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1           The excitatory events that trigger myotonic action potentials in the absence of stabilizing
2 slow afterdepolarization (AfD) that triggers myotonic action potentials.
3 vealed the absence of the exons 15 and 16 in myotonic animals.
4 on of the linear fragment of pumiliotoxin B (myotonic, cardiotonic) and enantioselective synthesis an
5 ncluding muscle histological morphology, and myotonic discharges and heart conduction abnormalities,
6 n shows delayed relaxation, and there are no myotonic discharges at electromyography, we recommend di
7 tal limbs of Tg26-hDMPK showed myopathy with myotonic discharges coupled with deficit in sarcolemmal
8 e sodium channel alpha-subunit, resulting in myotonic discharges in skeletal muscle of the lower urin
9                                              Myotonic discharges were more common in statin-associate
10 duction in the CUG(exp) mRNA, a reduction in myotonic discharges, a shift toward adult pre-mRNA splic
11 ty and deactivation kinetics, and eliminated myotonic discharges.
12                                          The myotonic dystrophies (DM) are human diseases in which th
13                       PURPOSE OF REVIEW: The myotonic dystrophies (DM1 and DM2) are the paradigm for
14  known RNA-mediated disorders, including the myotonic dystrophies and fragile X tremor ataxia syndrom
15 tor protein that plays a pivotal role in the Myotonic Dystrophies and Huntington's Disease, and sever
16                                              Myotonic dystrophies are the most common, comprising 28.
17                   The pathomechanism for the myotonic dystrophies is not well understood and the role
18 ansions of noncoding CUG and CCUG repeats in myotonic dystrophies type 1 (DM1) and DM2 cause complex
19                                              Myotonic dystrophies type 1 (DM1) and type 2 (DM2) are n
20                                              Myotonic dystrophies type 1 and type 2 are progressive m
21 tive approach to screening and management of myotonic dystrophies type 1 and type 2 requires a multid
22 c mechanisms that have been proposed for the myotonic dystrophies, the clinical and molecular feature
23 e splicing and polyadenylation in congenital myotonic dystrophy (CDM).
24                                              Myotonic dystrophy (DM) is a genetic disorder caused by
25                                              Myotonic dystrophy (DM) is a multi-system neuromuscular
26                                              Myotonic dystrophy (DM) is a multisystemic disease cause
27                                              Myotonic dystrophy (DM) is caused by a CTG expansion in
28                                              Myotonic dystrophy (DM) is caused by a triplet repeat ex
29                                              Myotonic dystrophy (DM) is caused by either an untransla
30                                              Myotonic dystrophy (DM) is caused by the expression of m
31  a topic of intense study due to its role in myotonic dystrophy (DM) pathogenesis.
32           The RNA-mediated disease model for myotonic dystrophy (DM) proposes that microsatellite C(C
33                                              Myotonic dystrophy (DM) type 1 is associated with an exp
34 (MBNL) protein family has been implicated in myotonic dystrophy (DM), a specific function for these p
35                                           In myotonic dystrophy (DM), expression of RNA containing ex
36 t roles in muscle and eye development and in myotonic dystrophy (DM), in which expanded CUG or CCUG r
37  foci by C(C)UG microsatellite expansions in myotonic dystrophy (DM), is essential for normal thymus
38 proposed first for the neuromuscular disease myotonic dystrophy (DM), which is associated with the ex
39                                              Myotonic dystrophy (DM)--the most common form of muscula
40 pathogenic event in the RNA-mediated disease myotonic dystrophy (DM).
41  is a key player in the disease mechanism of myotonic dystrophy (DM).
42 tal muscle development and are implicated in myotonic dystrophy (DM).
43 UGn RNA in the induction of stress in type 1 myotonic dystrophy (DM1) cells and in the stress-mediate
44                                              Myotonic dystrophy (DM1) is a highly variable, multi-sys
45                                       Type I myotonic dystrophy (DM1) is caused by a triplet repeat e
46                                              Myotonic dystrophy (DM1) is caused by an expansion of CU
47                                           In myotonic dystrophy (DM1), both inactivation of musclebli
48                                              Myotonic dystrophy (DM1), the most common muscular dystr
49 rections for many genetic diseases including myotonic dystrophy (DM1).
50 ein implicated in the pathogenesis of type I myotonic dystrophy (DM1).
51 ated with expanded repeat sequences, such as myotonic dystrophy (DM1).
52                                           In myotonic dystrophy (dystrophia myotonica [DM]), an incre
53                                              Myotonic dystrophy (dystrophia myotonica, DM) is a multi
54 ls have been implicated in schizophrenia and myotonic dystrophy (MD), and both conditions carry an in
55                                              Myotonic dystrophy 1 (DM1) is a multi-system disorder ch
56                                              Myotonic dystrophy 1 (DM1) is a multisystemic disease ca
57                                           In myotonic dystrophy 1 (DM1), aggregation of the mutant DM
58 f skeletal muscle pathology in patients with Myotonic Dystrophy 1 (DM1).
59 ts for Duchenne MD, various limb girdle MDs, myotonic dystrophy 1, facioscapulohumeral MD, dysferlino
60                                              Myotonic dystrophy 2 (DM2) is a multisystem skeletal mus
61                                              Myotonic dystrophy 2 (DM2) is an autosomal dominant, mul
62 the results with those of four patients with myotonic dystrophy and 12 healthy individuals.
63 ween the pathogenic RNA repeat expansions of myotonic dystrophy and MBNL1.
64                Using a cell culture model of myotonic dystrophy and myotonic dystrophy patient tissue
65 ls are key players in both the human disease myotonic dystrophy and the regulation of alternative spl
66 nic mouse model to show that derangements of myotonic dystrophy are reversed by a morpholino antisens
67              This process is dysregulated in myotonic dystrophy because MBNL proteins are sequestered
68  for a therapeutic strategy for treatment of myotonic dystrophy by ablating or silencing expression o
69 sis might have a clinically relevant role in myotonic dystrophy cardiac conduction defects and pathol
70                        The genetic lesion in myotonic dystrophy does not eliminate an essential muscl
71                                  Research on myotonic dystrophy has led to the recognition of a novel
72 unction is a prominent cause of mortality in myotonic dystrophy I (DM1), a disease where expanded CUG
73  in the development of RNA splice defects in myotonic dystrophy I (DM1), we purified RNA-independent
74                  Therapeutic development for myotonic dystrophy is moving rapidly with the developmen
75             RECENT FINDINGS: RNA toxicity in myotonic dystrophy is now associated with bi-directional
76                                           In myotonic dystrophy it is the RNA rather than protein pro
77 roteins HSP20, HSP25, alphaB-crystallin, and myotonic dystrophy kinase binding protein (MKBP) may reg
78                                        MRCK (myotonic dystrophy kinase-related Cdc42 binding kinase),
79                                              Myotonic dystrophy kinase-related Cdc42-binding kinase (
80 ation and invasion by binding and activating myotonic dystrophy kinase-related CDC42-binding kinase a
81                 Caspase-mediated cleavage of myotonic dystrophy kinase-related CDC42-binding kinase-a
82 cell culture model of myotonic dystrophy and myotonic dystrophy patient tissue, we have evidence that
83 L1, a splicing factor that is sequestered in myotonic dystrophy patients by binding to expanded r(CUG
84                          In human cells from myotonic dystrophy patients, treatment with 5-aza-CdR st
85 e variant CaV1.1e in the skeletal muscles of myotonic dystrophy patients.
86 sed Znf9 and Clc1 expression and rescued the myotonic dystrophy phenotype in Znf9+/- mice.
87 e Znf9 haploinsufficiency contributes to the myotonic dystrophy phenotype in Znf9+/- mice.
88 e basis for a new type of instability of the myotonic dystrophy protein kinase (DMPK) gene in patient
89                                              Myotonic dystrophy protein kinase (DMPK), a muscle- and
90 G)n tract in the 3' UTR of the gene encoding myotonic dystrophy protein kinase (DMPK), which results
91 ' untranslated region of the gene coding for myotonic dystrophy protein kinase (DMPK).
92                 Abnormal expression of human myotonic dystrophy protein kinase (hDMPK) gene products
93 -coil domain reminiscent of eukaryotic DMPK (Myotonic Dystrophy Protein Kinase) family kinases such a
94                By this mechanism, effects of myotonic dystrophy repeat expansions impact many differe
95  human samples from patients with congenital myotonic dystrophy type 1 (CDM1) and spinal muscular atr
96  with Huntington's disease (CAG repeats) and myotonic dystrophy type 1 (CTG repeats).
97 anded rCUG and rCAG repeat RNAs expressed in myotonic dystrophy type 1 (DM1) and spinocerebellar atax
98                                              Myotonic dystrophy type 1 (DM1) and type 2 (DM2) are cau
99 d CCUG are the underlying genetic causes for myotonic dystrophy type 1 (DM1) and type 2 (DM2), respec
100  sequence is considered a causative agent of myotonic dystrophy type 1 (DM1) because of its ability t
101 nscript (CUG(exp)) is the causative agent of myotonic dystrophy type 1 (DM1) by sequestering musclebl
102 man spinocerebellar ataxia type 8 (SCA8) and myotonic dystrophy type 1 (DM1) CAG expansion transcript
103  disease (HD) FEN1 +/- heterozygous mice and myotonic dystrophy type 1 (DM1) FEN1 +/- heterozygous mi
104                     Background Patients with myotonic dystrophy type 1 (DM1) increased their physical
105 A working hypothesis for the pathogenesis of myotonic dystrophy type 1 (DM1) involves the aberrant se
106                                              Myotonic dystrophy type 1 (DM1) is a complex neuromuscul
107                         The genetic basis of myotonic dystrophy type 1 (DM1) is a CTG expansion in th
108                                              Myotonic dystrophy type 1 (DM1) is a CTG microsatellite
109                                              Myotonic Dystrophy type 1 (DM1) is a dominant neuromuscu
110                                              Myotonic dystrophy type 1 (DM1) is a dominantly inherite
111                                              Myotonic dystrophy type 1 (DM1) is a genetic disorder in
112                                              Myotonic dystrophy type 1 (DM1) is a genetic disorder li
113                                              Myotonic dystrophy type 1 (DM1) is a life-threatening an
114                                              Myotonic dystrophy type 1 (DM1) is a microsatellite expa
115                                              Myotonic dystrophy type 1 (DM1) is a multisystem neuromu
116                                              Myotonic dystrophy type 1 (DM1) is a multisystemic genet
117                                              Myotonic dystrophy type 1 (DM1) is a neuromuscular disor
118                                              Myotonic dystrophy Type 1 (DM1) is a rare genetic diseas
119                                              Myotonic dystrophy type 1 (DM1) is a triplet repeating d
120                                              Myotonic dystrophy type 1 (DM1) is an autosomal dominant
121                                              Myotonic dystrophy type 1 (DM1) is an autosomal dominant
122                                              Myotonic dystrophy type 1 (DM1) is an autosomal dominant
123                                              Myotonic dystrophy type 1 (DM1) is an incurable neuromus
124                                              Myotonic dystrophy type 1 (DM1) is an inherited dominant
125                                              Myotonic dystrophy type 1 (DM1) is an RNA dominant disea
126                                              Myotonic dystrophy type 1 (DM1) is an RNA-dominant disea
127                                              Myotonic dystrophy type 1 (DM1) is associated with expan
128                                              Myotonic dystrophy type 1 (DM1) is caused by a CTG expan
129                                              Myotonic dystrophy type 1 (DM1) is caused by a CTG expan
130                                              Myotonic dystrophy type 1 (DM1) is caused by a CTG trinu
131                                              Myotonic dystrophy type 1 (DM1) is caused by an expanded
132                                              Myotonic dystrophy type 1 (DM1) is caused by expansion o
133                                              Myotonic dystrophy type 1 (DM1) is caused by expansion o
134                                              Myotonic dystrophy type 1 (DM1) is caused by the expansi
135                                              Myotonic dystrophy type 1 (DM1) is one of the most varia
136                                              Myotonic dystrophy type 1 (DM1) is one such disorder tha
137                                              Myotonic dystrophy type 1 (DM1) is the most common form
138 ion hypothesis for the CTG expansion causing myotonic dystrophy type 1 (DM1) located in the 3' noncod
139             The disease mechanism underlying myotonic dystrophy type 1 (DM1) pathogenesis in skeletal
140           Accumulation of RNA CUG repeats in myotonic dystrophy type 1 (DM1) patients leads to the in
141                                           In myotonic dystrophy type 1 (DM1), dystrophia myotonica pr
142  splicing has become a molecular hallmark of myotonic dystrophy type 1 (DM1), in which neonatal splic
143 ough cataract is a characteristic feature of myotonic dystrophy type 1 (DM1), little is known of the
144  and GAA.TTC are integral to the etiology of myotonic dystrophy type 1 (DM1), myotonic dystrophy type
145                                           In myotonic dystrophy type 1 (DM1), somatic mosaicism of th
146                                              Myotonic dystrophy type 1 (DM1), the most common adult m
147                                Among them is myotonic dystrophy type 1 (DM1), the most common form of
148                                              Myotonic dystrophy type 1 (DM1), the most common form of
149                                              Myotonic dystrophy type 1 (DM1), the most common form of
150                                              Myotonic dystrophy type 1 (DM1), the most common muscula
151                                              Myotonic dystrophy type 1 (DM1), the most prevalent musc
152       In the hereditary degenerative disease myotonic dystrophy type 1 (DM1), transcripts from the mu
153                                           In myotonic dystrophy type 1 (DM1), triplet repeat expansio
154 date disease for RNAi therapy application is myotonic dystrophy type 1 (DM1), which results from toxi
155 (hDMPK) gene products has been implicated in myotonic dystrophy type 1 (DM1), yet the impact of distr
156 h are disrupted on loss of MBNL1 function in myotonic dystrophy type 1 (DM1).
157 rophia myotonica protein kinase (DMPK) cause myotonic dystrophy type 1 (DM1).
158 k CTG expansion (CTG(exp)) knockin models of myotonic dystrophy type 1 (DM1).
159 S; trisomy 21) and the dementia component of myotonic dystrophy type 1 (DM1).
160 als with the inherited multisystemic disease myotonic dystrophy type 1 (DM1).
161 ting symptom experienced by individuals with myotonic dystrophy type 1 (DM1).
162 d pathogenic role of expanded CUG repeats in myotonic dystrophy type 1 (DM1).
163 ocess is impaired in patients afflicted with myotonic dystrophy type 1 (DM1).
164 rationally designed, multi-target agents for myotonic dystrophy type 1 (DM1).
165    METHODS AND We selected 855 patients with myotonic dystrophy type 1 (women, 51%; median age, 37 ye
166  cause dominantly inherited diseases such as myotonic dystrophy type 1 and 2 (DM1/2), Huntington's di
167                           Friedreich ataxia, myotonic dystrophy type 1 and 3 forms of intellectual di
168 detected in mouse models with DCM, including myotonic dystrophy type 1 and CELF1 overexpression model
169 s previously characterized in the context of myotonic dystrophy type 1 and epithelial-to-mesenchymal
170 se sequences are involved in the etiology of myotonic dystrophy type 1 and Friedreich's ataxia, respe
171 xias and the initial clinical application in myotonic dystrophy type 1 and Huntington's disease.
172                                              Myotonic dystrophy type 1 and type 2 (DM1 and DM2) are g
173 ress in elucidating the disease mechanism in myotonic dystrophy type 1 and type 2.
174                          Patients with adult myotonic dystrophy type 1 are at high risk for arrhythmi
175 ng in the molecular and clinical features of myotonic dystrophy type 1 as well as the screening of cl
176 epeats (CUG(exp)) are the causative agent of myotonic dystrophy type 1 by sequestering MBNL1.
177             Up to one-third of patients with myotonic dystrophy type 1 die suddenly.
178                  Historically, patients with myotonic dystrophy type 1 have not received the medical
179                                              Myotonic dystrophy type 1 is an autosomal dominant disor
180                                              Myotonic dystrophy type 1 is caused by the dysregulation
181                  The average age of death in myotonic dystrophy type 1 is in the fifth decade.
182                                              Myotonic dystrophy type 1 is the most prevalent muscular
183 he size of the CTG expansion in the blood of myotonic dystrophy type 1 patients is associated with to
184 n contrast to the CUG-RNA hairpins formed by myotonic dystrophy type 1 repeats, we found no evidence
185 umina sequencing in Huntington's disease and myotonic dystrophy type 1 subjects, we show that rs55787
186 der than 18 years with genetically confirmed myotonic dystrophy type 1 who were admitted to the Neuro
187   How this untranslated CTG expansion causes myotonic dystrophy type 1(DM1) has been controversial.
188  been implicated in human diseases including myotonic dystrophy type 1, Alzheimer's disease and multi
189                          Among patients with myotonic dystrophy type 1, an invasive strategy was asso
190  nine had myotonic dystrophy type 2, one had myotonic dystrophy type 1, and 17 had no identified muta
191 (P = 0.003) in both Huntington's disease and myotonic dystrophy type 1, and slower progression (P = 3
192 isease phenotype in Huntington's disease and myotonic dystrophy type 1, and suggests a common DNA rep
193 le for causing neurological diseases such as myotonic dystrophy type 1, but its binding mechanism rem
194 ples from individuals with one such disease, myotonic dystrophy type 1, provides an opportunity to pa
195 f Friedreich ataxia, fragile X syndrome, and myotonic dystrophy type 1, respectively.
196  dementia, fragile X tremor ataxia syndrome, myotonic dystrophy type 1, spinocerebellar ataxia type 8
197                                           In myotonic dystrophy type 1, the association between mutat
198                                   Similar to myotonic dystrophy type 1, the poly(CUG)n RNA co-localiz
199  atrophy, amyotrophic lateral sclerosis, and myotonic dystrophy type 1, were also reviewed.
200           Exon 2 is significantly reduced in myotonic dystrophy type 1, whose symptoms include dement
201 uation, out of 1014 patients included in the Myotonic Dystrophy Type 1-Heart Registry between January
202  disorders, including Huntington disease and myotonic dystrophy type 1.
203 er onset of symptoms and is less common than myotonic dystrophy type 1.
204  myotonica protein kinase (DMPK) gene causes myotonic dystrophy type 1.
205 able therapeutic target for the treatment of myotonic dystrophy type 1.
206 ive diseases, such as Huntington disease and myotonic dystrophy type 1.
207 tracts in the size range that is typical for myotonic dystrophy type 1.
208 n abnormalities in the neuromuscular disease myotonic dystrophy type 1.
209 06 adult patients with genetically confirmed myotonic dystrophy type 1.
210 expansion disorders Huntington's disease and myotonic dystrophy type 1.
211 en implicated in the cardiac pathogenesis of myotonic dystrophy type 1.
212  atrophy, amyotrophic lateral sclerosis, and myotonic dystrophy type 1.
213  atrophy, amyotrophic lateral sclerosis, and myotonic dystrophy type 1.
214 ranslated CCTG expansion in an intron causes myotonic dystrophy type 2 (DM2) have uncovered a new typ
215                                              Myotonic dystrophy type 2 (DM2) is a genetic disorder ch
216                                              Myotonic dystrophy type 2 (DM2) is a multisystemic disor
217                                              Myotonic dystrophy type 2 (DM2) is an incurable neuromus
218                                              Myotonic dystrophy type 2 (DM2) is caused by a CCTG expa
219                    The recent discovery that myotonic dystrophy type 2 (DM2) is caused by an untransl
220                                              Myotonic dystrophy type 2 (DM2) is caused by the extreme
221 ponsible for the massive expansions found in myotonic dystrophy type 2 (DM2) patients.
222 ribed but untranslated CCTG expansion causes myotonic dystrophy type 2 (DM2), along with other discov
223 oops in r(CCUG)(exp), the causative agent of myotonic dystrophy type 2 (DM2), and are transformed int
224 etiology of myotonic dystrophy type 1 (DM1), myotonic dystrophy type 2 (DM2), and Friedreich's ataxia
225 so examined the similarly slowly progressing myotonic dystrophy type 2 (DM2).
226 ofilm formation in Staphylococcus aureus and myotonic dystrophy type 2 in human, respectively.
227                                              Myotonic dystrophy type 2 is a genetic neuromuscular dis
228                                              Myotonic dystrophy type 2 is caused by a (CCTG)/(CCUG)n
229  not well understood and the role of ZNF9 in myotonic dystrophy type 2 pathogenesis has not been full
230                               In comparison, myotonic dystrophy type 2 tends to cause a milder phenot
231              We explored this question using myotonic dystrophy type 2, a multisystemic disease thoug
232 irst intron of the ZNF9 gene associated with myotonic dystrophy type 2, form slipped-strand DNA struc
233 s, 34 had sodium channel mutations, nine had myotonic dystrophy type 2, one had myotonic dystrophy ty
234 l mutations, chloride channel mutations, and myotonic dystrophy type 2.
235                    The neuromuscular disease myotonic dystrophy type I (DM1) affects multiple organ s
236                                              Myotonic dystrophy type I (DM1) exhibits distinctive dis
237                                              Myotonic dystrophy type I (DM1) is a disabling multisyst
238                                              Myotonic dystrophy type I (DM1) is a disabling neuromusc
239                                              Myotonic dystrophy type I (DM1) is a multisystemic autos
240                                              Myotonic dystrophy type I (DM1) is an RNA-mediated disea
241        They contain CUG repeats, relevant to myotonic dystrophy type I, and CAG repeats associated wi
242                   Molecular therapeutics for myotonic dystrophy will probably bridge the translationa
243 ment for clinical screening of patients with myotonic dystrophy with proactive and systematic managem
244 an skeletal actin (HSA)(LR) mice (a model of myotonic dystrophy) of various ages.
245 ar ataxia, amyotrophic lateral sclerosis and myotonic dystrophy) that involve mutations within the an
246 es of repeat instability and pathogenesis in myotonic dystrophy, a neurological disorder caused by an
247  disease process raises the possibility that myotonic dystrophy, among genetic disorders, may be unus
248 ts in Friedreich's ataxia, (CTG)n repeats in myotonic dystrophy, and (CGG)n repeats in fragile X synd
249 sity in humans as may occur in, for example, myotonic dystrophy, and possibly, the metabolically obes
250 leblind-like 1 (MBNL1), a gene implicated in myotonic dystrophy, as a robust suppressor of multiorgan
251 ated with multiple human diseases, including myotonic dystrophy, Fuchs endothelial corneal dystrophy,
252        Many neurological diseases, including myotonic dystrophy, Huntington's disease and several spi
253 AA)n, are associated with diseases including myotonic dystrophy, Huntington's disease, fragile X and
254 r phenotype reflects many of the features of myotonic dystrophy, including muscle histological morpho
255  3' UTR mRNA reproduced cardinal features of myotonic dystrophy, including myotonia, cardiac conducti
256                 In the best studied example, myotonic dystrophy, it appears that the main pathogenic
257 phasis on key updates in muscular dystrophy, myotonic dystrophy, mitochondrial myopathy, spinal muscu
258 hronic progressive external ophthalmoplegia, myotonic dystrophy, neurofibromatosis type 2, and basal
259 muscle cross-sectional area in patients with myotonic dystrophy, preferentially in healthy-appearing
260 d the pathobiology of disease mechanisms for myotonic dystrophy, spinal muscular atrophy, and fragile
261                                           In myotonic dystrophy, the expression of expanded CUG repea
262                                           In myotonic dystrophy, the lack of properly localized MBNL1
263 rnative splicing and have been implicated in myotonic dystrophy, the most common form of adult onset
264 muscleblind function and the pathogenesis of myotonic dystrophy, we generated Drosophila incorporatin
265 eases, including spinal muscular atrophy and myotonic dystrophy, where defects of splicing or alterna
266 operties of potential therapeutic agents for myotonic dystrophy, which is caused by sequestration of
267                      In mammalian cells, the myotonic dystrophy-related Cdc42-binding kinase possesse
268 sting a toxic RNA pathogenesis, as occurs in myotonic dystrophy.
269 e diseases, including Huntington disease and myotonic dystrophy.
270 uscle weakness and wasting characteristic of myotonic dystrophy.
271 disease severity and therapeutic response in myotonic dystrophy.
272  facioscapulohumeral muscular dystrophy, and myotonic dystrophy.
273 hogenic feature of the neuromuscular disease myotonic dystrophy.
274 ed and studied with respect to their role in myotonic dystrophy.
275 lular localization is a central component of myotonic dystrophy.
276 ead to muscle degeneration disorders such as myotonic dystrophy.
277 des to treat Duchenne muscular dystrophy and myotonic dystrophy.
278 g in corrective outcome for a mouse model of myotonic dystrophy.
279  skeletal actin, long repeat) mouse model of myotonic dystrophy.
280 ion disorders such as Huntington disease and myotonic dystrophy.
281 on diseases such as Huntington's disease and myotonic dystrophy.
282 ssues, including heart failure, diabetes, or myotonic dystrophy.
283 onduction delay, two predominant features of myotonic dystrophy.
284 causes symptoms in the neuromuscular disease myotonic dystrophy.
285 bset of the cardiac dysfunctions observed in myotonic dystrophy.
286 ical diseases such as Huntington disease and myotonic dystrophy.
287  transition, resulting in the development of myotonic dystrophy.
288 a potential drug target for the treatment of myotonic dystrophy.
289                                              Myotonic muscular dystrophy (DM1) is the most common inh
290                                              Myotonic muscular dystrophy (MMD) is an autosomal-domina
291                                              Myotonic muscular dystrophy types 1 and 2 (DM1 and DM2,
292                             In addition, the myotonic mutations G200R and Y261C abolished potentiatio
293 variable presentation that included proximal myotonic myopathy (PROMM) and type 2 DM (DM2) but withou
294 ypertrophic cardiomyopathy with dysrhythmia, myotonic myopathy and hypotension, all distinctive muscl
295                                          All myotonic pigs and their progenitors were homozygous rece
296              Interestingly, non-related, non-myotonic pigs expressed transcriptional levels of an alt
297 as identical to the deleted X1 transcript of myotonic pigs.
298 suggesting this may contribute to the end of myotonic runs.
299  defects may increase excitability and cause myotonic stiffness or may render fibres transiently inex
300 ks including myasthenia, periodic paralysis, myotonic stiffness, seizures, headache, dyskinesia, or e

 
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