ライフサイエンスコーパス: myasthenia gravis

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

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

3 sitive patients represent a unique subset of myasthenia gravis.

4 be of significant therapeutic value in human myasthenia gravis.

5 henia gravis and rat experimental autoimmune myasthenia gravis.

6 ecreasing the risk of developing generalized myasthenia gravis.

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

8 including congenital myasthenic syndrome and myasthenia gravis.

9 ioprine, and mycophenolate mofetil in ocular myasthenia gravis.

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

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

12 ummarize the results of newer treatments for myasthenia gravis.

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

14 toimmune antibodies in sera of patients with myasthenia gravis.

15 autoimmune disease of synaptic transmission, myasthenia gravis.

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

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

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

19 physiologic signs of experimental autoimmune myasthenia gravis.

20 eptor, and autoantibodies from patients with myasthenia gravis.

21 gnostic techniques, and treatment for ocular myasthenia gravis.

22 ession regulation, and EOM susceptibility to myasthenia gravis.

23 tor antibody-positive refractory generalised myasthenia gravis.

24 -year period in patients with nonthymomatous myasthenia gravis.

25 ients who met diagnostic criteria for ocular myasthenia gravis.

26 vels and progression from OMG to generalized myasthenia gravis.

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

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

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

30 passive induction of experimental autoimmune Myasthenia gravis.

31 effective strategy in the treatment of human myasthenia gravis.

32 er susceptibility to experimental autoimmune myasthenia gravis.

33 le to children and adolescents with juvenile myasthenia gravis.

34 entation, and treatment options for juvenile myasthenia gravis.

35 n for selected cases of generalized juvenile myasthenia gravis.

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

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

38 erse ongoing EAT and experimental autoimmune myasthenia gravis.

39 7357 in a model of the neuromuscular disease myasthenia gravis.

40 subunit of the nicotinic receptor linked to myasthenia gravis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 Myasthenia gravis, caused by IgG Ab against muscle acety

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

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

84 In myasthenia gravis, complement-mediated lysis directed at

85 The myasthenia gravis composite score addresses items common

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 Myasthenia gravis exacerbations were reported by six (10

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 Myasthenia gravis is a chronic, autoimmune, neuromuscula

138 Juvenile myasthenia gravis is a relatively rare autoimmune neurom

139 Myasthenia gravis is an acquired autoimmune disease caus

140 Myasthenia gravis is an autoimmune disorder that selecti

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

142 Myasthenia gravis is believed to be an autoimmune disord

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

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

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

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

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

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

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

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

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

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

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

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

155 Myasthenia gravis (MG) and experimental autoimmune myast

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

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

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

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

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

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

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

163 Myasthenia gravis (MG) is a neuromuscular transmission d

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

165 Myasthenia gravis (MG) is a prototypical autoimmune dise

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

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

168 Myasthenia gravis (MG) is a severely debilitating autoim

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

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

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

172 Myasthenia gravis (MG) is an autoimmune disease mediated

173 Myasthenia gravis (MG) is an autoimmune disease mediated

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

175 Myasthenia gravis (MG) is an autoimmune neuromuscular tr

176 Myasthenia gravis (MG) is an autoimmune syndrome caused

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 04; P = .007) and progression to generalized myasthenia gravis (OR, 2.92; 95% CI, 1.18-7.26; P = .02)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 In myasthenia gravis, the expression of acetylcholine recep

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

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

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

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

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

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

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

240 Immunosuppression remains the mainstay of myasthenia gravis treatment.

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

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

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

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

245 Myasthenia gravis was the most prevalent clinical manife

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

247 62 peptide-induced tolerance in experimental myasthenia gravis were examined.

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

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

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

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

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

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

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

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

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

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

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