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 individuals had significantly increased plasma level

3 SCA neutrophils display increased neutrophil-platelet ag

4 SCA occurrence is associated with a 10-fold higher morta

5 SCA-free droplets produce lower charge states because th

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

7 , we show that mixtures of these C(10)-C(15) SCAs form vesicles in aqueous solutions between pH ~6.5

8 of the seasonal cycle of atmospheric CO(2) (SCA) in the northern hemisphere is an emerging carbon cy

9 uments are based on model vesicles using 1-3 SCAs, even though Fischer-Tropsch-type synthesis under h

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

11 491,940 sulfonylurea users, and 714 and 385 SCA/VA events, in Medicaid and Optum, respectively.

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

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

14 n included 257 patients (JCP = 63; SEA = 95; SCA = 99).

15 pendent of segmental chromosome aberrations (SCAs); only 1p loss decreased EFS (5-year EFS +/- SD in

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

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

18 rs associated with increased mortality after SCA were age, heart failure, and extensive STEMI, while

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

20 sed by the addition of supercharging agents (SCAs) such as sulfolane.

21 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+

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

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

24 sicles formed from single-chain amphiphiles (SCAs) such as fatty acids probably played an important r

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

26 a major complication of sickle cell anaemia (SCA) and a leading cause for hospital admissions and dea

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

28 eased in red cells from sickle cell anaemia (SCA) patients.

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

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

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

32 ution method, statistical coupling analysis (SCA), to identify coevolving residue networks (sectors)

33 discovered by statistical coupling analysis (SCA).

34 es by applying specification curve analysis (SCA) across three large-scale social datasets (total n =

35 hniques are straight colorectal anastomosis (SCA), colon J -pouch (CJP), and side-to-end anastomosis

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

37 fferences in selectivity profiles of BCA and SCA processes.

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

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

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

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

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

43 serotonin (5-HT), and serotonin molecule and SCA plasma induced neutrophil CXCR4 expression in a sero

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

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

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

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

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

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

50 T2D genetic risk may predict both T2D and SCA.

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

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

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

54 ed that in patients with sickle cell anemia (SCA) genotypes, older age (95% confidence interval [CI],

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

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

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

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

59 In children with sickle cell anemia (SCA), high transcranial Doppler (TCD) velocities are ass

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

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

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

63 rocesses associated with sickle cell anemia (SCA).

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

65 diastolic dysfunction in sickle cell anemia (SCA).

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

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

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

69 n selected patients with sickle cell anemia (SCA).

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

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

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

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

74 ANOVA-simultaneous component analysis (ANOVA-SCA), stages 2 and 3 of reproduction show similarity in

75 erize sorghum tolerance to sugarcane aphids (SCA; Melanaphis sacchari Zehntner), a relatively new and

76 idal area (LCA), and stromal choroidal area (SCA) were analyzed.

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

78 Prehospital sudden cardiac arrest (SCA) became one of the most feared complications.

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

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

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

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

83 Sudden cardiac arrest (SCA) is one of the largest causes of mortality globally,

84 ogenic endpoints like sudden cardiac arrest (SCA) or ventricular arrhythmia (VA).

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

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

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

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

89 l defibrillators and sudden cardiac arrests (SCAs).

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

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

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

93 corresponding Specialty Coffee Association (SCA) cup scores were modeled by orthogonal partial least

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

95 The spinocerebellar ataxias (SCAs) are a genetically heterogeneous group of autosomal

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

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

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

99 n neurodegenerative spinocerebellar ataxias (SCAs).

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

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

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

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

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

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

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

107 Sensory recombination analysis by certified SCA Q-graders (n = 5) confirmed three out of four compou

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

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

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

111 tilization is the dominant cause of emergent SCA trends at northern sites south of 40 degrees N.

112 ically, SCAs are grouped as repeat expansion SCAs, such as SCA3/Machado-Joseph disease (MJD), and rar

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

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

115 ymmetries were broadly preserved in all five SCA groups.

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

117 No significant changes were recorded for SCA and CVI.

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

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

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

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

122 bellar dysfunction indexes for FRDA than for SCA.

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

124 For generating animal models for SCAs, genetic regulatory elements specifically targeting

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

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

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

128 Genetically, SCAs are grouped as repeat expansion SCAs, such as SCA3/

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

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

131 re is currently no treatment to slow or halt SCAs (many SCAs lead to premature death), the clinical c

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

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

134 .22 x 10(-4) ) and rs1805323 in PMS2 with HD+SCAs (p = 3.14 x 10(-5) ), all in the same direction as

135 Herein, SCA mice underwent a longitudinal comprehensive cardiac

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

137 sponse to aphids in sorghum plants, however, SCA feeding-induced salicylic acid levels were unaltered

138 kout lines and in transgenic models of human SCA.

139 race may provide opportunities for improved SCA prevention.

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

141 velocity (TRV) and exercise abnormalities in SCA.

142 pproaches to reduce neutrophil activation in SCA.

143 participants, with a significant decrease in SCA observed in one of these participants.

144 appears to underlie diastolic dysfunction in SCA.

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

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

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

148 RV hypertension, and myocardial fibrosis in SCA.

149 logical and behavioral changes manifested in SCA-affected patients will be suitable for investigating

150 olic dysfunction portends early mortality in SCA.

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

152 -driven eye-movement deficits as observed in SCA patients.

153 to mechanisms that promote vaso-occlusion in SCA; furthermore, circulating serotonin, derived from pl

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

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

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

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

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

159 ommon, early pathophysiological mechanism in SCAs.

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

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

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

163 were independently associated with increased SCA risk.

164 Through NBP, climate change increases SCA at MLO before the 1980s and decreases it afterwards.

165 hemisphere CO(2) record, shows an increasing SCA before the 1980s (p < .01), followed by no significa

166 tent to which population movements influence SCA distribution.

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

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

169 ur understanding of the pathobiology of many SCAs, revealing that they occur via interrelated mechani

170 proteins implicated in the pathology of many SCAs.

171 ntly no treatment to slow or halt SCAs (many SCAs lead to premature death), the clinical care of pati

172 t for diminished OS in patients < 18 months, SCAs (especially 11q loss) are risk factors for reduced

173 Most SCA mutations cause prominent damage to cerebellar Purki

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

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

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

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

178 solutions to the public health challenge of SCA will require greater awareness, societal debate and

179 o the anaemic and ischaemic complications of SCA.

180 tural intensification on the deceleration of SCA at MLO was elusive according to land-atmosphere CO(2

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

182 ect of climate change on the slowing-down of SCA at MLO is mainly exerted by intensified drought stre

183 We found that slowing-down of SCA at MLO is primarily explained by response of net bio

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

185 nes challenges in addressing the epidemic of SCA, along the framework of respond, understand and pred

186 We analyzed the potential driving factors of SCA slowing-down, with an ensemble of dynamic global veg

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

188 ghlights the persistently dramatic impact of SCA on STEMI and the major importance of PCI in this set

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

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

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

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

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

194 medical services were the main predictors of SCA.

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

196 Prevention of SCA must integrate these concepts, recognizing that all

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

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

199 ramatically associated with a higher risk of SCA.

200 assessed the comparative real-world risk of SCA/VA among users of second-generation sulfonylureas: g

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

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

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

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

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

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

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

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

209 In patients >= 18 months, only SCAs led to relapse and death, with 11q loss as the stro

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

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

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

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

214 Here, we identified heart-resident PDGFRa(+) SCA-1(+) cells as cardiac fibro/adipogenic progenitors (

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

216 d and efficient patient accrual in pediatric SCA studies.

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

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

219 ptoms recurred within the 24 hours preceding SCA.

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

221 Efforts to understand and predict SCA may be enhanced by refining taxonomy along phenotypi

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

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

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

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

226 me, and prognosis' predictors of prehospital SCA occurring after emergency medical services (EMS) arr

227 More than 1 of 20 STEMI presents prehospital SCA after EMS arrival.

228 9 (5.6%) presented EMS-witnessed prehospital SCA.

229 As in proteins, SCA reveals a hierarchical organization of evolutionary

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

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

232 SCA3/Machado-Joseph disease (MJD), and rare SCAs that are caused by non-repeat mutations, such as SC

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

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

235 nje neurons are only mildly affected in some SCAs.

236 ic acid biosynthesis pathway, in the sorghum SCA-tolerant SC35 plants.

237 Sports SCA cases presented with known preexisting cardiac disea

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

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

240 -resection, were randomized for standardized SCA, CJP, or SEA procedures.

241 ils was significantly higher in steady-state SCA individuals than in healthy control individuals and

242 rafish represent an excellent model to study SCAs in vivo We have isolated a 258 bp cross-species PC-

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

244 4.0% in the nonSCA group versus 37.7% in the SCA group ( P<0.001); 26.8% of deaths occurred before ho

245 g-induced cytokinins were accumulated in the SCA-tolerant sorghum genotype.

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

247 The genetic structures of the SCA cohorts from Brazil and US differ considerably on th

248 cular symptoms during the week preceding the SCA.

249 pies is hampered by the heterogeneity of the SCAs; specific therapeutic approaches may be required fo

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

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 tion.Subsequently, we generated a transgenic SCA type 13 (SCA13) model, using a zebrafish-variant mim

255 particular emphasis on chromosome 11 in two SCA admixed cohorts obtained from urban populations of B

256 equencing assay, we confirm that the top two SCA-predicted sectors contribute to ribosome function.

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

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

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

260 Outcomes were SCA/VA events precipitating hospital presentation.

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

262 antly elevated their CXCR4 expression, while SCA plasma was found to induce CXCR4(hi) neutrophil pola

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

264 One hundred adolescents and adults with SCA and hospital admissions for ACS were identified thro

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

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

267 Dataset-specific associations with SCA/VA for both glimepiride and glyburide (vs.

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

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

270 Sixty-seven children with SCA (median age, 7.6 years; 35 girls [52%]) were enrolle

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

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

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

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

275 Among children with SCA requiring chronic transfusion because of persistentl

276 Children with SCA were eligible if younger than 15 years, required chr

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

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

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

280 alities and sudden death seen in humans with SCA.

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

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

283 In a prospective study, individuals with SCA underwent CMR, echocardiography and exercise test.

284 ECV was increased in participant with SCA compared to our lab normal values (mean 0.44 +/- 0.0

285 Twenty-four participants with SCA were included (median age 20 years).

286 ments of CBF and OEF in 84 participants with SCA who were grouped by therapy: no disease-modifying th

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

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

289 neutrophils in a population of patients with SCA and investigated whether platelet-derived molecules

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

291 e death), the clinical care of patients with SCA focuses on managing the symptoms through physiothera

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

293 HSCT) can reduce velocities in patients with SCA is unknown.

294 Patients with SCA were enrolled between December 2010 and June 2013, w

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

296 In older patients with SCA, a randomized trial of postoperative chemotherapy co

297 g cerebral metabolic stress in patients with SCA, but not to the same degree as CTT.

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

299 locities, and had at least 1 sibling without SCA from the same 2 parents.

300 spital discharge compared with STEMI without SCA.