ライフサイエンスコーパス: myasthenia

1 scular synapse, and their absence results in myasthenia.

2 nd Escobar syndrome, two forms of congenital myasthenia.

3 Eaton myasthenic syndrome and 'seronegative' myasthenia.

4 N mutations have been reported in congenital myasthenia.

5 nosis continues to be challenging for ocular myasthenia.

6 J transmission cause muscle weakness, termed myasthenia.

7 has changed our previous view of congenital myasthenia.

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

9 t to be characterized for familial infantile myasthenia, acetylcholinesterase deficiency and ACh-rece

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

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

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

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

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

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

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

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

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

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

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

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

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

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 an animal model of human mya

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 Myasthenia gravis (MG) and experimental autoimmune myast

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

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

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

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

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

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

59 Myasthenia gravis (MG) is a neuromuscular transmission d

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

61 Myasthenia gravis (MG) is a prototypical autoimmune dise

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

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

64 Myasthenia gravis (MG) is a severely debilitating autoim

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

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 mediated

69 Myasthenia gravis (MG) is an autoimmune disease mediated

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

71 Myasthenia gravis (MG) is an autoimmune neuromuscular tr

72 Myasthenia gravis (MG) is an autoimmune syndrome caused

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 04; P = .007) and progression to generalized myasthenia gravis (OR, 2.92; 95% CI, 1.18-7.26; P = .02)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 The myasthenia gravis composite score addresses items common

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

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

128 Myasthenia gravis exacerbations were reported by six (10

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Myasthenia gravis is a chronic, autoimmune, neuromuscula

147 Juvenile myasthenia gravis is a relatively rare autoimmune neurom

148 Myasthenia gravis is an acquired autoimmune disease caus

149 Myasthenia gravis is an autoimmune disorder that selecti

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

151 Myasthenia gravis is believed to be an autoimmune disord

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 Immunosuppression remains the mainstay of myasthenia gravis treatment.

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

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

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

182 Myasthenia gravis was the most prevalent clinical manife

183 62 peptide-induced tolerance in experimental myasthenia gravis were examined.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 Myasthenia gravis, caused by IgG Ab against muscle acety

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

210 In myasthenia gravis, complement-mediated lysis directed at

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

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

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

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

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

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

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

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

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

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

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

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

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

224 In myasthenia gravis, the expression of acetylcholine recep

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

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

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

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

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

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

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

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

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

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

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

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

237 erse ongoing EAT and experimental autoimmune myasthenia gravis.

238 7357 in a model of the neuromuscular disease myasthenia gravis.

239 subunit of the nicotinic receptor linked to myasthenia gravis.

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

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

242 sitive patients represent a unique subset of myasthenia gravis.

243 including congenital myasthenic syndrome and myasthenia gravis.

244 be of significant therapeutic value in human myasthenia gravis.

245 henia gravis and rat experimental autoimmune myasthenia gravis.

246 ecreasing the risk of developing generalized myasthenia gravis.

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

248 ioprine, and mycophenolate mofetil in ocular myasthenia gravis.

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

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

251 ummarize the results of newer treatments for myasthenia gravis.

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

253 toimmune antibodies in sera of patients with myasthenia gravis.

254 autoimmune disease of synaptic transmission, myasthenia gravis.

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

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

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

258 physiologic signs of experimental autoimmune myasthenia gravis.

259 eptor, and autoantibodies from patients with myasthenia gravis.

260 gnostic techniques, and treatment for ocular myasthenia gravis.

261 tor antibody-positive refractory generalised myasthenia gravis.

262 -year period in patients with nonthymomatous myasthenia gravis.

263 ients who met diagnostic criteria for ocular myasthenia gravis.

264 vels and progression from OMG to generalized myasthenia gravis.

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

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

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

268 passive induction of experimental autoimmune Myasthenia gravis.

269 effective strategy in the treatment of human myasthenia gravis.

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

271 er susceptibility to experimental autoimmune myasthenia gravis.

272 le to children and adolescents with juvenile myasthenia gravis.

273 entation, and treatment options for juvenile myasthenia gravis.

274 n for selected cases of generalized juvenile myasthenia gravis.

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

276 4, a long-time candidate gene for congenital myasthenia, have now been described and a new pathogenic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 onstrated in a particular form of hereditary myasthenia syndrome.

296 ons for human neuromuscular diseases such as myasthenia syndromes.

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

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

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