ライフサイエンスコーパス: SCA

1 SCA does not have a major genetic component linked to a

2 SCA was associated with microvessel rarefaction, decreas

3 SCA-free droplets produce lower charge states because th

4 Of the 1247 SCA cases, 63 (5%) occurred during sports activities at

5 Despite the identification of 20 SCA genes, the cause of the disorder in a significant pr

6 sion network analysis was used to cluster 24 SCA genes into gene coexpression modules in an unsupervi

7 Of 3775 SCAs in all age groups, 186 (5%) occurred in the young (

8 Of the 4176 SCAs, 1255 (30%) occurred in public areas, with a highly

9 ties (TAMMV) >/=200 cm/s were detected in 92 SCA children at a mean age of 3.7 years (range, 1.3-8.3

10 CA38 to a 56 Mb region on chromosome 6p in a SCA-affected Italian family by whole-genome linkage anal

11 and diffusion tensor imaging (DTI) data of a SCA animal model that replicate recent PET studies in hu

12 g ability (GCA), specific combining ability (SCA) and mid-parental heterosis (MPH).

13 were levulinic acid (LLA) and succinic acid (SCA).

14 Synaptic excitation by sacrocaudal afferent (SCA) input of sacral relay neurons projecting rostrally

15 potently activated by sacrocaudal afferent (SCA) input.

16 rge is the addition of supercharging agents (SCAs) such as sulfolane or m-nitrobenzyl alcohol (m-NBA)

17 N1 with HD+SCAs (p = 1.52 x 10(-5) ) and all SCAs (p = 2.22 x 10(-4) ) and rs1805323 in PMS2 with HD+

18 ces and other Parisian agencies, data on all SCAs occurring in public places in Paris, France, were p

19 Although SCA-linked genes are quite diverse they share two key fe

20 tal SCA and used these variables to build an SCA prediction score, which we validated internally and

21 Sickle cell anaemia (SCA) is associated with structural manifestations in the

22 The global burden of sickle cell anaemia (SCA) is set to rise as a consequence of improved surviva

23 Stomach content analysis (SCA) showed that small juveniles consumed marine/estuari

24 Statistical coupling analysis (SCA) is a method for analyzing multiple sequence alignme

25 The statistical coupling analysis (SCA) is an approach to defining this pattern that involv

26 discovered by statistical coupling analysis (SCA).

27 developed Structural and Chemical Analyzer (SCA) to be a successful combination of Raman spectroscop

28 10; sickle cell trait carriers, n = 10; and SCA patients, n = 7) and underwent muscle biopsy of the

29 ncipal features of the NHC-catalyzed BCA and SCA processes are detailed.

30 fferences in selectivity profiles of BCA and SCA processes.

31 silyl conjugate addition reactions (BCA and SCA, respectively), which proceed without the need for a

32 we analyzed data on sudden cardiac death and SCA available from population studies that included larg

33 of standard cardiovascular risk factors and SCA, and sports as a trigger for SCA in the young.

34 The molar yields of LLA and SCA were quantified as 230 +/- 43% and 110 +/- 31%, resp

35 d Crus II-lobule VIIIB volumes in males) and SCA (contraction of total cerebellar, lobule IV, and Cru

36 ents, and missing data for some patients and SCA characteristics.

37 here was no relationship between seizure and SCA, implying that SCA in epilepsy patients often may no

38 aluate the relationship between seizures and SCA in patients with epilepsy.

39 n of these approaches shows that (1) sex and SCA effects on raw cerebellar volume are large and distr

40 d can therefore invert or exaggerate sex and SCA effects on subcortical anatomy.

41 Y, XYY, XXYY, XXXXY), we investigate sex and SCA effects on subcortical size and shape; focusing on t

42 fy brain size-independent effects of sex and SCA on cerebellar anatomy using a generalizable allometr

43 ll three structures as a function of sex and SCA.

44 T2D genetic risk may predict both T2D and SCA.

45 significantly modify age at onset in HD and SCAs, suggesting a common pathogenic mechanism, which co

46 saline in children with sickle cell anemia (SCA) admitted to the hospital for acute vaso-occlusive p

47 cohort of children with sickle cell anemia (SCA) and abnormal transcranial Doppler (TCD) velocities.

48 Sickle cell anemia (SCA) is a hemoglobinopathy leading to major hematologic,

49 Sickle cell anemia (SCA) is an inherited disorder associated with severe lif

50 levels in children with sickle cell anemia (SCA) is unclear, but increased levels can be associated

51 mended for children with sickle cell anemia (SCA) living in high-resource malaria-free regions, but i

52 situ gene correction of sickle cell anemia (SCA), a prototypical hemoglobinopathy.

53 prevention in pediatric sickle cell anemia (SCA), but the physiology conferring this benefit is uncl

54 astating complication of sickle cell anemia (SCA), occurring in 11% of patients before age 20 years.

55 Stroke risk in sickle cell anemia (SCA), predicted by high transcranial Doppler (TCD) veloc

56 ry are known to occur in sickle cell anemia (SCA), resulting in overt stroke and silent cerebral infa

57 screening of the Creteil sickle cell anemia (SCA)-newborn cohort, and rapid initiation of transfusion

58 Sickle cell anemia (SCA)-related cardiomyopathy is characterized by diastoli

59 (SCIs) in children with sickle cell anemia (SCA).

60 d with high mortality in sickle cell anemia (SCA).

61 mortality in adults with sickle cell anemia (SCA).

62 ng cause of mortality in sickle cell anemia (SCA).

63 ic: 36% in children with sickle cell anemia [SCA]), ischemic stroke (as low as 1% in children with SC

64 ith one of five sex-chromosome aneuploidies [SCAs; XXX (n = 28), XXY (n = 58), XYY (n = 26), XXYY (n

65 s five rare sex (X/Y) chromosome aneuploidy (SCA) syndromes, and (3) clarify brain size-independent e

66 s associated with sex-chromosome aneuploidy (SCA).

67 nd to be more prevalent (1.1%) in the ARREST SCA cohort compared with an ethnically and geographicall

68 at increased risk of sudden cardiac arrest (SCA) due to ECG-confirmed ventricular tachycardia/fibril

69 tification of risk of sudden cardiac arrest (SCA) in individual patients is a tool that is necessary

70 Prevention of sudden cardiac arrest (SCA) in the young remains a largely unsolved public heal

71 tients with epilepsy, sudden cardiac arrest (SCA) is a major cause of death.

72 Sudden cardiac arrest (SCA) is a major contributor to mortality, but data are l

73 Sudden cardiac arrest (SCA) ranks among the most common causes of death worldwi

74 spital mortality from sudden cardiac arrest (SCA) remains high and difficult to reduce.

75 Survival after sudden cardiac arrest (SCA) remains low, and tools for improved prediction of p

76 s at highest risk for sudden cardiac arrest (SCA).

77 o be at high risk for sudden cardiac arrest (SCA).

78 Sports-associated sudden cardiac arrests (SCAs) occur mostly during middle age.

79 l defibrillators and sudden cardiac arrests (SCAs).

80 s of erythema and hyperkeratosis, as well as SCA manifesting in the fourth or fifth decade of life.

81 enlargement: the "2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Ma

82 accuracy for single-copy sensitivity assays (SCA) of HIV RNA that was developed from first principles

83 l discharge was higher for sports-associated SCA (23.2% versus 13.6%; P=0.04).

84 Sports-associated SCA in middle age represents a relatively small proporti

85 A), in patients with spinocerebellar ataxia (SCA) and controls.

86 3'UTRs of the polyQ spinocerebellar ataxia (SCA) genes ATXN1, ATXN2, ATXN3, ATXN7, TBP and CACNA1A a

87 Spinocerebellar ataxia (SCA) in the Parson Russell Terrier (PRT) dog breed is a

88 ifferent subtypes of spinocerebellar ataxia (SCA).

89 autosomal dominant spinocerebellar ataxias (SCAs) are a complex group of neurodegenerative disorders

90 Spinocerebellar ataxias (SCAs) are a genetically heterogeneous group of disorders

91 Spinocerebellar ataxias (SCAs) are a heterogeneous group of autosomal-dominant ne

92 autosomal dominant spinocerebellar ataxias (SCAs) are caused by a variety of protein coding mutation

93 autosomal dominant spinocerebellar ataxias (SCAs) is cerebellar degeneration.

94 e (HD) and multiple spinocerebellar ataxias (SCAs), are among the commonest hereditary neurodegenerat

95 isk factors and subclinical atherosclerosis (SCA) predicts events in those with and without diabetes

96 Because SCA is most often lethal, yet mostly occurs in individua

97 Warning symptoms frequently occur before SCA, but most are ignored.

98 history, including nature of seizures before SCA.

99 , overall prevalence of warning signs before SCA was low (29%), and 26 (14%) were associated with spo

100 cal services (911) to report symptoms before SCA; these persons were more likely to be patients with

101 ral VF neurons serve as a major link between SCA and the hindlimb CPGs and that the ability of SCA to

102 rast, when the sacral CPGs were activated by SCA stimulation, rhythmic and nonrhythmic VF neurons wer

103 that 55% of the VF neurons were activated by SCA stimulation.

104 erted that the protein sectors identified by SCA are functionally significant, with different sectors

105 or output of the lumbar segments produced by SCA stimulation is enhanced by exposing the sacral segme

106 Rapid water loss causes SCA enrichment, ultimately forcing all remaining Na(+) t

107 factors identified low risk (44% of cohort; SCA <1%/year); whereas >/=2 factors identified high risk

108 factors identified high risk (20% of cohort; SCA approximately 12%/year).

109 Overall, the most common SCA-related conditions were sudden arrhythmic death synd

110 A composite SCA-related clinical outcome (vaso-occlusive painful cri

111 lternans can be either spatially concordant (SCA, all cells oscillate in phase) or spatially discorda

112 lcium homeostasis and signaling and contains SCA genes associated mostly with pure ataxia.

113 the ubiquitin-proteasome system and contains SCA genes usually associated with a complex phenotype, w

114 a reports of sudden cardiac arrest or death (SCA/SCD) keep alive a debate as to how best to prevent t

115 In contrast, patients developing SCA had greater amounts of sympathetic denervation (33 +

116 rate-drive locomotor rhythm developed during SCA stimulation.

117 lotype) in a cohort of 1440 unselected Dutch SCA victims included in the Amsterdam Resuscitation Stud

118 ctively ascertained subjects who experienced SCA between the ages of 5 and 34 years in the Portland,

119 Death Study (SUDS), individuals experiencing SCA in the Portland, OR, metropolitan area were identifi

120 ymmetries were broadly preserved in all five SCA groups.

121 ts for GCA and dominance-related effects for SCA and MPH, and additive-by-dominant effect for MPH was

122 patients generally and patients at risk for SCA and sudden cardiac death in particular is limited by

123 prediction of patients at long-term risk for SCA are lacking.

124 , the identification of patients at risk for SCA could save many lives.

125 scores per year were lower for FRDA than for SCA (CCFS index: 0.123+/-0.123 per year vs 0.163+/-0.179

126 bellar dysfunction indexes for FRDA than for SCA.

127 factors and SCA, and sports as a trigger for SCA in the young.

128 penicillin prophylaxis, and vaccination) for SCA in 2015, leading to significant reductions in excess

129 D PET predicts cause-specific mortality from SCA independently of LVEF and infarct volume.

130 he significantly worse rate of survival from SCA in epilepsy patients warrants urgent investigation.

131 ed fluorescence sensors, Fucci(CA) and Fucci(SCA), which enable real-time monitoring of interphase an

132 nct separation of G1, S, and G2, while Fucci(SCA) permitted a two-color readout of G1 and S/G2.

133 a genetic-only (adjusted for sex) and a full SCA risk factors-adjusted model (significance, P<0.01=0.

134 ower tertiles of sympathetic denervation had SCA rates of 1.2%/year and 2.2%/year, whereas the highes

135 All participants had SCA, were part of the prospective observational Sleep an

136 es, and clinical profile of subjects who had SCA by a detailed evaluation of emergency response recor

137 when grouping all polyglutamine diseases (HD+SCAs; p = 1.43 x 10(-5) ).

138 cant associations for rs3512 in FAN1 with HD+SCAs (p = 1.52 x 10(-5) ) and all SCAs (p = 2.22 x 10(-4

139 .22 x 10(-4) ) and rs1805323 in PMS2 with HD+SCAs (p = 3.14 x 10(-5) ), all in the same direction as

140 Herein, SCA mice underwent a longitudinal comprehensive cardiac

141 lar dynamics (MD) simulations to examine how SCAs affect the behavior of ESI nanodroplets.

142 kout lines and in transgenic models of human SCA.

143 lecular functions and mechanisms implicating SCA genes, as well as lists of relevant coexpressed gene

144 race may provide opportunities for improved SCA prevention.

145 In SCA in the young, overall prevalence of warning signs be

146 The brain in SCA is at constant threat of ischemia.

147 ngoing ischemia in other organs is common in SCA but has never been documented in the brain.

148 he development of cerebrovascular disease in SCA, but few candidate genetic modifiers have been valid

149 appears to underlie diastolic dysfunction in SCA.

150 en extraction fraction (OEF) are elevated in SCA, likely compensating for reduced arterial oxygen con

151 ssion modules were statistically enriched in SCA transcripts (P = .021 for the tan module and P = 2.8

152 nce conservation is the dominating factor in SCA, and can alone be used to make statistically equival

153 ated with microscopic myocardial fibrosis in SCA mice, but the cause of diastolic dysfunction in huma

154 olic dysfunction portends early mortality in SCA.

155 hythmias, and ischemic changes were noted in SCA mice before sudden death.

156 The mechanisms of pain in SCA remain poorly understood.

157 ified significant cell types and pathways in SCA pathogenesis.

158 ET-1 levels that are known to induce PHT in SCA.

159 d levels of placenta growth factor (PlGF) in SCA patients correlate with increased levels of the pote

160 e matter, a location at high infarct risk in SCA (P < .001).

161 arch for genetic modifiers of stroke risk in SCA.

162 We show that in SCA mice, anemia-induced hyperdynamic physiology was gra

163 the involvement of rare genetic variants in SCA risk at the population level by studying the prevale

164 was poor, with a nonsignificant increase in SCAs with population density (P=0.4).

165 ommon, early pathophysiological mechanism in SCAs.

166 Secondary outcomes included SCA-related adverse events (AEs), clinical and laborator

167 ermine whether this contributes to increased SCA risk in people with epilepsy.

168 n) are found to be associated with increased SCA risk.

169 Mutation screening of 456 independent SCA-affected individuals identified the same mutation in

170 tent to which population movements influence SCA distribution.

171 A sequencing of the regenerated donor Lin(-) SCA-1(+) KIT(+) (LSK) cells shows dysregulated expressio

172 on (n=8112; median age, 60 years; 78% male), SCA occurred in 452 patients (5.6%).

173 proteins implicated in the pathology of many SCAs.

174 and 2050 by combining estimates of national SCA frequencies with projected demographic data.

175 ld higher in sports-related versus nonsports SCA (28% versus 11%; P=0.05).

176 ssed genes as potential candidates for novel SCA causative or modifier genes.

177 a, smoking) with >/=1 risk factors in 58% of SCA cases.

178 n the known genes explain only 50% to 60% of SCA cases.

179 nd the hindlimb CPGs and that the ability of SCA to induce stepping can be enhanced by the sacral CPG

180 Allometric analysis of SCA reveals that supernumerary X- and Y-chromosomes both

181 approach confirms that the global burden of SCA is increasing, and highlights the need to develop sp

182 In this US community, the burden of SCA was significantly higher in blacks compared with whi

183 egon Sudden Unexpected Death Study, cases of SCA identified using prospective, multisource ascertainm

184 nts a provocative candidate for the cause of SCA in the PRT and a novel potential cause of ataxia in

185 Canadian family segregating a combination of SCA and erythrokeratodermia variabilis (EKV) in an autos

186 to protection from stroke in the context of SCA.

187 ing a systematic analysis of determinants of SCA in public places, we demonstrated the extent to whic

188 present study highlighted marked effects of SCA on microvascular, structural, and energetic characte

189 tic risk is associated with higher extent of SCA.

190 n and previously underappreciated feature of SCA that is associated with diastolic dysfunction, anemi

191 Specifically, SDA instead of SCA are observed.

192 olicies for the prevention and management of SCA.

193 med to determine whether ECG-risk markers of SCA are more prevalent in people with epilepsy.

194 We analysed ECGs for three markers of SCA risk: severe QTc prolongation (male >450 ms, female

195 risk score for association with measures of SCA, including coronary artery or abdominal aortic calci

196 nificantly associated with the occurrence of SCA (odds ratio, 1.48; 95% confidence interval, 1.34-1.6

197 the burden, characteristics, and outcomes of SCA during sports among middle-aged residents of a large

198 The overrepresentation of SCA transcripts in modules identified in the cerebellum

199 Multivariate predictors of SCA were PET sympathetic denervation, left ventricular e

200 medical services were the main predictors of SCA.

201 +/- 8% vs. 28 +/- 9%) were not predictors of SCA.

202 limitations for prediction and prevention of SCA and sudden cardiac death and provides justification

203 ches are needed for short-term prevention of SCA.

204 iduals at a sufficiently high probability of SCA to have a significant effect on clinical decision ma

205 assessed for the first time repercussions of SCA on skeletal muscle and its microvasculature.

206 ndividual patients selected for high risk of SCA early post-MI.

207 ly parameter identifying patients at risk of SCA who benefit from an implantable cardiac defibrillato

208 ramatically associated with a higher risk of SCA.

209 We report a new subtype of SCA presenting in patients as slow progressing ataxia wi

210 blacks were >6 years younger at the time of SCA and had a higher prearrest prevalence of diabetes me

211 Sports was a trigger of SCA in a minority of cases, and, in most patients, SCA o

212 We present the long-term follow-up of SCA children from the Creteil newborn cohort (1992-2012)

213 reas containing major train stations (12% of SCAs in 0.75% of the Paris area).

214 r 39% of SCAs in patients aged </=18, 13% of SCAs in patients aged 19 to 25, and 7% of SCAs in patien

215 Sports-related SCAs accounted for 39% of SCAs in patients aged </=18, 13% of SCAs in patients age

216 of SCAs in patients aged 19 to 25, and 7% of SCAs in patients aged 25 to 34.

217 eas, with a highly clustered distribution of SCAs, especially in areas containing major train station

218 SCA38 and SCA34 are examples of SCAs due to mutations in elongase-encoding genes, emphas

219 .56) for sports SCAs compared with all other SCAs (relative risk 2.58; 95% confidence interval, 2.12-

220 The droplets segregate into an outer SCA shell and an aqueous core.

221 a relatively small proportion of the overall SCA burden, reinforcing the idea of the high-benefit, lo

222 a minority of cases, and, in most patients, SCA occurred without warning symptoms.

223 that CTT mitigates infarct risk in pediatric SCA by relieving cerebral metabolic stress at patient- a

224 d and efficient patient accrual in pediatric SCA studies.

225 of 1,462 subjects with HD and polyglutamine SCAs, and genotyped single-nucleotide polymorphisms (SNP

226 demographics, arrest circumstances, and pre-SCA clinical profile were compared by race among cases f

227 ptoms recurred within the 24 hours preceding SCA.

228 essment of symptoms in the 4 weeks preceding SCA and association with survival to hospital discharge.

229 A score built from these variables predicted SCA, with the risk increasing 2-fold in patients with a

230 ts with STEMI at higher risk for prehospital SCA could facilitate rapid triage and intervention in th

231 ciated with an increased risk of prehospital SCA and used these variables to build an SCA prediction

232 arly phase of STEMI, the risk of prehospital SCA can be determined through a simple score of 5 routin

233 Hydroxyurea provides SCA-related laboratory and clinical efficacy, but optima

234 Occurrence of public SCAs was, in contrast, highly associated with population

235 Sports-related SCA cases were more likely to present with shockable rhy

236 Sports-related SCAs accounted for 39% of SCAs in patients aged </=18, 1

237 After 4.1 years follow-up, cause-specific SCA was 16.2%.

238 Sports SCA cases presented with known preexisting cardiac disea

239 Sports SCA was also more likely to be a witnessed event (87% ve

240 confidence interval, 2.50-139.56) for sports SCAs compared with all other SCAs (relative risk 2.58; 9

241 A shared T2D-SCA genetic basis, if any, might become apparent from be

242 nship between seizure and SCA, implying that SCA in epilepsy patients often may not involve seizure a

243 It is commonly thought that SCA in epilepsy occurs after a seizure, though the stren

244 The SCA approach permitted the individual PM analysis, allow

245 The SCA rate was 28.9% in patients with a score >/=30 compar

246 e sacral level of acetylcholine modulate the SCA-induced locomotor rhythm via muscarinic receptor-dep

247 sent here the principles and practice of the SCA and introduce new methods for sector analysis in a p

248 cular symptoms during the week preceding the SCA.

249 This SCA network acts as a signalling rheostat to integrate s

250 haplotype reconstruction further traced this SCA locus to a 0.66-cM interval flanked by D1S200 and D1

251 whether rare genetic variants contribute to SCA risk in the community is largely unexplored.

252 enetic variants contribute to some extent to SCA risk in the community.

253 ential contribution of these risk factors to SCA in the young has not been evaluated.

254 e approach to address pain and perhaps treat SCA.

255 tients post-MI, the WCD successfully treated SCA in 1.4%, and the risk was highest in the first month

256 encoding beta-III spectrin (SPTBN2) underlie SCA type-5 whereas homozygous mutations cause spectrin a

257 Unfavorable SCA solvation restricts Na(+) access to the droplet surf

258 In unselected SCA victims from the community, common genetic variants

259 The primary endpoint was SCA defined as arrhythmic death or ICD discharge for ven

260 the experimental focus to proteins for which SCA identifies several sectors.

261 231) and patients with stroke (n = 57) with SCA.

262 morrhagic stroke in children and adults with SCA (3% and 10%, respectively).

263 A prospective cohort of adults with SCA, followed in the Cooperative Study for Sickle Cell D

264 A cohort of 430 adults with SCA, mean age 32.6 +/- 9.5 (range, 21.0-67.8) years at t

265 In adults with SCA, the clinical history of SCI is poorly defined, alth

266 t mutation in ELOVL4 that is associated with SCA and EKV.

267 Blacks with SCA had a higher prearrest prevalence of risk factors be

268 e analytic sample included 131 children with SCA (median age, 11.2 years; age range, 6-18 years) foll

269 s primary stroke prevention in children with SCA and high transcranial Doppler (TCD) velocities; afte

270 and vascular abnormalities in children with SCA and stroke and support concerns about chronic transf

271 ary prevention of infarcts for children with SCA and strokes (Stroke With Transfusions Changing to Hy

272 t could be saved in under-five children with SCA by the implementation of different levels of health

273 Children with SCA experience ongoing (chronic, intermittent) cerebral

274 rea treatment appears safe for children with SCA living in malaria-endemic sub-Saharan Africa, withou

275 Twenty-one children with SCA receiving chronic transfusion therapy (CTT) underwen

276 chemic stroke (as low as 1% in children with SCA with effective screening and prophylaxis, but approx

277 axis, but approximately 11% in children with SCA without screening), and hemorrhagic stroke in childr

278 ess mortality among under-five children with SCA, could, by 2050, prolong the lives of 5,302,900 [CI:

279 levels of excess mortality for children with SCA, reflecting the benefits of implementing specific he

280 in a significant proportion of families with SCA remains unexplained.

281 in affected individuals from the family with SCA and EKV.

282 ause of diastolic dysfunction in humans with SCA is unknown.

283 alities and sudden death seen in humans with SCA.

284 e myocardial fibrosis in 25 individuals with SCA (mean age, 23 +/- 13 years) and determine the associ

285 w FEV1 percent predicted in individuals with SCA is warranted, enabling early intervention for those

286 ely that Nigeria (2010: 91,000 newborns with SCA [CI: 77,900-106,100]; 2050: 140,800 [CI: 95,500-200,

287 trends in the future number of newborns with SCA and the number of lives that could be saved in under

288 alculated projected numbers of newborns with SCA for each 5-y interval between 2010 and 2050 by combi

289 The estimated number of newborns with SCA globally will increase from 305,800 (confidence inte

290 000 (CI: 6,745,800-14,232,700) newborns with SCA globally, 85% (CI: 81%-88%) of whom will be born in

291 crease in the annual number of newborns with SCA in India (2010: 44,400 [CI: 33,700-59,100]; 2050: 33

292 ,900 [CI: 3,174,800-6,699,100] newborns with SCA.

293 riedreich's ataxia (FRDA), 205 patients with SCA and 168 controls.

294 Of 839 patients with SCA and comprehensive assessment of symptoms (mean age,

295 creening does not identify all patients with SCA at risk for SCI.

296 study includes 189 stroke-free patients with SCA from the Creteil newborn cohort (1992-2010) followed

297 Patients with SCA who were 35 to 65 years of age were identified in a

298 as more severe in FRDA than in patients with SCA, but with lower progression indexes, within the limi

299 findings in older homozygotic patients with SCA.

300 In the subset with witnessed SCA, clinical presentations were analyzed for evidence o