ライフサイエンスコーパス: MSA

1 MSA has been divided into two clinicopathological subtyp

2 MSA is a slowly evolving disorder characterized by progr

3 MSA populations remained consistently small by LSA stand

4 MSA results in significant manometric improvement of the

5 MSA values, ranging from 1 in natural rangelands to 0.3

6 MSA was associated with an overall increase in the media

7 MSA-P and MSA-C groups had higher median MD values (P <

8 Brain extracts from 14 MSA cases all transmitted neurodegeneration to TgM83(+/-

9 gnoses of PD (n=31), PSP (n=33), CBS (n=14), MSA (n=31), AD (n=26) and FTD (n=16).

10 In this first release, R3D-2-MSA provides manual and programmatic access to curated,

11 The R3D-2-MSA server maps these ranges to the appropriate columns

12 to-Multiple Sequence Alignment Server (R3D-2-MSA) is a new web service that seamlessly links RNA thre

13 umbers of supermarkets among tracts in all 4 MSAs.

14 ng findings on 6193 patients (1911 PSP, 4282 MSA) fulfilled the inclusion criteria.

15 nown congeners, de-6-MSA-pactamycin and de-6-MSA-pactamycate, lacking the 6-methylsalicylyl moiety.

16 , in parallel, the two known congeners, de-6-MSA-pactamycin and de-6-MSA-pactamycate, lacking the 6-m

17 we report a 3.1-A crystal structure of de-6-MSA-pactamycin bound to its target site on the Thermus t

18 Although de-6-MSA-pactamycin lacks the MSA moiety, it shares the same

19 Meanwhile, in vitro studies of recombinant 6-MSA synthases with both nonhydrolyzable and hydrolyzable

20 east 7900 patients (men; >/=65 years), in 92 MSAs.

21 Implantation of a MSA around the gastroesophageal junction has been shown

22 The logarithm of the total probability of a MSA under a stochastic model of sequence evolution along

23 ersity, expressed in mean species abundance (MSA) of the original rangeland native species assemblage

24 ations have relied exclusively on amino acid MSAs as inputs.

25 n that nucleation from methanesulfonic acid (MSA) and amines, which is enhanced with added water, can

26 ough transformation to methanesulfonic acid (MSA) and non-seasalt sulfate (NSS-SO(4)(2-)) aerosols.

27 tudies have shown that methanesulfonic acid (MSA) reacts with amines and ammonia to form particles, w

28 ssions of chloride and methanesulfonic acid (MSA), chemical tracers not associated with cooking emiss

29 Another precursor is methanesulfonic acid (MSA), produced simultaneously with SO2 during the atmosp

30 form sulfuric acid and methanesulfonic acid (MSA).

31 Methylseleninic acid (MSA) is a metabolite of selenium (Se) in animal cells th

32 e and increase that of methyl sulfonic acid (MSA), which is needed to close the gap between modeled a

33 ce of water, but NPF is enhanced when adding MSA to OxA-MA with and without water.

34 n = 121) evaluating manometric changes after MSA.

35 sed preoperatively and 6 and 12 months after MSA.

36 xic acid agar (CNA), and mannitol salt agar (MSA); and 25 enteric isolates grown on blood agar, xylos

37 k its roots in the African Middle Stone Age (MSA; approximately 200 to approximately 50 ka).

38 resistant to microtubule stabilizing agents (MSAs) and in human tumors resistant to Taxol.

39 mber of microtubule (MT)-stabilizing agents (MSAs) have demonstrated or predicted potential as antica

40 limited by the Master Settlement Agreement (MSA) after 1998, while alcohol is subject to self-regula

41 to use a single multiple sequence alignment (MSA) as the basis for various types of analysis.

42 the query-based multiple sequence alignment (MSA) implied by the pairwise alignments between the quer

43 Multiple sequence alignment (MSA) is a core method in bioinformatics.

44 While multiple sequence alignment (MSA) is a potent tool to detect the phylogenetic signal,

45 Multiple sequence alignment (MSA) is a prominent method for classification of DNA seq

46 re derived from multiple sequence alignment (MSA) of sequence homologs in a protein family.

47 ler for protein multiple sequence alignment (MSA) that, as implemented in the program GISMO and appli

48 ment for large multiple sequence alignments (MSA) and the fact that, in general, only the relatively

49 function from Multiple Sequence Alignments (MSA) are emerging as powerful tools in computational bio

50 e good-quality multiple sequence alignments (MSA) because the power of correlated mutation analysis f

51 sualization of multiple sequence alignments (MSAs) and sequence motifs.

52 Multiple sequence alignments (MSAs) are a prerequisite for a wide variety of evolution

53 Multiple sequence alignments (MSAs) are usually scored under the assumption that the s

54 gh-quality RNA multiple sequence alignments (MSAs) from diverse biological sources.

55 onstruction of multiple sequence alignments (MSAs) is a crucial step in most homology-based sequence

56 formation from multiple sequence alignments (MSAs) is becoming increasingly important.

57 tations within multiple sequence alignments (MSAs), most commonly through the information-theoretic a

58 e databases of multiple sequence alignments (MSAs), Uniboost10, Uniboost20 and Uniboost30, as a resou

59 types of local multiple sequence alignments (MSAs), we numerically computed the total contribution fr

60 d mutations in multiple sequence alignments (MSAs).

61 At baseline, patients with MSA-P (n=126) and MSA-C (n=49) had much the same symptoms and functional s

62 ificantly increased for PSP/CBD (HR=5.2) and MSA (HR=5.6) classified by PET, but for PSP/CBD only whe

63 al variation in impact on rangeland area and MSA between two agricultural production scenarios.

64 ed to examine how contributions of H2SO4 and MSA to particle formation will change in a large coastal

65 phy in AD, ALS, FTD and PSP (Crus I/II), and MSA and PSP (lobules I-IV), respectively.

66 The natural histories of MSA-P and MSA-C are similar and severe symptomatic autonomic failu

67 MSA-P and MSA-C groups had higher median MD values (P < .01) in th

68 types: MSA with predominant parkinsonism and MSA with predominant cerebellar ataxia, which generally

69 cantly lower in MSA-P and PSP than in PD and MSA-C patients and might therefore be of interest for di

70 cantly lower in MSA-P and PSP than in PD and MSA-C patients and might therefore be of interest for di

71 of PSP patients than in that of both PD and MSA-C patients.

72 of PSP patients than in that of both PD and MSA-C patients.

73 ate HR 1.22; 95% CI 0.83 to 1.80).In PSP and MSA, survival was predicted by early falls (multivariate

74 cantly lower hypothalamic binding in PSP and MSA-P than PD.

75 associated with shorter survival in PSP and MSA.

76 the developing leaves and main shoot apices (MSAs) of barley by RNA sequencing.

77 VD was devised using a multi-stage approach (MSA) with two or three stages, including both non-random

78 orithm that calculates the first-approximate MSA probability by multiplying total parsimonious contri

79 Suburbs, and Metropolitan Statistical Area (MSA) of Cincinnati was evaluated by using 29 social and

80 thin the same metropolitan statistical area (MSA).

81 cities, i.e. Metropolitan Statistical Area (MSA).

82 tions in the Metropolitan Statistical Areas (MSAs) of 4 US cities (Birmingham, Alabama; Chicago, Illi

83 ut using the Metropolitan Statistical Areas (MSAs), we obtain beta = 0.88 +/- 0.01.

84 with coexistence of multiple system atrophy (MSA) and amyotrophic lateral sclerosis (ALS) with hexanu

85 uclear palsy (PSP), multiple system atrophy (MSA) and corticobasal syndrome (CBS) carry a poor progno

86 uclear palsy (PSP), multiple system atrophy (MSA) and idiopathic Parkinson's disease (IPD) can be cli

87 minergic systems in multiple-system atrophy (MSA) and progressive supranuclear palsy (PSP) than in Pa

88 disease (IPD) from multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the most

89 ration (PSP/CBD) or multiple-system atrophy (MSA) by PET and clinical follow-up were associated with

90 Multiple system atrophy (MSA) is a progressive neurodegenerative disorder charact

91 Multiple system atrophy (MSA) is a sporadic orphan neurodegenerative disorder.

92 We report here that multiple system atrophy (MSA) is caused by a different human prion composed of th

93 al sclerosis (ALS), multiple system atrophy (MSA), progressive supranuclear palsy (MSP)).

94 's disease (PD) and multiple system atrophy (MSA).

95 body dementia, and multiple system atrophy (MSA).

96 ear palsy (PSP) and multiple system atrophy (MSA).

97 wy bodies (DLB) and multiple system atrophy (MSA).

98 y bodies (DLB), and multiple system atrophy (MSA).

99 insonian variant of multiple system atrophy (MSA-P), seven with the cerebellar variant of MSA (MSA-C)

100 uclear Palsy(PSP) or Multiple System Atrophy(MSA).

101 d impact of magnetic sphincter augmentation (MSA) on the lower esophageal sphincter (LES).

102 However, even with small autogenerated MSAs, maximum entropy-based CMMs contain information.

103 le methods and strategies based on available MSA size and computing resources.

104 there was no significant difference between MSA as measured by DASH compared with CT.

105 (123)I-FP-CIT SPECT binding to SERT between MSA, PSP, and PD.

106 thresholds for a heatwave episode in Boston MSA based on 16 years of daily observations.

107 We build MSA of highly stable sequences in target LP structures,

108 used to objectively characterize hernias by MSA, with accuracy demonstrated in the obese population

109 To characterize MSA errors using these tools, we constructed three sets

110 on combined analysis of amino acid and codon MSAs.

111 We report this family with coexisting MSA and ALS, highlighting the phenotypic variability in

112 rebellum and all basal ganglia compartments; MSA from the midbrain/brainstem and cerebellum and IPD f

113 omogenates from two pathologically confirmed MSA cases.

114 called MergeAlign which constructs consensus MSAs from multiple independent MSAs and assigns an align

115 the appropriate columns of the corresponding MSA and returns the contents of the columns, either for

116 detect the phylogenetic signal, the current MSA implementations are optimized to align the maximum n

117 n derived from review of nearly 200 definite MSA cases in the Mayo Clinic Brain Bank.

118 ochemical products of DMSP degradation (DMS, MSA, and NSS-SO(4)(2-)), carrying implications for the i

119 Overall, our results suggest that exogenous MSA inhibited angiogenesis at nutritional Se levels not

120 eled mouse serum albumin ((18)F-fluorobenzyl-MSA).

121 thm achieved 90% specificity and 85% PPV for MSA and 94% specificity and 94% PPV for PSP.

122 nic sources of OSCs, with contributions from MSA and H2SO4 of a similar order of magnitude.

123 mportant Cape turban shells and limpets from MSA layers along the south and west coasts of South Afri

124 ebellar atrophy were found for AD, ALS, FTD, MSA, and PSP.

125 e effective LP Hamiltonians used to generate MSA are not simple pairwise models due to the competitio

126 She was diagnosed as having MSA based on her clinical history and the hot cross bun

127 of them, can clearly visualize where and how MSA errors occurred and help disentangle composite error

128 Thus improving MSA accuracy and identifying potential errors in MSAs is

129 In MSA, severe dysautonomia and early development of combin

130 Both scenarios suggest a global decrease in MSA for rangelands until 2050.

131 he MSA was calculated, and the difference in MSA by DASH and CT was compared using the Wilcoxon signe

132 T binding to SERT are significantly lower in MSA-P and PSP than in PD and MSA-C patients and might th

133 T binding to SERT are significantly lower in MSA-P and PSP than in PD and MSA-C patients and might th

134 , binding ratios were significantly lower in MSA-P, PSP, and PD than MSA-C patients.

135 ize of rocky intertidal gastropod species in MSA and later coastal middens allows a test of this idea

136 amus were significantly lower in PSP than in MSA-C patients, and we observed significantly lower stri

137 amus were significantly lower in PSP than in MSA-C patients, and we observed significantly lower stri

138 We also review some controversial topics in MSA.

139 e objective functions and heuristics used in MSA methods, and (ii) affect downstream analyses.

140 accuracy and identifying potential errors in MSAs is important for a wide range of post-genomic resea

141 LOCUS T orthologs: FT1 in leaves and FT2 in MSAs.

142 ospitalization in a VA or non-VA hospital in MSAs that contained at least 1 VA and non-VA hospital.

143 with fast tau values; both were shortest in MSAs.

144 neurotoxicity in synucleinopathies including MSA.

145 gene families we demonstrate that increasing MSA performance leads to an increase in the performance

146 cts consensus MSAs from multiple independent MSAs and assigns an alignment precision score to each co

147 Different methods of inferring MSAs produce different results in all but the most trivi

148 alse positives (FPs) arise from insufficient MSA size, phylogenetic background and indirect couplings

149 ts in the formation of methanesulfonate ion (MSA(-))H3O(+) ion pair.

150 on of metabolic covariance patterns for IPD, MSA, and PSP.

151 consenting patients with a diagnosis of IPD, MSA or PSP, stages 3-5 Hoehn and Yahr(H&Y).

152 ividual scan data, the probabilities of IPD, MSA, and PSP were computed and used to classify each of

153 or symptoms in patients with late stage IPD, MSA and PSP.

154 a probability distribution of fairly likely MSAs, instead of just searching for a single optimum MSA

155 first-approximate probability of each local MSA with its absolute frequency in the MSAs created via

156 al parsimonious contributions from all local MSAs.

157 o close the gap between modeled and measured MSA concentrations.

158 ts we demonstrate that on average MergeAlign MSAs are more accurate than MSAs generated using any sin

159 ibiotic pactamycin and de-6-methylsalicylyl (MSA)-pactamycin have attracted recent interest as potent

160 Moreover, MSA effectively inhibited the sprouts of mouse aortic ri

161 ), seven with the cerebellar variant of MSA (MSA-C), 17 with progressive supranuclear palsy-Richardso

162 sonism [MSA-P], n = 9), cerebellar type MSA (MSA-C, n = 7), PSP (n = 13), and PD (n = 30).

163 sonism [MSA-P], n = 9), cerebellar type MSA (MSA-C, n = 7), PSP (n = 13), and PD (n = 30).

164 We present a novel multiple MSA methodology that scores TFBS DNA sequences by includ

165 lated with I(h) and I(h) density for all non-MSA LTMs, and for Adelta-nociceptors.

166 ombined autonomic and motor features but not MSA phenotype (multivariate HR 1.22; 95% CI 0.83 to 1.80

167 n and, to a lesser extent, global nucleotide MSAs are available, but less effort has been made to est

168 hase DMS oxidation produces equal amounts of MSA and sulfate, a result that has significant implicati

169 synuclein aggregates formed in the brains of MSA patients are transmissible and, as such, are prions.

170 Brains of MSA-inoculated mice exhibited prominent astrocytic glios

171 29 autopsy confirmed cases of MSA evaluated at the Mayo Clinic who had undergone forma

172 ecline proportionally with concentrations of MSA and amines if temperature also decreases, for exampl

173 nt role in clinicopathological correlates of MSA.

174 ostic accuracy and differential diagnosis of MSA as well as candidate biomarkers.

175 , which has been a non-supporting feature of MSA, is considered from both clinical and pathological p

176 , that clinical and pathological features of MSA are broader than previously considered.In this revie

177 ncertain gas phase mechanism of formation of MSA and (ii) a combination of published and experimental

178 vel mechanistic insight into the function of MSA for regulating angiogenesis and suggest that MSA cou

179 kinsonism; the neuropathological hallmark of MSA is glial cytoplasmic inclusions consisting of filame

180 The cytopathological hallmark of MSA is the accumulation of alpha-synuclein (alpha-syn) a

181 The natural histories of MSA-P and MSA-C are similar and severe symptomatic auton

182 (PLP-SYN) mice, a transgenic mouse model of MSA.

183 escribe recent advances in neuropathology of MSA from a review of the literature and from information

184 discrepancy is due to the overestimation of MSA areas.

185 e clinical phenotype is highly predictive of MSA.

186 xalic acid (OxA) on NPF from the reaction of MSA and methylamine (MA) at 1 atm and 294 K in the prese

187 chemistry from the heterogeneous reaction of MSA with an amine on a surface.

188 trometry (DRIFTS) studies of the reaction of MSA with trimethylamine (TMA) on a silicon powder at atm

189 of particle formation from the reactions of MSA with trimethylamine (TMA), dimethylamine (DMA), meth

190 terpretation of variability in delta(34)S of MSA and NSS-SO(4)(2-) that links them to changes in grow

191 The daylength sensitivity of MSA development had two phases, floret primordia initiat

192 MSA-P), seven with the cerebellar variant of MSA (MSA-C), 17 with progressive supranuclear palsy-Rich

193 To study the relative binding affinities of MSAs, tubulin from different sources, with distinct beta

194 atform for the joint explorative analysis of MSAs and phylogenetic trees, employing Sequence Bundles

195 vance to the possible use of combinations of MSAs to regulate MT activity and improve therapeutic pot

196 ogies, averaging over a very large number of MSAs.

197 dobenzoyl)taxol, alone or in the presence of MSAs.

198 to represent a distribution in the space of MSAs, and allows for existing algorithms to be efficient

199 stead of just searching for a single optimum MSA.

200 th a likely or confirmed diagnosis of PSP or MSA were eligible for inclusion.

201 GISMO fills a different niche than other MSA programs, namely identifying and aligning a conserve

202 tem atrophy with predominantly parkinsonism [MSA-P], n = 9), cerebellar type MSA (MSA-C, n = 7), PSP

203 tem atrophy with predominantly parkinsonism [MSA-P], n = 9), cerebellar type MSA (MSA-C, n = 7), PSP

204 to unravel how this mutant contributes to PD/MSA.

205 pare atmospheric concentrations of gas phase MSA, H2SO4, and SO2 under current emissions of fossil fu

206 sequences, is more accurate than the popular MSA programs MUSCLE, MAFFT, Clustal-Omega and Kalign.

207 esting pressure (18 pre-MSA vs 23 mm Hg post-MSA; P = 0.0003), residual pressure (4 vs 9 mm Hg; P < 0

208 he appearance of art in the MSA and its post-MSA florescence.

209 rom 1996 through 1999 compared with the post-MSA period from 2000 through 2009.

210 using a mouse albumin-based equivalent (pPB-MSA).

211 e in the median LES resting pressure (18 pre-MSA vs 23 mm Hg post-MSA; P = 0.0003), residual pressure

212 ounts and seconds of screen time for the pre-MSA period from 1996 through 1999 compared with the post

213 that whatever cognitive capacity precocious MSA artifacts imply, it was not associated with human po

214 In the proposed MSA, the major threat to the validity of the results of

215 cerebellar areas implicated for motor (PSP, MSA) or cognitive symptoms (FTD, ALS, PSP) in the diseas

216 considerable neighborhoods of reconstructed MSAs in about 80-99% of the erroneous segments for small

217 urther improve the accuracy of reconstructed MSAs would substantially differ depending on the types o

218 eously reconstructed segments, reconstructed MSAs by each aligner showed complete-likelihood scores n

219 Then, we reconstructed MSAs using MAFFT and Prank as representative state-of-th

220 recision in the absence of curated reference MSAs.

221 tween HMSA and (R1)(R2)NH, and the resulting MSA(-)(R1)(R2)NH2(+) complex is bound by one to four int

222 alignments than the original set of sampled MSAs, such that the effective sample size is greatly inc

223 The mean (SD) MSA measurements were similar between the modalities: DA

224 ools, we constructed three sets of simulated MSAs of selectively neutral mammalian DNA sequences, wit

225 date the MSA in Africa and Eurasia, but some MSA sites contain possible precursors, especially includ

226 Specifically, MSAs display isometric scaling emissions and we argue th

227 ble improvements when compared with standard MSA algorithms.

228 pe (MSA-P) or the cerebellar ataxia subtype (MSA-C)-at 12 neurology centres in the USA specialising i

229 atrophy-of either the parkinsonism subtype (MSA-P) or the cerebellar ataxia subtype (MSA-C)-at 12 ne

230 vided into two clinicopathological subtypes: MSA with predominant parkinsonism and MSA with predomina

231 gnificantly lower in MSA-P, PSP, and PD than MSA-C patients.

232 son and classification of DNA sequences than MSA.

233 erage MergeAlign MSAs are more accurate than MSAs generated using any single matrix of sequence subst

234 Our findings argue that MSA is caused by a unique strain of alpha-synuclein prio

235 Herein, we demonstrate that MSA inhibited angiogenesis at 2 microM, which falls in t

236 We also found that MSA down-regulated integrin beta3 at the levels of mRNA

237 We found that MSA treatments at 2 microM increased cell adherence, whi

238 Additionally, results showed that MSA inhibited the phosphorylation of AKT, IkappaBalpha,

239 objects have convinced most specialists that MSA people were behaviorally (cognitively) modern, and m

240 for regulating angiogenesis and suggest that MSA could be a potential candidate or adjuvant for anti-

241 The MSA also heralded a drop in tobacco screen time for yout

242 The MSA discards ineffective treatments quickly, while relia

243 The MSA is appropriate for the clinical evaluation of EVD tr

244 The MSA led to a smaller number of cases receiving ineffecti

245 The MSA measurements determined by DASH and CT were also sim

246 The MSA prion represents a unique human pathogen that is let

247 The MSA was calculated, and the difference in MSA by DASH an

248 The MSA, an agreement signed in 1998 between the state attor

249 y mass index of this group was 39.2, and the MSA measurements by DASH and CT were similar (P = .26).

250 Both the MSA and SRCT led to substantially fewer deaths than a co

251 Assuming 100 new EVD cases per day, the MSA led to between 6% and 15% greater reductions in epid

252 variables were also selected to describe the MSA's environmental component (1980-2009).

253 s were built on parameters that describe the MSA, the predicted secondary structure, the predicted so

254 two epidemic scenarios were compared for the MSA, a sequential randomised controlled trial (SRCT) wit

255 growth explains the appearance of art in the MSA and its post-MSA florescence.

256 e because the true covariation signal in the MSA is often masked by biases from many ancillary indire

257 irectly coupled mutation correlations in the MSA.

258 Although de-6-MSA-pactamycin lacks the MSA moiety, it shares the same binding site as pactamyci

259 in population size is obvious only near the MSA/LSA transition, when it is dramatically reflected in

260 More than 50% of the MSA and PSP patients died over the year.

261 d mutation analysis falls as the size of the MSA decreases.

262 All of the MSA extracts also induced aggregation of alpha-syn*A53T-

263 seemed due to inadequate exploration of the MSA space.

264 After implementation of the MSA, tobacco brand appearances dropped exponentially by

265 re" here) can serve as an ideal score of the MSA.

266 ers for further growth, their effects on the MSA-amine system are not known.

267 ecome common only in sites that postdate the MSA in Africa and Eurasia, but some MSA sites contain po

268 We expected that the MSA would be associated with declines in tobacco but not

269 For less effective treatments, the MSA had a high probability of including an RCT component

270 ng effective treatments correctly, while the MSA was less likely to recommend treatments that were in

271 local MSA with its absolute frequency in the MSAs created via a genuine sequence evolution simulator,

272 earch clusters by keywords and explore their MSAs, taxonomic representation, and annotations.

273 I) consisting of alpha-synuclein; therefore, MSA is included in the category of alpha-synucleinopathi

274 The inhibitory effects elicited by these MSAs on photolabeling were distinct for beta-tubulin fro

275 ctive pairwise Potts Hamiltonians from those MSA.

276 The contribution of livestock grazing to MSA loss is, however, expected to diminish after 2030, i

277 The addition of OxA to MSA-MA mixtures yields a modest NPF enhancement, whereas

278 enhancement, whereas the addition of OxA to MSA-MA-H2O has no effect.

279 s by position-shift maps indicated that true MSAs are in considerable neighborhoods of reconstructed

280 hood scores not lower than those of the true MSAs.

281 rence in each residue's position between two MSAs onto one of them, can clearly visualize where and h

282 arkinsonism [MSA-P], n = 9), cerebellar type MSA (MSA-C, n = 7), PSP (n = 13), and PD (n = 30).

283 arkinsonism [MSA-P], n = 9), cerebellar type MSA (MSA-C, n = 7), PSP (n = 13), and PD (n = 30).

284 We included patients with parkinsonian type MSA (multiple-system atrophy with predominantly parkinso

285 We included patients with parkinsonian type MSA (multiple-system atrophy with predominantly parkinso

286 Uniboost MSAs of three diversities are built by enriching the Uni

287 sities are built by enriching the Uniclust30 MSAs with local sequence matches from MMseqs2 profile se

288 Clinical diagnosis at last visit was MSA for 28 cases.

289 To determine whether MSA brains contain alpha-synuclein prions, we inoculated

290 However, it remains unclear whether MSA exerts its effects on cancer prevention by influenci

291 7 patients with PSP, 14 with IPD and 19 with MSA were scanned using structural MRI along with 19 heal

292 eres were used to discriminate patients with MSA-C and those with MSA-P from patients with PD and tho

293 At baseline, patients with MSA-P (n=126) and MSA-C (n=49) had much the same symptom

294 res can be used to distinguish patients with MSA-P and those with MSA-C from patients with PSP-RS and

295 epeat expansions in C9orf72 can present with MSA as well as ALS or frontotemporal dementia.

296 d 67% of the time to a normal sphincter with MSA.

297 stinguish patients with MSA-P and those with MSA-C from patients with PSP-RS and those with PD.

298 criminate patients with MSA-C and those with MSA-P from patients with PD and those with PSP-RS (P < .

299 Mean aggregated within-MSA differences in mortality and readmission rates were

300 In within-MSA comparisons, VA hospitals had lower mortality rates