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 pathology was produced in NMO-IgG-treated spinal cor

4 NMO was previously associated with a poor prognosis; how

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

6 NMO-IgG alone caused astrocyte activation and AQP4 loss.

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

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

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

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

14 LiNi(0.5)Mn(1.5)O(4) and Ni(0.5)Mn(1.5)O(4) (NMO).

15 f (2E,6E)-octa-2,6-diene catalyzed by OsO(4)/NMO has been studied using density functional theory (DF

16 experimental results for reactions of OsO(4)/NMO with 1,5-dienes with acid (oxidative cyclization) an

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

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

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

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

21 32 samples from 50 (64%) NMO sera and 34 from 51 (67%) NMOSD sera were positive o

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

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

24 more commonly and earlier compared to adult NMO.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 nt facilitates direct electron transfer, and NMO accelerates rate-limiting electron transfer by stron

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

43 Binding of AQP4-specific antibodies (NMO-IgG) triggers activation of the complement cascade,

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

45 85 genes are annotated in the GenBank(TM) as NMO.

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

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

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

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

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

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

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

53 On average, NMO patients had a higher proportion of Native American

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

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

56 may hold promise for differentiating between NMO and MS.

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

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

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

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

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

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

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

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

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

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

67 stry and to seek genetic variants conferring NMO susceptibility in admixed Mexican patients.

68 en considering only those fulfilling current NMO diagnostic criteria.

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

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 seropositivity increased from 56% to 75% for NMO, 5% to 22% for CRION, 6% to 7% for RION, 0% to 7% fo

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

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

79 nducted at a single UK specialist center for NMO.

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

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

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

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

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

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

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

87 egative patients, including those fulfilling NMO diagnostic criteria.

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

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

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

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

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

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

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

95 direct administration, may be beneficial in NMO.

96 ed the molecular determinants driving CDC in NMO using recombinant AQP4-specific autoantibodies (AQP4

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

98 plement proteins in astrocyte destruction in NMO is well established, little is known regarding the i

99 ation, and is consistent with differences in NMO epidemiology in Mexico and Latin America.

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

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

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

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

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

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

106 potential early therapeutic intervention in NMO.

107 abnormalities have not been investigated in NMO.

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

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

110 this commensal microbe might participate in NMO pathogenesis.

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

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

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

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

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

116 croglia may serve as a therapeutic target in NMO.

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

118 oping imaging markers for clinical trials in NMO.

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

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

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

122 otein environment, increases by 85 mV inside NMO, corresponding to a DeltaDeltaG (0)' of 2.0 kcal mol

123 ization of the Os(VI) dioxoglycolate, or its NMO complex, through protonation of an oxo ligand to giv

124 A total of 164 Mexican NMO patients and 1,208 controls were included.

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

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

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

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

129 Nogalamycin monooxygenase (NMO) from Streptomyces nogalater is a cofactor-independe

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

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

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

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

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

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

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

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

138 of CRION, 10% of SION, 0% of MSON and 0% of NMO.

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

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

141 of NMO that led to reduced agglomeration of NMO.

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

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

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

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

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

147 Other causes of NMO (such as paraneoplastic disorders and neurosarcoidos

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

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

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

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

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

153 tant laboratory finding for the diagnosis of NMO.

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

155 Other features of NMO include female preponderance, longitudinally extensi

156 icity (CDC) is critical for the formation of NMO lesions, the molecular mechanisms governing optimal

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

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

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

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

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

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

163 pinal cord slice culture and mouse models of NMO.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 12 (25%) negative for neuromyelitis optica (NMO) IgG (per IIF of serial serum specimens).

190 Neuromyelitis optica (NMO) is a central nervous system (CNS) inflammatory auto

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

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

193 Neuromyelitis optica (NMO) is an autoimmune CNS disorder mediated by pathogeni

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

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

196 Neuromyelitis Optica (NMO) is an autoimmune disease with a higher prevalence i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 hemorrhage (ICH), and neuromyelitis optica (NMO).

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

216 r its association with neuromyelitis optica (NMO).

217 dinal manifestation of neuromyelitis optica (NMO).

218 myelinating lesions in neuromyelitis optica (NMO).

219 pathologic changes in neuromyelitis optica (NMO).

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

221 Neuromyelitis optica (NMO; also known as Devic syndrome) is a clinical syndrom

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

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

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

225 0, and April 1, 2013, seen within the Oxford NMO service and who tested positive for MOG-Abs or AQP4-

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

227 hat oxidation by N-methylmorpholine N-oxide (NMO) is selective for the C4-borylated 1,2-azaborine, an

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

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

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

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

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

233 In most patients, NMO is caused by pathogenetic serum IgG autoantibodies t

234 ited CDC induced by AQP4 rAbs and polyclonal NMO patient sera.

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

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

237 06 criteria or aquaporin-4 antibody-positive NMO spectrum disorder (NMOSD).

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

239 roved for the treatment of AQP4-IgG-positive NMO and its formes frustes.

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

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

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

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

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

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

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

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

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

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

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

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

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

253 In summary, NMO's protein environment facilitates direct electron tr

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

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

256 and mutagenesis methods, we demonstrate that NMO initially activates the substrate, lowering its pK(a

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

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

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

260 ocal ancestry estimates suggest that all the NMO-associated alleles within the HLA region are of Nati

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 erican ancestry significantly contributes to NMO susceptibility in an admixed population, and is cons

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 otential new therapeutic avenue for treating NMO.

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

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

275 eagues evaluated the precytolytic phase when NMO-IgG binds astrocytes in vivo in the absence of exoge

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

277 GWAS identified a HLA region associated with NMO, led by rs9272219 (OR = 2.48, P = 8 x 10(-10)).

278 howed the most significant associations with NMO risk.

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

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

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

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

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

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

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

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

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

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

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

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 QP4 gene were found in Mexican patients with NMO or multiple sclerosis.

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

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

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

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

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