ライフサイエンスコーパス: NMO

1 NMO brain scan lesions compared to controls were large (

2 NMO differs from MS, however, in the distribution and hi

3 NMO lesions were greatly reduced by intracerebral admini

4 NMO lesions were produced in mice by intracerebral injec

5 NMO pathology was produced in NMO-IgG-treated spinal cor

6 NMO-F(ab')(2) competitively displaced pathogenic NMO-IgG

7 NMO-IgG and human complement-induced placentitis caused

8 NMO-IgGs have a polyclonal origin and recognize differen

9 NMO/NMOSD represented a higher proportion of IDD in Mart

10 NMOs catalyze the hydroxylation of sine and ornithine in

11 Pattern 1 NMO rAbs were insensitive to loop A mutations and could

12 A total of 871 attacks in 185 patients (142 NMO/43 NMOSD, 82% female) were analyzed.

13 d the gut microbiome by PhyloChip G3 from 16 NMO patients, 16 healthy controls (HC), and 16 multiple

14 Alternatively, pattern 2 NMO rAbs showed significantly reduced binding following

15 At presentation, 40% NMO cases had unilateral optic neuritis (ON); 20% bilate

16 We report 5 NMO-related cases, all with longitudinally extensive les

17 MO patients, and AQP4 antibodies in 48 of 56 NMO and 1 of 50 anti-NMDAR patients (p<0.0001 for all co

18 antibodies in 3 of 50 anti-NMDAR and 1 of 56 NMO patients, and AQP4 antibodies in 48 of 56 NMO and 1

19 32 samples from 50 (64%) NMO sera and 34 from 51 (67%) NMOSD sera were positive o

20 or otherwise therapy-resistant highly active NMO and NMO spectrum disorder.

21 tly reduced NMO lesions in mice administered NMO-IgG and human complement.

22 more commonly and earlier compared to adult NMO.

23 CDC and ADCC, even when IdeS was added after NMO-IgG was bound to AQP4.

24 as also prevented by addition of EndoS after NMO-IgG binding to AQP4.

25 onformation and abolished the binding of all NMO rAbs and NMO-IgG, indicating the global importance o

26 Whereas all NMO rAbs required conserved loop C ((137)TP(138) and Val

27 aporin-4 (AQP4) antibody (AQP4-antibody), an NMO-specific autoantibody to AQP4, the dominant water ch

28 active AQP4-ab-seropositive NMO (n = 6) and NMO spectrum disorder (n = 2) whose disease had been res

29 Cytotoxicity and NMO pathology were measured in cell and spinal cord slic

30 MO-IgG/eosinophil-dependent cytotoxicity and NMO pathology.

31 s, IdeS treatment of monoclonal NMO-IgGs and NMO patient sera abolished CDC and ADCC, even when IdeS

32 loss is a common clinical feature in MS and NMO.

33 of 14 aquaporin-4 antibody positive NMO and NMO spectrum disorder patients treated with methotrexate

34 gnificantly reduces relapse rates in NMO and NMO spectrum disorder patients.

35 ysis of relapses in 90 patients with NMO and NMO spectrum disorder treated with azathioprine, mycophe

36 wise therapy-resistant highly active NMO and NMO spectrum disorder.

37 ures, immunopathology and therapy of NMO and NMO spectrum disorders.

38 nd abolished the binding of all NMO rAbs and NMO-IgG, indicating the global importance of loop C conf

39 h includes bacterial, fungal, and two animal NMOs.

40 d a wealth of information to better approach NMO pathogenesis.

41 85 genes are annotated in the GenBank(TM) as NMO.

42 y brain/brainstem disease are referred to as NMO spectrum disorders (NMOSD).

43 g of anti-aquaporin-4 (AQP4) autoantibodies (NMO-IgG) to AQP4 on astrocytes.

44 Circulating autoantibodies (NMO-immunoglobulin [Ig]G) against astrocyte water channe

45 by binding of pathogenic IgG autoantibodies (NMO-IgG) to astrocyte water channel aquaporin-4 (AQP4).

46 c nerve caused by pathogenic autoantibodies (NMO-IgG) against astrocyte aquaporin-4 (AQP4).

47 y the presence of pathogenic autoantibodies (NMO-IgGs) against supra-molecular assemblies of aquapori

48 sed by binding of pathogenic autoantibodies (NMO-immunoglobulin G [IgG]) to aquaporin-4 (AQP4) on ast

49 porin-4 in the presence of NMO autoantibody (NMO-IgG).

50 are identified in the structure of bacterial NMO, defining Class I NMO, which includes bacterial, fun

51 munological treatments are different between NMO and MS, making early differential diagnosis of these

52 may hold promise for differentiating between NMO and MS.

53 l microbial communities was observed between NMO and HC (Adonis test, p = 0.001).

54 ple sclerosis (MS), the relationship between NMO and MS has long been controversial.

55 d berbamine alkaloids, each of which blocked NMO-IgG binding to AQP4 without affecting AQP4 expressio

56 ients, who have overlapping features of both NMO and MS, test negative for AQP4-Abs and may be diffic

57 P4 can damage astrocytes via complement, but NMO histopathology also shows demyelination, and - impor

58 Nitronate monooxygenases encoded by NMO genes catalyse the oxidative denitrification of nitr

59 common with the biochemically characterized NMO from Cyberlindnera saturnus are identified in the st

60 In children, NMO is associated with early recurrence and visual impai

61 IdeS efficiently cleaved NMO-IgG in mice in vivo, and greatly reduced NMO lesions

62 In the CNS, NMO-IgG causes complement-mediated astrocyte damage, inf

63 come these limitations, we sought to compare NMO/NMOSD seroepidemiology across two ethnically diverge

64 Current NMO therapies, which have limited efficacy, include immu

65 en considering only those fulfilling current NMO diagnostic criteria.

66 Early active demyelinating NMO lesions may show complement within macrophages and o

67 In live mice, demyelinating NMO lesions produced by continuous intracerebral injecti

68 stablishing a new mechanism of OAP-dependent NMO pathogenesis.

69 ith different monoclonal and patient-derived NMO-IgGs, that CDC was greatly (>100-fold) reduced in ce

70 NMO-IgG are the most sensitive for detecting NMO spectrum disorders.

71 -4 (AQP4), which unequivocally differentiate NMO from MS.

72 antification of myo-inositol may distinguish NMO from MS.

73 tool to study the formation of experimental NMO-related lesions caused by human AQP4 antibodies in m

74 Thus, PA4202 is the first NMO identified and characterized in bacteria.

75 h may determine permanent deficits following NMO relapses.

76 ted cell sorting and cell binding assays for NMO-IgG are the most sensitive for detecting NMO spectru

77 Novel treatment strategies are available for NMO, but other causes need to be excluded in NMO-IgG-ser

78 nducted at a single UK specialist center for NMO.

79 -Abs can fulfill the diagnostic criteria for NMO, there are differences when compared with those with

80 extracellular loop amino acids critical for NMO-IgG binding and identified regions of AQP4 extracell

81 n of patients with LETM who are negative for NMO-IgG may lead to an alternate cause for myelopathy.

82 vide additional clues for new strategies for NMO treatment and a wealth of information to better appr

83 ey role of aspartate 69 (Asp(69)) of TM2 for NMO-IgG epitope assembly.

84 sequence, and efficacy of therapies used for NMO attacks.

85 Apart from NMO, some patients with recurrent ON or recurrent longit

86 T cells from NMO patients and HC proliferated to intact AQP4 or AQP4

87 Peripheral blood T cells from NMO patients and HC were examined for recognition of AQP

88 T cells from NMO patients proliferated to this homologous bacterial s

89 tion of immunoglobulin G (IgG) isolated from NMO patient serum and human complement.

90 egative patients, including those fulfilling NMO diagnostic criteria.

91 Neuromyelitis optica-immunoglobulin G (NMO-IgG) binds to aquaporin-4 (AQP4) water channels in t

92 addition to characteristic histopathological NMO features, namely loss of AQP4 and astrocytes.

93 Immunostaining of human NMO lesions for neutrophil elastase revealed many degran

94 The generation of human NMO rAbs has allowed the first high resolution mapping o

95 structure of bacterial NMO, defining Class I NMO, which includes bacterial, fungal, and two animal NM

96 ble lacks the four motifs, defining Class II NMO.

97 ion of Asp(69) to histidine severely impairs NMO-IgG binding for 85.7% of the NMO patient sera analyz

98 In NMO, AQP4 p61-80-specific T cells exhibited Th17 polariz

99 is review aims to discuss recent advances in NMO diagnosis and treatment, and to discuss the differen

100 4-specific T-cell responses are amplified in NMO, exhibit a Th17 bias, and display cross-reactivity t

101 ndoS treatment of blood may be beneficial in NMO, and may be accomplished, for example, by therapeuti

102 direct administration, may be beneficial in NMO.

103 AQP4 assembly in OAPs is required for CDC in NMO, establishing a new mechanism of OAP-dependent NMO p

104 ding development of AQP4-reactive T cells in NMO.

105 Tocilizumab might be effective in NMO, here in a patient not responding to leukocyte deple

106 MO to investigate the role of eosinophils in NMO pathogenesis and the therapeutic potential of eosino

107 implicate the involvement of eosinophils in NMO pathogenesis by ADCC and CDCC mechanisms and suggest

108 NMO, but other causes need to be excluded in NMO-IgG-seronegative patients.

109 atures, MRI and other laboratory findings in NMO have been clarified further.

110 The dynamics of astrocyte injury in NMO and the mechanisms by which toxicity spreads to axon

111 potential early therapeutic intervention in NMO.

112 abnormalities have not been investigated in NMO.

113 ommend methotrexate as a treatment option in NMO patients who do not tolerate first-line therapy, exp

114 ingly, C. perfringens was overrepresented in NMO (p = 5.24 x 10(-8) ).

115 this commensal microbe might participate in NMO pathogenesis.

116 strocytic damage is the primary pathology in NMO, and experimental studies confirm the pathogenicity

117 pport a potential role for C. perfringens in NMO pathogenesis.

118 NMO pathology was produced in NMO-IgG-treated spinal cord slice cultures by inclusion

119 prine significantly reduces relapse rates in NMO and NMO spectrum disorder patients.

120 ong-term efficacy and safety of rituximab in NMO.

121 longest follow-up of rituximab treatment in NMO, which provide reassurance regarding the long-term e

122 oping imaging markers for clinical trials in NMO.

123 ealed that brain lesions are not uncommon in NMO, and some patterns appear to be unique to NMO.

124 ed drug in general practice and when used in NMO it reduces relapse frequency, stabilises disability

125 Intraperitoneally injected NMO-IgG binds mouse placental aquaporin-4, activates coi

126 providing new perspectives for investigating NMO pathogenesis.

127 ed hafnium oxide (nHfO2) was used as a model NMO.

128 cell cultures, IdeS treatment of monoclonal NMO-IgGs and NMO patient sera abolished CDC and ADCC, ev

129 an AQP4 using a human recombinant monoclonal NMO-IgG and transfected Fisher rat thyroid cells stably

130 Nitronate monooxygenase (NMO) oxidizes the mitochondrial toxin propionate 3-nitro

131 substrate for the nogalamycin monooxygenase (NMO) from Streptomyces nogalater As with flavin, dithran

132 N-Hydroxylating monooxygenases (NMOs) are essential for pathogenesis in fungi and bacter

133 sis of multialignment analysis, mutagenesis, NMO-IgG binding, and cytotoxicity assay, we have disclos

134 Since patients with AQP4-Ab negative NMO/SD require different management, the use of both app

135 Patients with AQP4-Ab-negative NMO/NMOSD should be tested for MOG-Abs.

136 a and AQP4-Ab-positive and antibody-negative NMO/NMO spectrum disorder cohorts should be analyzed sep

137 -selective cleavage by IdeS thus neutralizes NMO-IgG pathogenicity, and yields therapeutic F(ab')(2)

138 body (AQP4-Ab) status, and compared to a non NMO control cohort.

139 njected with NMO-IgG without complement, non-NMO-IgG with human complement, or in aquaporin-4 null mi

140 The EndoS-treated, nonpathogenic NMO-IgG competitively displaced pathogenic NMO-IgG bound

141 11) and prevalence (on December 31, 2011) of NMO/NMOSD and aquaporin-4-IgG seroincidence and seroprev

142 ed prior optic neuritis compared with 71% of NMO eyes without microcystic abnormalities).

143 ported a wide range of binding affinities of NMO-IgGs to AQP4 in separate tetramers versus intramembr

144 of NMO that led to reduced agglomeration of NMO.

145 tuses were born normal when lower amounts of NMO-IgG and human complement were injected.

146 onformation of which enables the assembly of NMO-IgG epitopes.

147 , and we evaluated the effects on binding of NMO AQP4-reactive rAbs by quantitative immunofluorescenc

148 Binding of NMO-IgG to AQP4 was similar to that of the NMO-F(ab')(2)

149 First, the binding of NMO-IgG to the ectodomain of astrocytic AQP4 has isoform

150 gh-throughput screen to identify blockers of NMO-IgG binding to human AQP4 using a human recombinant

151 n be effective in therapy-resistant cases of NMO.

152 hat a high proportion of CSF plasma cells of NMO patients produce antibody to the extracellular domai

153 peutic strategies for LETM in the context of NMO include eculizumab, which could be considered in pat

154 spinal cord reveals the swift development of NMO-related acute axon injury following AQP4 antibody-me

155 Recent advances in the diagnosis of NMO have led to very sensitive and specific tests and ad

156 IgG seropositivity, and a final diagnosis of NMO or NMOSD.

157 tant laboratory finding for the diagnosis of NMO.

158 However, since the discovery of NMO-IgG or aquaporin-4 (AQP4) antibody (AQP4-antibody),

159 in the nature and anatomical distribution of NMO lesions, and in the clinical and imaging manifestati

160 Other features of NMO include female preponderance, longitudinally extensi

161 itical molecule in the immunopathogenesis of NMO, and a critical role for T cells in the pathogenesis

162 mediated cytotoxicity, without impairment of NMO-IgG binding to AQP4.

163 ced by continuous intracerebral injection of NMO-IgG and complement showed marked eosinophil infiltra

164 Moreover, the majority of NMO patients carry IgG autoantibodies against aquaporin-

165 ings have implications for the management of NMO during pregnancy.

166 nal cord slices, and in vivo mouse models of NMO to investigate the role of eosinophils in NMO pathog

167 pinal cord slice culture and mouse models of NMO.

168 inal cord slice, and in vivo mouse models of NMO.

169 uccessfully inhibited the Brownian motion of NMO that led to reduced agglomeration of NMO.

170 rnative strategy involving neutralization of NMO-IgG effector function by selective IgG heavy-chain d

171 LETM is not pathognomonic of NMO, therefore it is important to investigate for other

172 ino acids for binding, two broad patterns of NMO-IgG recognition could be distinguished based on diff

173 es expressing aquaporin-4 in the presence of NMO autoantibody (NMO-IgG).

174 lecule trap had an effect in the presence of NMO.

175 Patients who have a clinical presentation of NMO, who have been tested with older ELISA or immunofluo

176 This study reports the highest prevalence of NMO/NMOSD in any population (10/100,000 in Martinique),

177 s for therapy of NMO, based on prevention of NMO-IgG binding to AQP4.

178 of the spinal cord, one of the main sites of NMO pathology, as a powerful tool to study the formation

179 Thus, the spectrum of NMO is wider than mere ON and TM.

180 ying the mechanisms underlying the spread of NMO pathology beyond astrocytes, as well as in evaluatin

181 ing features, immunopathology and therapy of NMO and NMO spectrum disorders.

182 l-molecule blocker strategies for therapy of NMO, based on prevention of NMO-IgG binding to AQP4.

183 EndoS treatment of NMO patient serum reduced by >95% CDC and antibody-depen

184 assay can be used to identify inhibitors of NMOs.

185 c neuritis attack for those with rLETM-onset NMO followed a median of 3 myelitis attacks (range, 2-19

186 -positive patients with rLETM or rLETM-onset NMO were similar in age at onset, sex ratio, attack seve

187 attacks of transverse myelitis (rLETM-onset NMO).

188 For patients with rLETM-onset NMO, the median time from onset to first optic neuritis

189 Most patients with neuromyelitis optica (NMO) and many with NMO spectrum disorder have autoantibo

190 e; two presenting with neuromyelitis optica (NMO) and one with isolated optic neuritis (ON).

191 Neuromyelitis optica (NMO) attacks often are severe, are difficult to treat, a

192 ific IgG distinguishes neuromyelitis optica (NMO) from multiple sclerosis and causes characteristic i

193 Neuromyelitis optica (NMO) has been described as a disease clinically characte

194 Neuromyelitis optica (NMO) has long been considered as a variant of multiple s

195 12 (25%) negative for neuromyelitis optica (NMO) IgG (per IIF of serial serum specimens).

196 Neuromyelitis optica (NMO) is a chronic inflammatory disease of the CNS that i

197 Neuromyelitis Optica (NMO) is a severe and rare inflammatory condition, where

198 Neuromyelitis optica (NMO) is a severe autoimmune inflammatory disorder associ

199 Neuromyelitis optica (NMO) is an autoimmune disease of the central nervous sys

200 Neuromyelitis optica (NMO) is an autoimmune disease of the CNS, which resemble

201 Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of spinal

202 Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the cen

203 Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the cen

204 Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the cen

205 Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the CNS

206 Neuromyelitis optica (NMO) is an inflammatory disease of the optic nerves and

207 Neuromyelitis optica (NMO) is caused by binding of pathogenic autoantibodies (

208 Neuromyelitis optica (NMO) is characterized by disabling relapses of optic neu

209 Neuromyelitis optica (NMO) is characterized by the presence of pathogenic auto

210 in 4 antibody-negative neuromyelitis optica (NMO) is rare when good assays are used.

211 athological feature of neuromyelitis optica (NMO) lesions and is clinically relevant.

212 les from patients with neuromyelitis optica (NMO) or NMOSD (101) and controls (92) were tested at 15

213 cells are expanded in neuromyelitis optica (NMO) patients and exhibit Th17 polarization.

214 T cells from neuromyelitis optica (NMO) patients, which recognize the immunodominant epitop

215 tment in patients with neuromyelitis optica (NMO) revealed significant improvements in relapse rates

216 ndependent episodes of neuromyelitis optica (NMO) spectrum disorder (5 cases, 4 anti-AQP4 positive) o

217 d noncharacteristic of neuromyelitis optica (NMO) spectrum disorders (NMOSDs).

218 orin-4 (AQP4)-negative neuromyelitis optica (NMO), and chronic relapsing inflammatory optic neuritis

219 hows pathologically to neuromyelitis optica (NMO), including that demyelination in both is secondary

220 rent groups: controls, neuromyelitis optica (NMO), longitudinally extensive transverse myelitis (LETM

221 dinal manifestation of neuromyelitis optica (NMO).

222 myelinating lesions in neuromyelitis optica (NMO).

223 pathologic changes in neuromyelitis optica (NMO).

224 ple sclerosis (MS) and neuromyelitis optica (NMO).

225 alomyelitis (EAE), and neuromyelitis optica (NMO).

226 r its association with neuromyelitis optica (NMO).

227 s derived from non-mineralising osteoblasts (NMO-EVs) were not found to enhance mineralisation beyond

228 Notably, the only other NMO from Neurospora crassa for which biochemical evidenc

229 ents with LETM identified through the Oxford NMO clinical database.

230 0, and April 1, 2013, seen within the Oxford NMO service and who tested positive for MOG-Abs or AQP4-

231 o fabrication of nanostructured metal oxide (NMO) based cancer biosensor.

232 We describe a national paediatric NMO cohort's clinical, MRI, outcome, and prognostic feat

233 ion to the recognition of AQP4 by pathogenic NMO Abs.

234 EndoS deglycosylation converts pathogenic NMO-IgG autoantibodies into therapeutic blocking antibod

235 c NMO-IgG competitively displaced pathogenic NMO-IgG bound to AQP4, and prevented NMO pathology in sp

236 F(ab')(2) competitively displaced pathogenic NMO-IgG, preventing cytotoxicity, and the Fc fragments g

237 range, 26-40 years) and aquaporin 4-positive NMO.

238 e series of 14 aquaporin-4 antibody positive NMO and NMO spectrum disorder patients treated with meth

239 06 criteria or aquaporin-4 antibody-positive NMO spectrum disorder (NMOSD).

240 we review distinct features of AQP4-positive NMO and MS, which might then be useful in the diagnosis

241 hogenic NMO-IgG bound to AQP4, and prevented NMO pathology in spinal cord slice culture and mouse mod

242 Prior NMO/NMOSD epidemiological studies are limited by lack of

243 NMO-IgG in mice in vivo, and greatly reduced NMO lesions in mice administered NMO-IgG and human compl

244 inophil-stabilizing actions, greatly reduced NMO-IgG/eosinophil-dependent cytotoxicity and NMO pathol

245 r aquaporin-4 binding, significantly reduced NMO-IgG and human complement induced placentitis and fet

246 erosis, including 30 patients with relapsing NMO or NMOSD.

247 e damage and downstream inflammation require NMO-IgG effector function to initiate complement-depende

248 Second, NMO-IgG binding to either isoform impairs water flux dir

249 ed on 92 control samples and 35 seronegative NMO/SD patient samples.

250 nly 6.5% of patients had "true" seronegative NMO and 6.5% had idiopathic LETM.

251 ssays, leaving 35 patients with seronegative NMO/spectrum disorder (SD).

252 with highly active aquaporin 4-seropositive NMO who failed numerous immunosuppressive interventions,

253 city with highly active AQP4-ab-seropositive NMO (n = 6) and NMO spectrum disorder (n = 2) whose dise

254 his raises important practical issues, since NMO and MS respond differently to immunomodulatory treat

255 tients with NMO have circulating Abs, termed NMO-IgG, against the astrocytic water channel protein aq

256 scarriage, thus challenging the concept that NMO affects only the CNS.

257 Experimental evidence is emerging that NMO is partly driven by the proinflammatory cytokine int

258 4 in different M1/M23 ratios, indicated that NMO-IgG-dependent CDC requires AQP4 OAP assembly.

259 Our data suggest that NMO-IgG can cause miscarriage, thus challenging the conc

260 This suggested that NMO both accelerated the formation and directed the reco

261 were not significantly different between the NMO and MS-ON groups, the patients with NMO had a signif

262 gnificantly thinner than in controls for the NMO, MS-ON, and MS non-ON groups (P<0.001 for the 3 grou

263 ctious disorders should be exclusions in the NMO diagnostic criteria and AQP4-Ab-positive and antibod

264 ely impairs NMO-IgG binding for 85.7% of the NMO patient sera analyzed here.

265 f NMO-IgG to AQP4 was similar to that of the NMO-F(ab')(2) generated by IdeS cleavage.

266 c damage, were consistently found within the NMO lesions when compared with healthy controls and pati

267 a K(d) value of 0.60 +/- 0.05 muM and to the NMOs from Aspergillus fumigatus and Mycobacterium smegma

268 Evolution to NMO can be anticipated in AQP4-IgG-positive patients.

269 e to the predilection of these structures to NMO pathologic changes.

270 MO, and some patterns appear to be unique to NMO.

271 in mice exposed to control or EndoS-treated NMO-IgG.

272 Twenty NMO cases (females = 90%; AQP4-Ab positive = 60%; median

273 uctive central nervous system lesions of two NMO patients, two previously unappreciated histopatholog

274 inor myelin proteins, in addition to typical NMO features.

275 Inclusion criteria were NMO according to Wingerchuk's 2006 criteria or aquaporin

276 ith typical anti-NMDAR encephalitis, 56 with NMO, and 30 with multiple sclerosis; NMDAR antibodies we

277 umab, a nonpathogenic IgG that competes with NMO-IgG for aquaporin-4 binding, significantly reduced N

278 transverse myelitis (TM) are diagnosed with NMO and those who show an incomplete phenotype with isol

279 n AQP4 expression between an individual with NMO and the control samples.

280 Optic nerve tissue from an individual with NMO did not differ in AQP4 expression from control sampl

281 t, or in aquaporin-4 null mice injected with NMO-IgG and human complement.

282 placentitis was found in mice injected with NMO-IgG without complement, non-NMO-IgG with human compl

283 ith neuromyelitis optica (NMO) and many with NMO spectrum disorder have autoantibodies against aquapo

284 ges were identified in 5 of 25 patients with NMO (20%) and 7 of 48 total eyes, including 7 of 29 eyes

285 Seventeen patients with NMO (mean age, 45 years; 14 women) were compared with 17

286 icker than in controls for the patients with NMO (P = 0.003) and LETM (P = 0.006) but not for those w

287 ter analysis of relapses in 90 patients with NMO and NMO spectrum disorder treated with azathioprine,

288 , the INL thickening occurs in patients with NMO and patients with LETM, and study of this layer may

289 x 10(23) mm(2)/sec +/- 0.04 in patients with NMO compared with 0.75 +/- 0.02, 0.33 x 10(23) mm(2)/sec

290 ersistent visual disability in patients with NMO following optic neuritis.

291 the NMO and MS-ON groups, the patients with NMO had a significantly thicker INL than the patients wi

292 Most patients with NMO have circulating Abs, termed NMO-IgG, against the as

293 logy occurs in a proportion of patients with NMO in eyes previously affected by acute optic neuritis.

294 ting disorders, and conversely patients with NMO or demyelinating disorders with atypical symptoms (e

295 ignificant differences between patients with NMO with and without microcystic changes in terms of age

296 rum and cerebrospinal fluid of patients with NMO, induces AQP4-ab production by plasmablasts and repr

297 included 140 AQP4-IgG-positive patients with NMO, of whom a subgroup of 20 initially presented with 2

298 her with or without ON, and in patients with NMO.

299 tensive white matter damage in patients with NMO.

300 Here, we showed that patients with NMO/NMOSD with MOG-Abs demonstrate differences when comp