ライフサイエンスコーパス: myasthenia

1 J transmission cause muscle weakness, termed myasthenia.

2 has changed our previous view of congenital myasthenia.

3 nd Escobar syndrome, two forms of congenital myasthenia.

4 Eaton myasthenic syndrome and 'seronegative' myasthenia.

5 N mutations have been reported in congenital myasthenia.

6 nosis continues to be challenging for ocular myasthenia.

7 scular synapse, and their absence results in myasthenia.

8 derlie familial limb-girdle myasthenia (DOK7 myasthenia), a neuromuscular disease characterized by sm

9 Heterozygous null mice have latent myasthenia and a right shift of the force-stimulus relat

10 alleles is rare and has been associated with myasthenia and congenital myopathy, while a mix of loss

11 hE should be avoided during the treatment of myasthenia and the pharmacological reversal of residual

12 mutants (which cause slow-channel congenital myasthenia) and therefore would contribute significantly

13 First, the clinical features of Dok-7 myasthenia are highly variable.

14 type can be distinguished from 'limb-girdle' myasthenia associated with tubular aggregates, where DOK

15 l transfer of these antibodies in women with myasthenia can cause fetal or neonatal weakness and occa

16 and cognitive function and is compromised in myasthenias, cardiovascular diseases, and neurodegenerat

17 rted in humans, with a propensity for pseudo-myasthenia caused by a marginal Na(+) current density to

18 Congenital myasthenias (CMs) arise from defects in neuromuscular ju

19 s been recently associated with the onset of myasthenia, common neuromuscular disorders mainly charac

20 At 2 years, generalized myasthenia developed in 8 of 76 patients in the treated

21 DOK7 mutations underlie familial limb-girdle myasthenia (DOK7 myasthenia), a neuromuscular disease ch

22 rs) examined at Mayo Clinic with any form of myasthenia from January 1 1966, through December 31, 201

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 Myasthenia gravis (MG) and experimental autoimmune myast

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

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

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

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

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

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

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

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

60 Myasthenia gravis (MG) is a neuromuscular transmission d

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

62 Myasthenia gravis (MG) is a prototypical autoimmune dise

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

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

65 Myasthenia gravis (MG) is a severely debilitating autoim

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

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

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

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

70 Myasthenia gravis (MG) is an autoimmune disease mediated

71 Myasthenia gravis (MG) is an autoimmune disease mediated

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

73 Myasthenia gravis (MG) is an autoimmune neuromuscular tr

74 Myasthenia gravis (MG) is an autoimmune syndrome caused

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 04; P = .007) and progression to generalized myasthenia gravis (OR, 2.92; 95% CI, 1.18-7.26; P = .02)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 The myasthenia gravis composite score addresses items common

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

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

130 Myasthenia gravis exacerbations were reported by six (10

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Myasthenia gravis is a chronic, autoimmune, neuromuscula

148 Juvenile myasthenia gravis is a relatively rare autoimmune neurom

149 Myasthenia gravis is an acquired autoimmune disease caus

150 Myasthenia gravis is an autoimmune disorder that selecti

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

152 Myasthenia gravis is believed to be an autoimmune disord

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Immunosuppression remains the mainstay of myasthenia gravis treatment.

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

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

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

185 Myasthenia gravis was the most prevalent clinical manife

186 62 peptide-induced tolerance in experimental myasthenia gravis were examined.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 In myasthenia gravis, the expression of acetylcholine recep

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

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

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

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

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

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

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

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

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

238 effective strategy in the treatment of human myasthenia gravis.

239 er susceptibility to experimental autoimmune myasthenia gravis.

240 le to children and adolescents with juvenile myasthenia gravis.

241 entation, and treatment options for juvenile myasthenia gravis.

242 n for selected cases of generalized juvenile myasthenia gravis.

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

244 erse ongoing EAT and experimental autoimmune myasthenia gravis.

245 7357 in a model of the neuromuscular disease myasthenia gravis.

246 subunit of the nicotinic receptor linked to myasthenia gravis.

247 in patients with generalised non-thymomatous myasthenia gravis.

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

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

250 sitive patients represent a unique subset of myasthenia gravis.

251 be of significant therapeutic value in human myasthenia gravis.

252 henia gravis and rat experimental autoimmune myasthenia gravis.

253 ecreasing the risk of developing generalized myasthenia gravis.

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

255 ioprine, and mycophenolate mofetil in ocular myasthenia gravis.

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

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

258 ummarize the results of newer treatments for myasthenia gravis.

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

260 toimmune antibodies in sera of patients with myasthenia gravis.

261 autoimmune disease of synaptic transmission, myasthenia gravis.

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

263 tor antibody-positive refractory generalised myasthenia gravis.

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

265 including congenital myasthenic syndrome and myasthenia gravis.

266 -year period in patients with nonthymomatous myasthenia gravis.

267 ients who met diagnostic criteria for ocular myasthenia gravis.

268 vels and progression from OMG to generalized myasthenia gravis.

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

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

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

272 passive induction of experimental autoimmune Myasthenia gravis.

273 4, a long-time candidate gene for congenital myasthenia, have now been described and a new pathogenic

274 ord, where he continued to see patients with myasthenia, he was the President of the Association of B

275 mic abnormalities and cellular immunology of myasthenia, identified antibody-mediated mechanisms in a

276 typic and molecular genetic aspects of Dok-7 myasthenia in 16 patients.

277 impair Dok-7 are a major cause of congenital myasthenia in humans.

278 ants in MACF1 are associated with congenital myasthenia in humans.

279 he diagnostic tests that may help to confirm myasthenia in patients without acetylcholine receptor an

280 KDeltaCRD mice developed signs of congenital myasthenia, including severe NMJs dismantlement, muscle

281 the neonatal period; (3) provided that their myasthenia is under good control before pregnancy, the m

282 nt myasthenic weakness, even if the mother's myasthenia is well-controlled, and should have rapid acc

283 fore leading investigators to a diagnosis of myasthenia, is once again highlighted.

284 rimarily proximal limb muscles ['limb-girdle myasthenia' (LGM)].

285 loss of rapsyn function may cause congenital myasthenia, more severe loss of function can result in a

286 This case highlights the overlap of myasthenia, neuromyotonia, and thymoma, emphasizing the

287 patients with myotonia, periodic paralysis, myasthenia, or congenital myopathy.

288 found to be only rarely identified in ocular myasthenia patients and therefore the majority of patien

289 , their toxicity is poorly defined in ocular myasthenia patients and whether they reduce the risk of

290 y to transient symptomatic attacks including myasthenia, periodic paralysis, myotonic stiffness, seiz

291 echanisms of complement-mediated myopathies, myasthenia, peripheral neuropathies, neuromyelitis and o

292 The visual compromise of ocular myasthenia responds poorly to nonpharmacological and cho

293 patient that causes slow channel congenital myasthenia syndrome was shown to be cholesterol-sensitiv

294 onstrated in a particular form of hereditary myasthenia syndrome.

295 ons for human neuromuscular diseases such as myasthenia syndromes.

296 Here, we show in a mouse model of DOK7 myasthenia that therapeutic administration of an adeno-a

297 whereas most mutations that cause congenital myasthenia truncate the C-terminal domain.

298 implications for both autoimmune and genetic myasthenias where anticholinesterase medication is a sta

299 ogenous clinical entity combining congenital myasthenia with distal muscle weakness and atrophy remin

300 ne for the diagnosis and treatment of ocular myasthenia within the limits of largely retrospective ca