ライフサイエンスコーパス: myasthenia gravis

1 n for selected cases of generalized juvenile myasthenia gravis.

2 mptom of recurrent thymoma in a patient with myasthenia gravis.

3 erse ongoing EAT and experimental autoimmune myasthenia gravis.

4 7357 in a model of the neuromuscular disease myasthenia gravis.

5 subunit of the nicotinic receptor linked to myasthenia gravis.

6 heumatoid arthritis, Sjogren's syndrome, and myasthenia gravis.

7 re frequent respiratory crises than non-MuSK myasthenia gravis.

8 sitive patients represent a unique subset of myasthenia gravis.

9 in patients with generalised non-thymomatous myasthenia gravis.

10 be of significant therapeutic value in human myasthenia gravis.

11 henia gravis and rat experimental autoimmune myasthenia gravis.

12 ecreasing the risk of developing generalized myasthenia gravis.

13 ave been the first-line treatment for ocular myasthenia gravis.

14 ioprine, and mycophenolate mofetil in ocular myasthenia gravis.

15 s, autoimmune thyroid disease, vitiligo, and myasthenia gravis.

16 diseases may help to guide the treatment of myasthenia gravis.

17 ummarize the results of newer treatments for myasthenia gravis.

18 support its use for long-term improvement in myasthenia gravis.

19 toimmune antibodies in sera of patients with myasthenia gravis.

20 autoimmune disease of synaptic transmission, myasthenia gravis.

21 of anti-TAChR Ab, and prevented experimental myasthenia gravis.

22 as stroke, the Guillain-Barre syndrome, and myasthenia gravis.

23 of P. wickerhamii algaemia in a patient with myasthenia gravis.

24 tor antibody-positive refractory generalised myasthenia gravis.

25 physiologic signs of experimental autoimmune myasthenia gravis.

26 eptor, and autoantibodies from patients with myasthenia gravis.

27 gnostic techniques, and treatment for ocular myasthenia gravis.

28 ession regulation, and EOM susceptibility to myasthenia gravis.

29 cacy and safety in patients with generalised myasthenia gravis.

30 and efficacious in patients with generalised myasthenia gravis.

31 ases characterized by reduced AChRs, such as myasthenia gravis.

32 including congenital myasthenic syndrome and myasthenia gravis.

33 -year period in patients with nonthymomatous myasthenia gravis.

34 ients who met diagnostic criteria for ocular myasthenia gravis.

35 vels and progression from OMG to generalized myasthenia gravis.

36 ated loci for early- and late-onset forms of myasthenia gravis.

37 of a lesion on the forearm of a patient with myasthenia gravis.

38 cell-dependent and B cell-mediated model for myasthenia gravis.

39 passive induction of experimental autoimmune Myasthenia gravis.

40 effective strategy in the treatment of human myasthenia gravis.

41 er susceptibility to experimental autoimmune myasthenia gravis.

42 le to children and adolescents with juvenile myasthenia gravis.

43 entation, and treatment options for juvenile myasthenia gravis.

44 who did not develop symptoms of generalized myasthenia gravis (12.7 [16.5] nmol/L vs 4.2 [7.9] nmol/

45 her systemic autoimmune disorders, including myasthenia gravis (40%) and rheumatoid arthritis (20%).

46 luded Guillain-Barre syndrome (99 cases) and myasthenia gravis (76 cases) and, rarely, gastrointestin

47 anti-rat FcRn mAb, 1G3, in two rat models of myasthenia gravis, a prototypical Ab-mediated autoimmune

48 , inducing muscle weakness characteristic of myasthenia gravis, a T cell-dependent Ab-mediated autoim

49 ogic disorders (eg, autoimmune encephalitis, myasthenia gravis) accounted for 6 526 278 claims and co

50 hR; acetylcholine receptor antibody positive myasthenia gravis (AChR-MG)] by the radioimmunoprecipita

51 oundation of America severity class II-IV, a Myasthenia Gravis Activities of Daily Living (MG-ADL) sc

52 patients were aged at least 18 years, with a Myasthenia Gravis-Activities of Daily Living (MG-ADL) sc

53 actor (SCF) mRNA were elevated in normal and myasthenia gravis-aged thymuses, and correlated with dec

54 imilar findings may be seen in patients with myasthenia gravis, although disrupted peripheral toleran

55 In this study we demonstrate that myasthenia gravis, an autoimmune disease strongly identi

56 ing acetylcholine receptor antibody-positive myasthenia gravis and 1998 race/ethnicity-matched contro

57 Forty percent of the patients had associated myasthenia gravis and 27% had a secondary primary malign

58 t of a single case of a 53-year-old man with myasthenia gravis and a prior thymectomy presenting with

59 ance (59 and 28%, respectively)-particularly myasthenia gravis and acetylcholine receptor (AChR) anti

60 sidered a primary disease mechanism in human myasthenia gravis and animal models of experimentally ac

61 sed in progressive multiple sclerosis and in myasthenia gravis and autoimmune neuropathies that are r

62 e is also new literature on childhood ocular myasthenia gravis and childhood neurosarcoidosis.

63 nfection in three patients thymectomized for myasthenia gravis and determined the effect of antiretro

64 hat inhibit complement are being explored in myasthenia gravis and Guillain-Barre syndrome (GBS).

65 inhibitors in autoimmune diseases, including myasthenia gravis and immune thrombocytopenia, provides

66 Immunotherapy with sophisticated agents for myasthenia gravis and inflammatory myopathies, neuroprot

67 her autoimmune neurological diseases such as myasthenia gravis and multiple sclerosis.

68 the autoantibodies to muscle AChRs in human myasthenia gravis and rat experimental autoimmune myasth

69 lar-blocking agent be used for patients with myasthenia gravis and that the dose should be based on p

70 died from treatment-related adverse events (myasthenia gravis and worsening of renal failure), and o

71 er developed as a novel approach to treating myasthenia gravis and, even more broadly, other diseases

72 ith thymoma, chronic visceral leishmaniasis, myasthenia gravis, and a marked increase of rare gammade

73 ncomplete resection, preoperative absence of myasthenia gravis, and advanced Lattes/Bernatz pathologi

74 ibly perpetuate the autoantibody response in myasthenia gravis, and are a rational target for strateg

75 antiphospholipid syndrome, Sjogren syndrome, myasthenia gravis, and celiac disease.

76 icient mice developed an exacerbated form of myasthenia gravis, and demonstrated that NOS2 expression

77 , are increasingly prescribed for refractory myasthenia gravis, and drugs that inhibit complement are

78 approval after visual disturbances, syncope, myasthenia gravis, and hepatotoxicity were noted.

79 y in stiff-person syndrome, dermatomyositis, myasthenia gravis, and Lambert-Eaton myasthenic syndrome

80 iopathy, antiphospholipid antibody syndrome, myasthenia gravis, and neuromyelitis optica.

81 Brachial plexopathy, myasthenia gravis, and NMJ Disorders showed statisticall

82 rimental studies on MuSK antibody associated myasthenia gravis, and summarize the results of newer tr

83 e thyroiditis (EAT), experimental autoimmune myasthenia gravis, and type 1 diabetes, and could also r

84 ar weakness and fatigability associated with myasthenia gravis are engendered by autoantibodies direc

85 in patients with generalised non-thymomatous myasthenia gravis at 3 years.

86 ars and older, with seropositive generalised myasthenia gravis (autoantibodies to the acetylcholine r

87 ed in 267 patients with clinically confirmed myasthenia gravis between January 1, 1995, and December

88 Three patients also had myasthenia gravis, bulbar weakness, or symptoms that ini

89 th the Lambert-Eaton myasthenic syndrome and myasthenia gravis but had a variable, mild, or unsubstan

90 ely to have a role in refractory generalised myasthenia gravis, but no approved therapies specificall

91 tomy has been a mainstay in the treatment of myasthenia gravis, but there is no conclusive evidence o

92 ariety of autoimmune diseases, most commonly myasthenia gravis caused by anti-acetylcholine receptor

93 Myasthenia gravis, caused by IgG Ab against muscle acety

94 myasthenia gravis (OMG), a localized form of myasthenia gravis clinically involving only the extraocu

95 eing applied to medical decision making, but myasthenia gravis, commonly considered the best understo

96 in patients with generalised non-thymomatous myasthenia gravis compared with prednisone alone.

97 In myasthenia gravis, complement-mediated lysis directed at

98 The myasthenia gravis composite score addresses items common

99 roliferative maintenance is described.Median myasthenia gravis composite scores reduced by >50% after

100 nital myasthenic syndrome, and patients with myasthenia gravis develop antibodies against agrin, LRP4

101 An 81-year-old male with myasthenia gravis developed a cutaneous infection with M

102 Data were drawn from the Adelphi Real World myasthenia gravis Disease Specific Programme(TM), a cros

103 Double-seronegative myasthenia gravis (dSNMG) includes patients with myasthe

104 eaths were due to complications arising from myasthenia gravis (durvalumab 10 mg/kg every 4 weeks plu

105 enia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG) are caused by Ab-mediated autoi

106 s the development of experimental autoimmune myasthenia gravis (EAMG) has not been studied.

107 ptor (TAChR) induces experimental autoimmune myasthenia gravis (EAMG) in C57BL/6 (B6) mice.

108 r the development of experimental autoimmune myasthenia gravis (EAMG) in C57BL/6 mice.

109 thepsin S (Cat S) in experimental autoimmune myasthenia gravis (EAMG) induced by AChR immunization.

110 r the development of experimental autoimmune myasthenia gravis (EAMG) induced by AChR immunization.

111 Experimental autoimmune myasthenia gravis (EAMG) is an animal model of human mya

112 Experimental autoimmune myasthenia gravis (EAMG) is severe in RIIIS/J mice, desp

113 e been implicated in experimental autoimmune myasthenia gravis (EAMG) pathogenesis in susceptible H-2

114 Experimental autoimmune myasthenia gravis (EAMG), a disorder of the neuromuscula

115 sease progression in experimental autoimmune myasthenia gravis (EAMG), a T cell-dependent and B cell-

116 this possibility in experimental autoimmune myasthenia gravis (EAMG), an animal model of human myast

117 nd its animal model, experimental autoimmune myasthenia gravis (EAMG), are antibody (Ab)-mediated aut

118 or a role of IL-6 in experimental autoimmune myasthenia gravis (EAMG), IL-6 gene KO (IL-6(-/-)) mice

119 of clinical signs of experimental autoimmune myasthenia gravis (EAMG), we treated mice with clinical

120 and animal models of experimentally acquired myasthenia gravis (EAMG).

121 lity to induction of experimental autoimmune myasthenia gravis (EAMG).

122 ologue of HLA-DQ, in experimental autoimmune myasthenia gravis (EAMG).

123 cause the symptoms of human and experimental myasthenia gravis (EMG).

124 ylcholine receptor (AChR) cause experimental myasthenia gravis (EMG).

125 lcholine receptor (AChR) causes experimental myasthenia gravis (EMG).

126 vely define the genetic basis of early onset myasthenia gravis (EOMG).

127 motor unit disorders with weakness occur in myasthenia gravis, especially with thymoma, a myopathy a

128 Myasthenia gravis exacerbations were reported by six (10

129 rats had evidence of experimental autoimmune myasthenia gravis; five of five tested had electrophysio

130 of Daily Living (MG-ADL) score of 6 or more, Myasthenia Gravis Foundation of America (MGFA) class II-

131 y department visits and hospitalizations and Myasthenia Gravis Foundation of America (MGFA) clinical

132 less than 5 years were included if they had Myasthenia Gravis Foundation of America clinical class I

133 abnormal single fibre electromyography), had Myasthenia Gravis Foundation of America Clinical Classif

134 tactin antibodies, 6 had ocular MG and 3 had Myasthenia Gravis Foundation of America clinical classif

135 BFR score correlated positively with current Myasthenia Gravis Foundation of America grades and with

136 sion, or minimal manifestations based on the Myasthenia Gravis Foundation of America postintervention

137 in receptor-related protein 4 [LRP4-IgG]), a Myasthenia Gravis Foundation of America severity class I

138 ent trans-sternal thymectomy for symptomatic myasthenia gravis from 1969 through 1996 at the Johns Ho

139 Among individuals with generalized myasthenia gravis (gMG), risk factors for increased seve

140 mune-mediated diseases including generalized myasthenia gravis (gMG).

141 neuropathies, systemic lupus erythematosus, myasthenia gravis, Guillain-Barre syndrome, skin blister

142 tients who developed symptoms of generalized myasthenia gravis had a significantly higher mean (SD) a

143 Incubation with control human IgG (normal or myasthenia gravis) had no effect.

144 ns for antigen-specific immunosuppression of myasthenia gravis has the potential to be specific, robu

145 Randomized clinical studies of myasthenia gravis have been carried out primarily in adu

146 , neuromyelitis optica spectrum disorder and myasthenia gravis, have shown dramatic clinical response

147 ith unique paraneoplastic syndromes, such as myasthenia gravis, hypogammaglobulinemia, and pure red c

148 testing, and progression time to generalized myasthenia gravis (if this occurred) were recorded for e

149 f the integrated management of patients with myasthenia gravis in a large series of patients from a s

150 Although relatively rare, myasthenia gravis in children has 2 predominant forms, C

151 There he began to work on myasthenia gravis in collaboration with Ricardo Miledi a

152 uppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas a

153 n an active model of experimental autoimmune myasthenia gravis in which rats were immunized with AChR

154 hree patients with adult acquired autoimmune myasthenia gravis in whom AChR loss results directly fro

155 Adults (aged >=18 years) with generalised myasthenia gravis inadequately controlled with standard-

156 in an experimental model of human autoimmune myasthenia gravis induced by a self-Ag, the acetylcholin

157 We used an animal model, experimental myasthenia gravis induced in C57Bl/6 mice by immunizatio

158 enia gravis (EAMG), an animal model of human myasthenia gravis, induced by immunization of C57BL/6 mi

159 Myasthenia gravis is a chronic, autoimmune, neuromuscula

160 Juvenile myasthenia gravis is a relatively rare autoimmune neurom

161 Myasthenia gravis is an acquired autoimmune disease caus

162 Myasthenia gravis is an autoimmune disorder that selecti

163 te that some, but not all, adult research on myasthenia gravis is applicable to children and adolesce

164 Myasthenia gravis is believed to be an autoimmune disord

165 The prevalence and incidence of myasthenia gravis is higher than previously thought.

166 l condition, the genetic etiology underlying myasthenia gravis is not well understood.

167 As juvenile myasthenia gravis is rare, it has been difficult to coll

168 The pathophysiology of juvenile myasthenia gravis is similar to that of adult myasthenia

169 Preventing progression to generalized myasthenia gravis is still under debate and needs to be

170 e score addresses items commonly affected in myasthenia gravis, is sensitive to detect clinical chang

171 uscle-specific kinase protein in generalized myasthenia gravis, it has been found to be only rarely i

172 In myasthenia gravis, it should be reserved for difficult c

173 The incidence of juvenile myasthenia gravis (JMG) and congenital myasthenic syndro

174 Conversion rates from ocular to generalized myasthenia gravis may be lower than previously reported

175 Ocular myasthenia gravis may mimic any pupil-spared, painless,

176 To update our current concepts of ocular myasthenia gravis medical management and to provide a sh

177 g neuromuscular junction destruction in both myasthenia gravis (MG) and experimental autoimmune MG (E

178 Myasthenia gravis (MG) and experimental autoimmune myast

179 it of acetylcholine receptor (AChR) in human myasthenia gravis (MG) and in experimental autoimmune MG

180 e end-plate region in patients with acquired myasthenia gravis (MG) and in rats with experimental aut

181 Myasthenia gravis (MG) and its animal model, experimenta

182 Myasthenia gravis (MG) and its animal model, experimenta

183 )-specific IgG4 autoantibodies in autoimmune myasthenia gravis (MG) are functionally monovalent as a

184 Some patients with myasthenia gravis (MG) do not respond to conventional tr

185 All adults (>=18 years) diagnosed with myasthenia gravis (MG) from January 1, 1990, through Dec

186 Approximately 80% of patients with myasthenia gravis (MG) have autoantibodies against acety

187 Only around 80% of patients with generalized myasthenia gravis (MG) have serum antibodies to acetylch

188 f skeletal muscles and cause the symptoms of myasthenia gravis (MG) in humans, as well as in experime

189 Myasthenia gravis (MG) is a neuromuscular transmission d

190 Myasthenia gravis (MG) is a neuromuscular, autoimmune di

191 Myasthenia gravis (MG) is a prototype Ab-mediated autoim

192 Myasthenia gravis (MG) is a prototypical autoimmune dise

193 Myasthenia gravis (MG) is a prototypical B cell-mediated

194 Juvenile myasthenia gravis (MG) is a relatively rare autoimmune d

195 Myasthenia gravis (MG) is a severely debilitating autoim

196 Myasthenia gravis (MG) is a T cell-dependent, Ab-mediate

197 Myasthenia gravis (MG) is a well-recognised disorder of

198 Myasthenia gravis (MG) is an autoimmune disease caused b

199 Myasthenia gravis (MG) is an autoimmune disease in which

200 Myasthenia gravis (MG) is an autoimmune disease mediated

201 Myasthenia gravis (MG) is an autoimmune disease mediated

202 Acquired myasthenia gravis (MG) is an autoimmune disorder of the

203 Myasthenia gravis (MG) is an autoimmune neuromuscular tr

204 Myasthenia gravis (MG) is an autoimmune syndrome caused

205 The muscle weakness in myasthenia gravis (MG) is mediated by autoantibodies aga

206 Susceptibility to myasthenia gravis (MG) is positively linked to expressio

207 The early-onset form of Myasthenia Gravis (MG) is prevalent in women and associa

208 Myasthenia gravis (MG) is the most common disorder affec

209 Studies in myasthenia gravis (MG) patients demonstrate that polymor

210 utoantigen has been definitively identified, myasthenia gravis (MG) provides a unique opportunity for

211 nvironment (TME) were evaluated to determine myasthenia gravis (MG) severity in patients with thymoma

212 We have analyzed 87 normal and 31 myasthenia gravis (MG) thymus tissues from patients rang

213 Patients with myasthenia gravis (MG) who do not respond to conventiona

214 in the autoimmune regulator (AIRE) gene, and myasthenia gravis (MG) with thymoma, show intriguing but

215 A proportion of patients with myasthenia gravis (MG) without acetylcholine receptor (A

216 thenia gravis (dSNMG) includes patients with myasthenia gravis (MG) without detectable antibodies to

217 AChR) is a major target of autoantibodies in myasthenia gravis (MG), an autoimmune disease that cause

218 Myasthenia gravis (MG), an autoimmune disorder of neurom

219 n association with paraneoplastic autoimmune myasthenia gravis (MG), an IgG-mediated impairment of sy

220 is considered a rare pathogenic mechanism in myasthenia gravis (MG), but is usually studied on AChRs

221 In myasthenia gravis (MG), extraocular muscle (EOM) weaknes

222 and had preexisting multiple sclerosis (MS), myasthenia gravis (MG), Guillain-Barre syndrome (GBS), a

223 In myasthenia gravis (MG), TNF and IL-1beta polymorphisms a

224 tomy in humans is performed for treatment of myasthenia gravis (MG), we have studied patients with MG

225 ached on the ideal therapeutic algorithm for myasthenia gravis (MG).

226 and in certain autoimmune disorders, such as myasthenia gravis (MG).

227 lecule that reportedly predisposes humans to myasthenia gravis (MG).

228 e target of the pathogenic autoantibodies in myasthenia gravis (MG).

229 ia gravis (EAMG) is an animal model of human myasthenia gravis (MG).

230 receptor (AChR) antibodies in patients with myasthenia gravis (MG).

231 e counterparts in animal models of lupus and myasthenia gravis (MG).

232 e major phenotypes in MuSK antibody positive myasthenia gravis (MMG) patients: indistinguishable from

233 pecific kinase [MuSK; MuSK antibody positive myasthenia gravis (MuSK-MG)] make up a variable proporti

234 ereferral diagnostic considerations included myasthenia gravis, myopathies, and psychiatric disorders

235 t enrolment, had generalised non-thymomatous myasthenia gravis of less than 5 years' duration, had ac

236 ody testing is thought to be lower in ocular myasthenia gravis (OMG) compared with generalized diseas

237 establish a novel model of autoimmune ocular myasthenia gravis (oMG) in mice and study the pathogenic

238 (2) compared the binding of sera from ocular myasthenia gravis (OMG) patients with fetal (alpha2 beta

239 PURPOSE OF REVIEW: To review ocular myasthenia gravis (OMG), a localized form of myasthenia

240 s with chronic inflammatory diseases such as myasthenia gravis or organ transplant recipients.

241 04; P = .007) and progression to generalized myasthenia gravis (OR, 2.92; 95% CI, 1.18-7.26; P = .02)

242 yositis (PM), inclusion body myositis (IBM), myasthenia gravis, or genetically determined myopathies

243 unction in patients with spinal cord injury, myasthenia gravis, or multiple sclerosis.

244 le sclerosis, inflammatory bowel disease and myasthenia gravis, or systemic diseases, including syste

245 th a cohort of patients affected by juvenile myasthenia gravis over a number of years.

246 The incidence of myasthenia gravis, particularly in patients older than 5

247 ntibody (mAb 131) previously isolated from a myasthenia gravis patient by immortalization of thymic B

248 Further, 3D co-culture treatments with myasthenia gravis patient sera shows the ease of studyin

249 we incubated these co-cultures with IgG from myasthenia gravis patients and active complement.

250 The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) s

251 The UPSIT scores of the myasthenia gravis patients were markedly lower than thos

252 ariable proportion of AChR antibody negative myasthenia gravis patients who are often, but not exclus

253 Some of the 20% of myasthenia gravis patients who do not have antibodies to

254 row B cells of 12 healthy individuals, eight myasthenia gravis patients, and six systemic lupus eryth

255 bodies (IgG4-AID) include diseases like MuSK myasthenia gravis, pemphigus vulgaris or thrombotic thro

256 iction, dyschromatopsia, worsening of ocular myasthenia gravis, posterior reversible leukoencephalopa

257 nical status as measured by the Quantitative Myasthenia Gravis (QMG) score in patients with generalis

258 diseases) and neuromuscular syndromes (e.g. myasthenia gravis) raises the possibility that future th

259 e group should be monitored in patients with myasthenia gravis receiving neuromuscular-blocking agent

260 ic medical records were searched to identify myasthenia gravis-related symptoms before (</= 14 days)

261 ignificantly associated with exacerbation of myasthenia gravis-related symptoms.

262 a exchange in that disease, he established a myasthenia gravis research group at the Royal Free Hospi

263 fic tyrosine kinase (MuSK) antibody positive myasthenia gravis results in neuromuscular transmission

264 a potentially useful reagent for studies of myasthenia gravis, rhabdomyosarcoma and arthrogryposis m

265 were the time-weighted average Quantitative Myasthenia Gravis score (on a scale from 0 to 39, with h

266 d a lower time-weighted average Quantitative Myasthenia Gravis score over a 3-year period than those

267 d by a majority of human, feline, and canine myasthenia gravis sera.

268 ified as a cytoplasmic antigen recognized by myasthenia gravis sera.

269 tor (AChR) are found in 85% of patients with myasthenia gravis (seropositive MG [SPMG]) and are thoug

270 llowed by clinically meaningful decreases on myasthenia gravis severity scales at up to 9 months of f

271 dentified in some generalized "seronegative" myasthenia gravis (SNMG) patients, who are often females

272 MuSK antibodies define a form of myasthenia gravis that can be difficult to diagnose, can

273 In myasthenia gravis, the expression of acetylcholine recep

274 ssible, patients were maintained on existing myasthenia gravis therapies and rescue medication was al

275 yasthenia gravis is similar to that of adult myasthenia gravis, though there remain important differe

276 rospective series suggests that, as in adult myasthenia gravis, thymectomy is a viable therapeutic op

277 ormal human (aged 3 days to 78 years) and 34 myasthenia gravis thymuses (aged 4 to 75 years) during a

278 did not fall with aging in either normal or myasthenia gravis thymuses.

279 izes, describe the response of patients with myasthenia gravis to thymectomy primarily with respect t

280 An adolescent patient with myasthenia gravis treated with thymectomy subsequently d

281 Immunosuppression remains the mainstay of myasthenia gravis treatment.

282 e treatment; and (4) in contrast to acquired myasthenia gravis, treatment with acetylcholinesterase i

283 ts across the genome and risk for developing myasthenia gravis using logistic regression modeling.

284 nt issues related to pregnancy in women with myasthenia gravis was held in May 2011.

285 Passive experimental autoimmune myasthenia gravis was induced by administration of an an

286 Myasthenia gravis was the most prevalent clinical manife

287 to T cells is critical to the development of myasthenia gravis, we examined the role of cathepsin S (

288 62 peptide-induced tolerance in experimental myasthenia gravis were examined.

289 nge for managing Guillain-Barre syndrome and myasthenia gravis were published.

290 ic antibody (ANCA)-associated vasculitis and myasthenia gravis were rather disappointing.

291 ge, male sex, and progression to generalized myasthenia gravis were significantly associated with a p

292 First, in myasthenia gravis, what mechanisms are likely to underli

293 fic tyrosine kinase (MuSK) antibody positive myasthenia gravis will be reviewed.

294 rs of age who had generalized nonthymomatous myasthenia gravis with a disease duration of less than 5

295 ripheral neuromuscular symptoms analogous to myasthenia gravis with no known central nervous system i

296 o be reduced, have been used in all types of myasthenia gravis with some success, but they have not b

297 l strains of immunized mice developed ocular myasthenia gravis with varying disease incidence and sev

298 a component of the integrated management of myasthenia gravis, with significant improvement seen in

299 This is proving relevant to seronegative myasthenia gravis, with the discovery of anti-MuSK antib

300 uded in the study were diagnosed with ocular myasthenia gravis without the presence of generalized di