antitubercular drug isoniazid (INH).

213 due to the antituberculosis drug isoniazid (INH).

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

215 sed for setting up direct DST for isoniazid (INH) and rifampin (RIF).

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

217 uation of a rapid breath test for isoniazid (INH)-sensitive TB based on detection of labelled N2 gas

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

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

220 cynomolgus macaques with 6 mo of isoniazid (INH) effectively prevented anti-TNF antibody-induced rea

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

222 s drugs used in the United States-isoniazid (INH), rifampin (RMP), ethambutol (EMB), and pyrazinamide

223 Streptomycin (STR), isoniazid (INH), rifampin (RIF), ethambutol (EMB) (collectively kno

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

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

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

227 BL/PA, in combination or not with isoniazid (INH), dramatically reduced lung and, to a lesser extent,

228 2 y), and recently infected with isoniazid (INH)-resistant strains.

229 ifampin [RIF] and 9.3% for RIF or isoniazid [INH]).

230 pin (RIF), isoniazid [isonicotinylhydrazine (INH)], pyrazinamide, and ethambutol, among other drug th

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

232 led N2 gas formed specifically from labelled INH by mycobacterial KatG enzyme.

233 ance was observed for strains with low-level INH resistance, RMP resistance, and EMB-resistant strain

234 In contacts with LTBI, INH therapy plays no role in observed decreases in Mycob

235 icipants received a 6-month course of 900 mg INH twice weekly or a matching placebo.

236 d autoimmune MRL/Mp-lpr/lpr mice, G-modified INH-ODN 24888 was significantly more efficient than unmo

237 lly inhibited by INH-ODN 2088 and G-modified INH-ODNs such as INH-ODN 24888, TLR7-induced TNF-alpha r

238 was more efficiently impaired by G-modified INH-ODNs.

239 re significantly more impaired by G-modified INH-ODNs.

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

241 potential advantages over a standard 9-month INH regimen for the treatment of latent tuberculosis inf

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

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

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

245 2088 is a prototypic member of this class of INH-ODN and acts as a TLR7 and TLR9 antagonist.

246 ment of latent animals with a combination of INH and rifampicin (RIF) was highly effective at prevent

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

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

249 ry, G modification allows the development of INH-ODNs with superior inhibitory potency for inflammato

250 We demonstrate that the gain of INH resistance in the M.tb.

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

252 ed, blinded, and placebo-controlled trial of INH in EC ELISPOT and Mantoux test positive participants

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

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

255 ligonucleotides (inhibitory oligonucleotide [INH-ODN]) are characterized by a phosphorothioate backbo

256 ants with idiopathic cholestatic jaundice or INH were enrolled.

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

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

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

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

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

262 % were treated with approved therapies (pdC1-INH or icatibant), 15% were with tranexamic acid, and 35

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

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

265 The most prevalent INH resistance mutation was S315T (78%) in the katG codo

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

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 irectly observed isoniazid plus rifapentine (INH/RPT) combination could have potential advantages ove

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

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

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

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

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

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

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

277 %) and 110 (72%) were started on 12-week RPT/INH and 9-month INH, respectively.

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

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

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

281 Surprisingly, INH-ODN 2088 stimulated B cells to proliferate when used

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

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

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

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

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

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

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 B, we further showed that addition of MTZ to INH/RIF effectively treated animals with active TB withi

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

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

295 significantly more efficient than unmodified INH-ODN 2088.

296 direct DST, there was 95.1% concordance with INH and 96.1% with rifampin.

297 ear of age, they often are misdiagnosed with INH, leading to difficulty in determining the true preva

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

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

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