ライフサイエンスコーパス: AS

1 AS OCT provides an assessment of structural changes occu

2 AS-CA has worse clinical presentation and a trend toward

3 AS-OCTA provides novel, quantitative, and noninvasive pa

4 already been diagnosed by MS-HRM (20 PWS, 1 AS, and 24 healthy individuals).

5 f axillary nodes from StMSI1-OE and StBMI1-1-AS lines revealed downregulation of auxin and brassinost

6 Further, grafting of StMSI1-OE or StBMI1-1-AS on wild-type stock resulted in reduced root biomass a

7 Here, we identified 1723 AS events and 41 splicing factors regulated in a breast

8 Plasma YKL-40 was analyzed in 2 AS populations, one severe AS (n=572) with outcome measu

9 Measurements were taken from 21 AS patients and 13 non-AS subjects.

10 The ultratight binding affinity of P[5]AS and P[6]AS toward quaternary (di)ammonium ions render

11 to as Pillar[6]MaxQ along with analogues P[5]AS and P[7]AS toward guests 1-18.

12 ltratight binding affinity of P[5]AS and P[6]AS toward quaternary (di)ammonium ions renders them prim

13 properties of pillar[n]arene derivative P[6]AS, which we refer to as Pillar[6]MaxQ along with analog

14 r[6]MaxQ along with analogues P[5]AS and P[7]AS toward guests 1-18.

15 Altogether, our studies establish aberrant AS landscape caused by dysregulated SRGs as a hallmark o

16 ith training for establishing and leading an AS program (ASP), we describe the rationale for, and the

17 th Framingham risk score (FRS) (r = 0.2) and AS (r = 0.39), respectively.

18 ions that led to changes in degree of AI and AS did not seem to influence change in aortic dimensions

19 Microbiome analysis in both AS and AS + Ck culture samples indicated strong enrichment towa

20 0.38, and 7.67 +/- 0.37 g/L for AS, Ck, and AS + Ck cultures, respectively.

21 tive Behavioral Scales, Second Edition), and AS-specific symptoms (AS Clinical Severity Scale).

22 ncing revealed extensive gene expression and AS changes in mice overexpressing nuclear and naturally

23 e association between the FADS1 genotype and AS may implicate effects on valvular fatty acids.

24 ocular examination including gonioscopy and AS-OCT imaging.

25 cing (AS), and its transcriptional level and AS are significantly affected by BdFTL2.

26 es with significantly lower age, K-mean, and AS-OCT stages and higher pachymetric values (always P <

27 Clinical course, slit lamp photographs, and AS OCT findings were the main outcomes.

28 capable of accuracy in detecting all PWS and AS individuals.

29 urce of many methodologies to detect PWS and AS, however, the need of WB makes a massive screening di

30 signals via Toll-like receptor 4 (TLR4), and AS-ODN for TLR4 mRNA administered intrathecally, attenua

31 d transcriptome analysis on them from WT and AS mice, followed by in vitro functional assays and conf

32 Prader-Willi (PWS) and Angelman (AS) syndromes are two clinically distinct imprinted diso

33 StMSI1-OE and StBMI1-1-antisense (AS) lines produced pleiotropic effects, including altere

34 ration of an oligodeoxynucleotide antisense (AS-ODN) to mRNA for cluster of differentiation 44 (CD44)

35 d the regulatory role of HIF-1alpha in BACE1-AS/BACE1 in Tat-mediated amyloidosis.

36 ting, in turn, in the formation of the BACE1-AS/BACE1 RNA complex, subsequently leading to increased

37 A (lncRNA) BACE1-antisense transcript (BACE1-AS), resulting, in turn, in the formation of the BACE1-A

38 Boulware DR, Pullen MF, Bangdiwala AS, et al.

39 chanism, we established a luminescence-based AS reporter system in Nicotiana benthamiana to screen pa

40 f two GEC subpopulations that differ between AS and healthy mice or humans.

41 LV biopsies (AS and non-pressure-loaded heart biopsy) were analyzed f

42 Microbiome analysis in both AS and AS + Ck culture samples indicated strong enrichme

43 rimination between bubble types, followed by AS-OCT stage, pachymetry, K-mean, and astigmatism (respe

44 a-hydroxy fatty acids and sphingosines (Cer[AS]) decreased, with larger alkyl chain lengths in Cer[N

45 del of malaria (Plasmodium chabaudi chabaudi AS).

46 -specific Th cells from P. chabaudi chabaudi AS-infected mice and is downregulated in Malat1(-/-) Th1

47 Here we describe the first comprehensive AS landscape in the spectrum of human prostate cancer (P

48 It is unknown whether concomitant AS-CA has worse outcomes or results in futility of trans

49 lusively express analog-sensitive CRK9 (CRK9(AS) ).

50 Inhibition of CRK9(AS) in these cells by the ATP-competitive inhibitor 1-NM

51 In the second cycle, AS microbiome was enriched toward caproate production an

52 the output and shortcomings of, a dedicated AS rotation.

53 The aim of this study is to describe AS OCT findings in cases of PUK.

54 Different AS cessation criteria had similar expected infection dyn

55 1 display a less severe electrophysiological AS phenotype.

56 250, and 299 differentially expressed exons (AS exons) at 4, 24, 48, and 72 hpi, respectively, showin

57 ypertension, history of atrial fibrillation, AS-related symptoms, left ventricular ejection fraction,

58 or artificial saliva (AS)] separated by five AS rinse licks on a variable ratio 5 schedule.

59 corresponding to the protective genotype for AS, was associated with higher FADS2 mRNA levels in calc

60 43, 7.86 +/- 0.38, and 7.67 +/- 0.37 g/L for AS, Ck, and AS + Ck cultures, respectively.

61 ascular magnetic resonance (CMR) methods for AS assessment.

62 ion for the development of new therapies for AS.

63 new platforms for developing treatments for AS and various forms of autism.

64 Four AS-OCT images from one eye per subject were analyzed and

65 Four AS-OCT images were analyzed per eye.

66 lear gene regulatory variation in PBMCs from AS patients, providing a foundational framework for the

67 otentiation (LTP) in hippocampal slices from AS mice by enhancing SK2 internalization.

68 nadjusted and adjusted for age and sex, FRS, AS, and FRS plus AS (HR = 2.4, 2.8, 2.8, 2.3, and 2.6; P

69 S unadjusted, adjusted for age and sex, FRS, AS, and FRS plus AS were significantly associated with e

70 Further, AS-OCTA parameters were correlated to clinical parameter

71 on and transcription can influence host gene AS and/or APA.

72 Here, we examined the global AS changes in tomato leaves infected with Phytophthora i

73 For the DS group, AS-OCT imaging revealed the frequent presence of small d

74 n low-gradient (LG, mean gradient <40 mm Hg) AS are conflicting.

75 tion and responses to immune reactions, host AS events that occur as a result of T. cruzi infection h

76 and 72 hpi, respectively, showing that host AS mechanism may have a significant role in the intracel

77 Moreover, identified AS genes may provide new potential molecular candidates

78 Altogether, our data identify AS programs controlled by ZRANB2 and SYF2 and converging

79 plants, hence the chromatin state can impact AS.

80 In AS mice, dim(tdT) and bright(tdT) cells had different ex

81 In AS mice, the bright(tdT) cell number increased and prese

82 In AS-OCT, an intrascleral hyper-reflective shadow signifie

83 on/aggregation by a factor of 1.3 +/- 0.4 in AS solution in the first 60 min of reaction time.

84 8 TF motifs with decreased accessibility in AS.

85 med a new pro-inflammatory role of Apelin in AS mice and in cultured human GEC.

86 w rate determines prognostic value of AVA in AS.

87 t of flow rate on prognostic value of AVA in AS.

88 2000 genes exhibiting significant changes in AS are not differentially expressed, indicating that AS

89 ranslation by CELF1, with minimal changes in AS.

90 ne the landscape of active regulatory DNA in AS.

91 on but has failed to demonstrate efficacy in AS that is largely a spinal polyenthesitis.

92 YKL-40 levels were elevated in AS and associated with mortality but not with other metr

93 egy to prevent and treat systolic failure in AS.

94 derstanding of the pathogenic role of GEC in AS progression and could lead to novel therapeutic targe

95 ng from oscillation in the genes involved in AS and APA.

96 eover, natural killer cells were involved in AS by increasing the accessibility to TF motifs TEAD1 an

97 ogics do not prevent the fusion of joints in AS patients.

98 rment of synaptic plasticity and learning in AS mice.

99 nt and independent predictor of mortality in AS.

100 Imitation performance in AS appears to be more modulated by the social context co

101 ued anatomical and behavioural phenotypes in AS mice.

102 Despite scientific rationale for its role in AS, the clinical utility of circulating YKL-40 as a biom

103 minent elevations in plasma sphingolipids in AS progressors that, together with plasma Cav-1, yield a

104 Therefore, TAVR should not be withheld in AS-CA.

105 ients with chronic kidney disease, including AS were compared with our findings in mice.

106 f several cardiovascular outcomes, including AS.

107 ight and noncoronary cusp fusion, increasing AS and AI, and older age were independently associated w

108 leosome occupancy influence the cold-induced AS remains poorly understood.

109 ucleosome positioning modulates cold-induced AS.

110 Our results demonstrate how integrating AS activity can substantially improve the detection of c

111 m(2) is unknown and is not incorporated into AS assessment.

112 ptome may provide new potential insight into AS regulation in human foreskin fibroblast (HFF) cells i

113 c digester sludge with Clostridium kluyveri (AS + Ck) on caproic acid production from a mixed substra

114 from wild type (WT) and col4alpha5 knockout AS mice, a hereditary disorder characterized by progress

115 index of LV stiffness may be important in LF AS.

116 vere diastolic dysfunction, especially in LF AS.

117 CLF-LG was the most common pattern of LG AS and was associated with higher rates of death, rehosp

118 Clinical outcomes were as good in the LG AS groups with preserved left ventricular ejection fract

119 The LG AS pattern was highly prevalent (36.5%) in the PARTNER 2

120 ating the role of the HIF-1alpha/lncRNABACE1-AS/BACE1 axis in Tat-mediated induction of astrocytic am

121 survival post-TAVR did not differ from lone AS (p = 0.36).

122 h AS-CA (grade: 1 to 3) than those with lone AS (24.5% vs. 13.9%; p = 0.05).

123 ics and outcomes of AS-CA compared with lone AS.

124 oorer clinical outcomes in medically-managed AS.

125 improved survival versus medical management; AS-CA survival post-TAVR did not differ from lone AS (p

126 Using MATLAB, AS-OCT images were analysed and lens opacities calculate

127 A recent case study reported mild AS phenotypes in individuals lacking one specific isofor

128 d as severe AS were reclassified as moderate AS.

129 mpairment is already established in moderate AS and suggest that a fall in CK flux is not by itself a

130 delivery is reduced earlier, at the moderate AS stage, where LV function remains preserved.

131 d the mechanisms by which pathogens modulate AS remain poorly understood.

132 c changes in nucleosome positioning modulate AS in plants in response to cold.

133 lant AS machinery and subsequently modulates AS-mediated plant immunity.

134 n an allyl-sulfide-containing azide monomer (AS-N(3) ) is used to form the network, the network exhib

135 Moreover, AS-related genes exhibited rhythmic AS and APA regulatio

136 hort of patients with BAV, valve morphology, AS, and AI are independently associated with ascending a

137 Wilson ME, Dobler CC, Morrow AS, et al.

138 In contrast, MPP-AS programming generated greater clinical composite scor

139 cular single-site pacing and 43 received MPP-AS.

140 nt pacing with wide anatomic separation (MPP-AS: >=30 mm).

141 r hearts was observed when programmed to MPP-AS pacing.

142 failure event occurred in patients with MPP-AS programming between 3 and 9 months in LVEDVI(>Median)

143 Reverse remodeling trended better with MPP-AS programming.

144 N-AS then acetylates serine 565 (S565) of COX2, and the N-

145 model of AD, microglia show a reduction in N-AS generation, leading to decreased acetyl-S565 COX2 and

146 together, these results identify a role of N-AS in the dysfunction of microglia in AD.

147 Here we show that N-acetyl sphingosine (N-AS) is first generated by acetyl-CoA and sphingosine thr

148 tylates serine 565 (S565) of COX2, and the N-AS-acetylated COX2 induces the production of specialized

149 en phthalocyanines, yellow and red (naphthol AS) azo pigments, red quinacridone, anthraquinone, and d

150 In patients with neither AS nor AI, 37% had ascending aorta dilatation (4% severe

151 have poorer prognosis than normal-flow (NF) AS, though its pathophysiology remained unclear.

152 ts were taken from 21 AS patients and 13 non-AS subjects.

153 uring infection but also establishes a novel AS screening tool to identify SREs from a wide range of

154 Upon Strap deletion, there are numerous AS events observed in mouse embryoid bodies (EBs) underg

155 This study employed anterior segment OCT (AS-OCT) and slit-lamp (SL) photography to image the crys

156 native method for non-invasive assessment of AS.

157 deep learning tools on the classification of AS.

158 e elevated and associated with the degree of AS severity and outcome in patients with symptomatic AS.

159 but levels were not related to the degree of AS severity.

160 of disease severity including the degree of AS severity.

161 Finally, we examined the effects of AS-associated TYK2 SNPs on TYK2 expression and function

162 s, and found evidence for a reduced level of AS activity during leaf senescence.

163 ) is vital for elucidating the mechanisms of AS pathogenesis.

164 d virus and administered to a mouse model of AS during the embryonic and early postnatal stages, when

165 ied clinical characteristics and outcomes of AS-CA compared with lone AS.

166 Concomitant pathology of AS-CA is common in older patients with AS and can be pre

167 ailure, CK flux was lower in the presence of AS (by 32%, P=0.04), driven primarily by reduction in ph

168 es) was developed to predict the presence of AS-CA (area under the curve: 0.86; 95% confidence interv

169 al of CMR for the diagnosis and prognosis of AS.

170 diagnosis, classification, and prognosis of AS.

171 his histone mark is not a major regulator of AS or APA in our model system.

172 ent of the left ventricular repercussions of AS by CMR is not routinely performed in clinical practic

173 ere assessed for BAV morphology, severity of AS and AI, history of coarctation, and aortic dimensions

174 s for the treatment (either SAVR or TAVR) of AS in Ontario, Canada, and to understand the drivers of

175 TAPSE <17 mm at the time of AS diagnosis is a marker of poor survival under conserva

176 Multiple years of AS without case detections is a valuable measure to asse

177 imit, thickness, depth%, area, and volume on AS-OCTA compared to mild.

178 ease in wait-times (P<0.001) for the overall AS cohort as well as each of the TAVR (P<0.0001) and SAV

179 Stable pH values were measured for pure PB, AS, and AN droplets at different concentrations.

180 o screen pathogen effectors modulating plant AS.

181 sically binds U1-70K to manipulate the plant AS machinery and subsequently modulates AS-mediated plan

182 However, the prevalence of genome-wide plant AS changes during infection and the mechanisms by which

183 Our study not only unveils genome-wide plant AS reprogramming during infection but also establishes a

184 usted for age and sex, FRS, AS, and FRS plus AS (HR = 2.4, 2.8, 2.8, 2.3, and 2.6; P < .001, respecti

185 usted for age and sex, FRS, AS, and FRS plus AS were significantly associated with events (hazard rat

186 Postoperative AS-OCT was performed to detect the position of the hapti

187 ation of cDCs and CD123(+)AXL(+)CD327(+) pre/AS-DCs.

188 S severity of the participants of the PRIMID-AS study (Prognostic Importance of Microvascular Dysfunc

189 3 and showed that exon 3 loss altered PTCHD1-AS splicing without affecting expression of the neighbor

190 us to explore the roles of PTCHD1 and PTCHD1-AS in genetic risk for ASD and other neurodevelopmental

191 nd a novel ASD-associated deletion of PTCHD1-AS exon 3 and showed that exon 3 loss altered PTCHD1-AS

192 Finally, targeted disruption of PTCHD1-AS exon 3 recapitulated diminished miniature excitatory

193 f deleting a single conserved exon of PTCHD1-AS.

194 o the PTCHD1 locus disrupted exons of PTCHD1-AS.

195 D1, DDX53, and the long noncoding RNA PTCHD1-AS is frequently disrupted in male subjects with autism

196 findings provide strong evidence that PTCHD1-AS deletions are risk factors for ASD, and human iPSC-de

197 , and its role in evaluating and quantifying AS is not yet well established.

198 ernative splicing (AS) factors that regulate AS process, and found evidence for a reduced level of AS

199 for nervous system development and regulates AS through preferred binding positions, as demonstrated

200 oreover, AS-related genes exhibited rhythmic AS and APA regulation, adding another layer of complexit

201 citric acid, quinine, or artificial saliva (AS)] separated by five AS rinse licks on a variable rati

202 epidemiology and level of active screening (AS) both influenced the predicted time to EOT.

203 x), 8.36 mg/day) and accumulation secretion (AS, 50.8 mg) were observed for milk RRR-alpha-tocopherol

204 ertion position 4 [TIP4]); anterior segment (AS) OCT tube parameters, including posterior cornea-to-t

205 s including gonioscopy and anterior segment (AS)-OCT imaging with the Tomey CASIA SS-1000 (Tomey Corp

206 pool of candidate ligands in two sequential AS-MS analyses.

207 ticipants, 45% (56/124) classified as severe AS were reclassified as moderate AS.

208 Eighteen patients with clinically severe AS were recruited.

209 ght ventricular dysfunction occurs in severe AS.

210 ients with medically-managed isolated severe AS (aortic valve area < 1 cm(2)) and preserved LVEF (>50

211 Compared to NF, LF severe AS had higher LV stiffness indices (>0.11 ml(-1) OR 3.06

212 Conclusions Among patients with LG severe AS and preserved left ventricular ejection fraction, dec

213 LG severe AS may be subdivided in classical low-flow (left ventric

214 olume index, SVI < 35 ml/m(2)) and NF severe AS.

215 was analyzed in 2 AS populations, one severe AS (n=572) with outcome measures and one with mixed seve

216 otal, 1,131 patients with moderate or severe AS and complete clinical follow-up were included as part

217 referred for treatment of symptomatic severe AS awaiting either SAVR or TAVR.

218 ot a good diagnostic marker for truly severe AS.

219 In asymptomatic patients with severe AS and preserved ejection fraction, TAPSE <17 mm was ind

220 VR even in asymptomatic patients with severe AS.

221 ing by affinity selection-mass spectrometry (AS-MS).

222 Alternative splicing (AS) and alternative polyadenylation (APA) generate diver

223 pha induces changes in alternative splicing (AS) and first exon usage, increasing the diversity of tr

224 mined 28 DEGs known as alternative splicing (AS) factors that regulate AS process, and found evidence

225 dysregulation of mRNA alternative splicing (AS) in the development and progression of solid tumors r

226 Alternative splicing (AS) is a major gene regulatory mechanism in plants.

227 Alternative splicing (AS) is frequent during early mouse embryonic development

228 Alternative splicing (AS) is involved in cell fate decisions and embryonic dev

229 Although alternative splicing (AS) is involved in virtually every biological function i

230 l rhythmic genome-wide alternative splicing (AS) of pre-mRNAs encoding regulators of peptidergic secr

231 networks of postnatal alternative splicing (AS) transitions, while in the cytoplasm, CELF1 regulates

232 polyadenylation (APA), alternative splicing (AS), and fusion transcripts.

233 , BdFTL1 is subject to alternative splicing (AS), and its transcriptional level and AS are significan

234 lating neuron-specific alternative splicing (AS), previously associated with an acquired neurologic c

235 criptional mechanisms, alternative splicing (AS; especially intron retention) and alternative polyade

236 arthritis (PsA), and ankylosing spondylitis (AS) from 526 subjects overall.

237 Ankylosing spondylitis (AS) is the prototypic form of SpA in which progressive d

238 egulatory network in ankylosing spondylitis (AS) is vital for elucidating the mechanisms of AS pathog

239 athies (SpA) include ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, the

240 Older patients with severe aortic stenosis (AS) are increasingly identified as having cardiac amyloi

241 dy on the classification of aortic stenosis (AS) based on cardio-mechanical signals collected using n

242 Aortic stenosis (AS) contributes to cardiovascular mortality and morbidit

243 management of patients with aortic stenosis (AS) crucially depends on accurate diagnosis.

244 th low-gradient (LG) severe aortic stenosis (AS) despite preserved left ventricular ejection fraction

245 oxical low-flow (LF) severe aortic stenosis (AS) with preserved left ventricular ejection fraction (L

246 Valve morphology, aortic stenosis (AS), and aortic insufficiency (AI) have been proposed as

247 predictor in patients with aortic stenosis (AS), but the prognostic impact of right ventricular dysf

248 n high-gradient (HG) severe aortic stenosis (AS), the results in low-gradient (LG, mean gradient <40

249 magnetic resonance (CMR) in aortic stenosis (AS).

250 tification in patients with aortic stenosis (AS).

251 R) for patients with severe aortic stenosis (AS).

252 in the definition of severe aortic stenosis (AS).

253 ng characteristic of severe aortic stenosis (AS).

254 We identified 3 types of angioid streaks (AS) using AO: "crack," "band," and "hypopigmented." The

255 ere prepared by mixing 1 M ammonium sulfate (AS), ammonium nitrate (AN), sodium sulfate (SS), or sodi

256 These systems contain ammonium sulfate (AS)/nitrate (AN) and C3-C5 dicarboxylic acids, namely, m

257 ospective cohort of 491 active surveillance (AS) participants indicates prominent elevations in plasm

258 In patients with severe symptomatic AS awaiting aortic valve replacement, there has been a t

259 ity and outcome in patients with symptomatic AS.

260 , Second Edition), and AS-specific symptoms (AS Clinical Severity Scale).

261 GEC affect the pathology of Alport syndrome (AS) however, is unclear.

262 Individuals with Angelman syndrome (AS) are characterized by severe cognitive impairments al

263 Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by a

264 Angelman Syndrome (AS) is a severe neurodevelopmental disorder due to impai

265 its deficiency results in Angelman Syndrome (AS) while its over-expression increases the risk for aut

266 enomic imprinting, causes Angelman syndrome (AS), a rare neurodevelopmental disorder.

267 target RNA sequences and to regulate target AS events.

268 ot differentially expressed, indicating that AS is a distinct layer of transcriptome reprogramming du

269 The AS OCT findings were found to correlate with the ocular

270 ially engaging or emotionally neutral in the AS group, while this modulation was not present in the c

271 beyond UBE3A as contributing factors in the AS phenotype, and provide important information for the

272 gulators of plant immunity and promoting the AS of susceptibility factors.

273 We reclassified the AS severity of the participants of the PRIMID-AS study (

274 ans subverts host immunity by repressing the AS of positive regulators of plant immunity and promotin

275 tory ability for events as compared with the AS (area under the receiver operating curve: 0.80 vs 0.6

276 Their AS-OCTA images were measured for CoNV anterior limit, Co

277 approach to relate global hPTM enrichment to AS regulation during mammalian tissue development.

278 e subgroup of participants, adding the RS to AS resulted in a significant improvement in the discrimi

279 studies have linked the Janus kinase TYK2 to AS.

280 terior segment optical coherence tomography (AS OCT) is a helpful tool used to diagnose and manage ma

281 terior segment optical coherence tomography (AS-OCT) was performed in order to detect intrascleral hy

282 terior segment optical coherence tomography (AS-OCT)-based stage of ectasia.

283 nformatically investigated the transcriptome AS dynamics of T. cruzi (Y strain) infected human foresk

284 iated with the type and abundance of various AS events under normal and cold temperature conditions i

285 However, whether EOT has been achieved when AS ends is critically dependent on the stopping criteria

286 However, because ATP demands increase with AS severity, this could increase susceptibility to systo

287 y data on a large sample of individuals with AS (n = 250, 848 assessments), including clinical scales

288 We examined how 23 individuals with AS and 21 typically developing young children with simil

289 Individuals with AS imitated as frequently and as accurately as typical y

290 In participants with AS of less than 300, RS association with events remained

291 ed aortic valve tissue from 58 patients with AS (mean age, 74.2; SD, 5.9).

292 gy of AS-CA is common in older patients with AS and can be predicted clinically.

293 omparable to the biopsies from patients with AS and focal segmental glomerulosclerosis, possibly indi

294 We found (1) patients with AS had upregulated circulating YKL-40 compared with heal

295 essed in aortic valves from 25 patients with AS using gas chromatography.

296 ar Dysfunction in Asymptomatic Patients With AS), using the 2017 guidelines, determined their risk of

297 t-times and access to care for patients with AS, irrespective of treatment modality.

298 ear mortality was worse in all patients with AS-CA (grade: 1 to 3) than those with lone AS (24.5% vs.

299 n tricuspid aortic valves from patients with AS.

300 ession and function and correlated them with AS disease progression.