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2 PHOMS were present in 16% of patients with relapsing-remitting, 16% of patients with progressive, a
3 7 healthy control subjects, 27 patients with relapsing-remitting, 23 with secondary-progressive and 2
4 : 119 (72%) had multiple sclerosis [94 (57%) relapsing-remitting, 25 (15%) secondary progressive], 45
5 lthy controls and 122 patients comprising 58 relapsing-remitting, 28 primary progressive and 36 secon
6 with a clinically isolated syndrome, 29 with relapsing-remitting, 28 with secondary-progressive and 2
7 ars, disease duration 14.6+/-10 years; 67.8% relapsing-remitting, 28% secondary progressive and 4.2%
8 tients (22 clinically isolated syndrome, 198 relapsing remitting, 39 secondary progressive, 31 primar
9 6 +/- 1.39 versus 49.13 +/- 1.19, P < 0.01), relapsing-remitting (48.86 +/- 2.89 versus 47.44 +/- 2.7
10 icipants included 36 individuals with MS (30 relapsing-remitting, 6 secondary or primary progressive)
11 ts (31 clinically isolated syndrome, and 416 relapsing-remitting, 84 secondary progressive, and 73 pr
13 ith distance from the ventricles in both the relapsing remitting and secondary progressive multiple s
14 d degenerating brain and spinal cord in both relapsing-remitting and progressive forms of MS and may
16 cervical spinal cord of patients with early relapsing-remitting and secondary progressive multiple s
17 ealthy donors and MS patients in the initial relapsing-remitting and subsequent secondary-progressive
18 nearest the subpial surfaces for those with relapsing-remitting and the central canal CSF surface in
19 rrently being evaluated for the treatment of relapsing, remitting, and primary progressive multiple s
22 fected with M. amphoriforme manifesting as a relapsing-remitting bacterial load, interspersed by peri
23 em traditionally characterized by an initial relapsing-remitting clinical course and focal inflammato
26 ed syndrome (coefficient = -0.32, P = 0.03), relapsing-remitting (coefficient = -0.48, P < 0.01), sec
27 2 of 268 (94.0%) patients who maintained the relapsing-remitting course and 58 of 66 (87.8%) patients
30 secondary progressive disease and 14 with a relapsing remitting disease course) underwent T1- and T2
32 s (MS) is a neuroinflammatory disease with a relapsing-remitting disease course at early stages, dist
34 ression was more common in younger patients, relapsing-remitting disease course, and after a smaller
35 y of myelin-reactive CD4 T cells that elicit relapsing-remitting disease have not been quantified.
37 e determined that pEVs induced a spontaneous relapsing-remitting disease phenotype in MOG(35-55)-immu
39 AZD1480 delays disease onset of PLP-induced relapsing-remitting disease, reduces relapses and dimini
43 g the first relapse in a SJL animal model of relapsing-remitting EAE abrogated clinical disease, infl
47 preclinically, could suppress progression of relapsing-remitting experimental autoimmune encephalomye
48 ition of system Xc(-) attenuates chronic and relapsing-remitting experimental autoimmune encephalomye
49 Moreover, guanabenz ameliorates relapse in relapsing-remitting experimental autoimmune encephalomye
50 causal role of IL-11 in the exacerbation of relapsing-remitting experimental autoimmune encephalomye
51 d progressive, as well as PLP138-151-induced relapsing-remitting experimental autoimmune encephalomye
52 BE1 mutations can cause an early adult-onset relapsing-remitting form of polyglucosan body disease di
53 d on the 2010 McDonald criteria (34 with the relapsing-remitting form, 2 with clinically isolated syn
54 ges were significant in both progressive and relapsing-remitting forms of the disease and correlated
55 , whereas the classifier that differentiates relapsing-remitting from progressive MS achieved a valid
58 males with progressive disease compared with relapsing-remitting males (RRMS) and female MS subjects,
59 disease relapses and remissions in the SJL/J-relapsing-remitting model of EAE, and could comparably a
61 se episode alleviated clinical symptoms in a relapsing-remitting model of proteolipid protein139-151-
62 of Gli1 improves the functional outcome in a relapsing/remitting model of experimental autoimmune enc
63 d in MS by comparing the fecal microbiota in relapsing remitting MS (RRMS) (n = 31) patients to that
64 ith secondary progressive MS [SPMS], 27 with relapsing remitting MS [RRMS]) and 30 healthy volunteers
65 ants with secondary progressive MS than with relapsing-remitting MS (3.6 lesions/year +/- 4.2 vs 1.1
67 ectroscopic imaging data in 46 patients with relapsing-remitting MS (median disease duration, 0.8 yea
69 ts with a diagnosis of either PPMS (n = 16), relapsing-remitting MS (n = 20), or benign MS (n = 20) a
72 expression is reduced in CD4(+) T cells from relapsing-remitting MS (RR-MS) patients during relapse.
73 can serve as a biomarker of regeneration in relapsing-remitting MS (RRMS) and whether disease-modify
75 ethylenediaminetetraacetic acid plasma in 10 relapsing-remitting MS (RRMS) patients, 9 secondary prog
76 secondary-progressive MS (SPMS) patients, 12 relapsing-remitting MS (RRMS) patients, and 14 matched h
79 were reconstructed from diffusion data in 58 relapsing-remitting MS (RRMS), 28 primary progressive MS
80 ulatory (EDSS scores <=3.5), all of whom had relapsing-remitting MS (RRMS), 3 (4%) had RRMS and EDSS
82 inically isolated syndrome (CIS) and 69 with relapsing-remitting MS (RRMS; mean age: CIS: 31.4 +/- 9.
83 nal fluid (CSF) and blood from subjects with relapsing-remitting MS (RRMS; n = 12), other neurologic
85 nd April 2019, 120 patients with MS (58 with relapsing-remitting MS [RRMS] and 62 with progressive MS
86 atic carriers of HTLV-1 (AC), 47 HAM/TSP, 74 relapsing-remitting MS [RRMS], 17 secondary progressive
87 (52 clinically isolated syndrome [CIS], 196 relapsing-remitting MS [RRMS], 34 progressive MS [PMS]),
88 terials and Methods Twenty participants with relapsing-remitting MS and 13 with secondary progressive
89 In a prospective study, 326 patients with relapsing-remitting MS and 163 patients with progressive
96 diagnosis of clinically isolated syndrome or relapsing-remitting MS and a minimum of 7 years of prosp
97 sability Status Scale score of 3.5 to 6.5 or relapsing-remitting MS and an Expanded Disability Status
98 nce images were acquired from 133 women with relapsing-remitting MS and analyzed using voxel-based mo
99 eters to explain IPS and EF in patients with relapsing-remitting MS and confirms the central role of
100 the lateral funiculi and gray matter (GM) in relapsing-remitting MS and GM atrophy in patients with p
101 mean age 33.4 yrs) with clinically definite, relapsing-remitting MS and mild disability (EDSS - Expan
102 written informed consent, six patients with relapsing-remitting MS and six healthy control subjects
104 ters in 21 countries examining patients with relapsing-remitting MS commencing DMTs (or clinical moni
105 ognitive performance of 99 clinically stable relapsing-remitting MS for whom data from four consequen
106 onal cohort study included 312 patients with relapsing-remitting MS in 2 independent cohorts (72 pati
108 eased in patients with clinically definitive relapsing-remitting MS in comparison with healthy contro
109 t study, 14 healthy control participants, 18 relapsing-remitting MS multiple sclerosis ( RRMS relaxin
111 e measured in CD14+ monocytes from untreated relapsing-remitting MS patients and compared to healthy
112 ssessed in a training set of 334 consecutive relapsing-remitting MS patients and in an independent va
114 volume suitably explains the probability of relapsing-remitting MS patients evolving into the progre
115 to analyze data from a large cohort of 1,697 relapsing-remitting MS patients in British Columbia, Can
122 the phase 2 studies) and diagnosed as having relapsing-remitting MS were eligible to participate in t
127 6 with clinically isolated syndrome, 42 with relapsing-remitting MS) and 23 control subjects underwen
128 onset (clinically isolated syndrome [CIS] or relapsing-remitting MS) and were also compared to two ot
129 summarise emerging injectable therapies for relapsing-remitting MS, and discuss pharmacological mech
130 either clinically isolated syndrome (CIS) or relapsing-remitting MS, as well as for 15 age- and sex-m
131 d July 7, 2016, a total of 110 patients with relapsing-remitting MS, at least 2 relapses while receiv
132 age, shorter durations of MS, female gender, relapsing-remitting MS, higher educational attainment an
134 ing tool for identifying novel therapies for relapsing-remitting MS, it has proven to be less success
136 In this preliminary study of patients with relapsing-remitting MS, nonmyeloablative HSCT, compared
137 the disease activity, among 99 patients with relapsing-remitting MS, who underwent blinded clinical a
149 XA1 to influence T cell effector function in relapsing/remitting MS (RRMS), an autoimmune disease sus
151 ntegrity of processing of structural RNAs in relapsing remitting multiple sclerosis (RRMS) and other
152 rom the cerebrospinal fluid of patients with relapsing remitting multiple sclerosis (RRMS) have highe
153 progressive multiple sclerosis compared with relapsing remitting multiple sclerosis group, and these
156 were enrolled in this study, 24 patients had relapsing remitting multiple sclerosis, six had progress
157 s, and more so in secondary progressive than relapsing remitting multiple sclerosis, tissue structura
164 3 years disease duration), 18 subjects with relapsing-remitting multiple sclerosis (>/= 4 years dise
165 -progressive (49.3 +/- 8.0 mM) compared with relapsing-remitting multiple sclerosis (43.0 +/- 8.5 mM,
167 rimary and secondary-progressive compared to relapsing-remitting multiple sclerosis (coefficients = -
168 atients with clinically isolated syndrome or relapsing-remitting multiple sclerosis (Expanded Disabil
170 e cerebrospinal fluid of patients with early relapsing-remitting multiple sclerosis (MS) and in activ
171 n the brains and spinal cords of people with relapsing-remitting multiple sclerosis (MS) and progress
172 des of onset, 80% of untreated patients with relapsing-remitting multiple sclerosis (MS) convert to a
174 The use of natalizumab for highly active relapsing-remitting multiple sclerosis (MS) is influence
176 on medications and disease progression among relapsing-remitting multiple sclerosis (MS) patients in
179 iety of human autoimmune diseases, including relapsing-remitting multiple sclerosis (MS), in which in
184 ts with clinically isolated syndrome (n=74), relapsing-remitting multiple sclerosis (n=664), or progr
185 ger-type lesion' in an independent cohort of relapsing-remitting multiple sclerosis (RRMS) and AQP4-a
186 cting fingolimod (FTY) treatment response in relapsing-remitting multiple sclerosis (RRMS) are lackin
187 TCR stimulation is impaired in subjects with relapsing-remitting multiple sclerosis (RRMS) because of
188 tokine polarization profile in patients with relapsing-remitting multiple sclerosis (RRMS) by high-di
189 umab is a newly licensed treatment of active relapsing-remitting multiple sclerosis (RRMS) in Europe,
190 mbulatory function in disabled subjects with relapsing-remitting multiple sclerosis (RRMS) or seconda
191 e total circulating exosome transcriptome in relapsing-remitting multiple sclerosis (RRMS) patients a
192 e previously showed that memory B cells from relapsing-remitting multiple sclerosis (RRMS) patients e
194 (CSF) samples collected over 12 months from relapsing-remitting multiple sclerosis (RRMS) patients.
196 le SclerOsis (ALLEGRO), a phase III study in relapsing-remitting multiple sclerosis (RRMS), oral laqu
204 l trials (Natalizumab Safety and Efficacy in Relapsing-Remitting Multiple Sclerosis [AFFIRM], Safety
205 a control cohort of neurologic autoimmunity (relapsing-remitting multiple sclerosis [MS] n = 110, HD
206 ion With Interferon Beta-1a in Patients With Relapsing-Remitting Multiple Sclerosis [SENTINEL], and I
207 al, we enrolled adults aged 18-55 years with relapsing-remitting multiple sclerosis and at least one
209 58 years) with relapsing multiple sclerosis (relapsing-remitting multiple sclerosis and secondary pro
210 atents for the first approved treatments for relapsing-remitting multiple sclerosis are expiring, cre
211 their effects on disability in patients with relapsing-remitting multiple sclerosis are maintained an
212 ratio values in the outer cord were lower in relapsing-remitting multiple sclerosis compared with cli
213 DMTs by comparing a cohort of patients with relapsing-remitting multiple sclerosis enrolled in the U
214 ed cohort study, we identified patients with relapsing-remitting multiple sclerosis experiencing rela
215 trial, patients aged 18-60 years with active relapsing-remitting multiple sclerosis from 84 centres i
217 d data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase a
218 In the clinically isolated syndrome and relapsing-remitting multiple sclerosis groups, outer cor
219 tive disease-modifying treatments (DMTs) for relapsing-remitting multiple sclerosis have been license
220 at have regulatory approval for treatment of relapsing-remitting multiple sclerosis have little or no
221 igher in secondary-progressive compared with relapsing-remitting multiple sclerosis in cortical grey
223 nd extra-cellular sodium concentration in 19 relapsing-remitting multiple sclerosis patients and 17 h
224 xonal analysis could define axonal damage in relapsing-remitting multiple sclerosis patients earlier
225 nd 4-6 and 18-26 mo Tecfidera-treated stable relapsing-remitting multiple sclerosis patients using mu
227 312 on MRI Lesion Given Once Daily) Study in relapsing-remitting multiple sclerosis provides evidence
228 disagreement among devices in patients with relapsing-remitting multiple sclerosis regarding the ON
230 , phase 3 study involving 1841 patients with relapsing-remitting multiple sclerosis to compare dacliz
231 The mechanism underlying the progression of relapsing-remitting multiple sclerosis to secondary prog
232 olimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to
234 autoimmune encephalomyelitis (EAE) model of relapsing-remitting multiple sclerosis when administered
235 The drug might be an effective treatment for relapsing-remitting multiple sclerosis with less frequen
236 ggestive of CNS demyelination and typical of relapsing-remitting multiple sclerosis, a complete neuro
237 Eligible patients were aged 18-55 years, had relapsing-remitting multiple sclerosis, and had complete
238 ears old) with clinically isolated syndrome, relapsing-remitting multiple sclerosis, and progressive
239 ging has been examined in small cohorts with relapsing-remitting multiple sclerosis, but has not been
240 than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy
242 lusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one
244 A) is widely prescribed for the treatment of relapsing-remitting multiple sclerosis, however, the mec
245 ns is the underlying pathological process in relapsing-remitting multiple sclerosis, the gradual accu
247 a woman in her late 30s with a diagnosis of relapsing-remitting multiple sclerosis, who continued to
248 tified adult patients (aged >=18 years) with relapsing-remitting multiple sclerosis, with at least 6
249 ligible patients-those aged 18-55 years with relapsing-remitting multiple sclerosis-to receive fingol
270 he CSF of multiple sclerosis patients with a relapsing remitting (n = 15) or a progressive (secondary
271 ation reflected behaviour in the subgroup of relapsing remitting patients (rho = 0.74, P = 0.008).
272 ctions of white matter lesion enlargement in relapsing remitting patients and is associated with grea
274 3.6 +/- 2.7% and 2.9 +/- 2.4%), compared to relapsing-remitting patients (1.6 +/- 2.1%, both P < 0.0
275 ve MS patients are immunologically closer to relapsing-remitting patients as compared with patients w
276 cretion in urine samples from a cohort of 70 relapsing-remitting patients with MS who were followed f
277 quency was higher in progressive compared to relapsing-remitting patients, with significant bilateral
281 ent disease-modifying agents for its initial relapsing-remitting phase, these therapies show limited
282 e with a clinically isolated syndrome (CIS), relapsing remitting (RR) and secondary progressive (SP)
285 ate neuroinflammation at different phases of relapsing-remitting (RR) experimental autoimmune encepha
286 sed DNA methylation in the CD4(+) T cells of relapsing-remitting (RR) MS patients compared to healthy
287 raphically matched normal controls (NC), and relapsing-remitting (RR) MS patients, also matched with
288 copy, we analysed the lipoprotein profile of relapsing-remitting (RR) MS patients, progressive MS pat
291 rations were measured by ELISA in cases with relapsing-remitting (RR)-MS (n=81), secondary progressiv
292 still possible, and even favored, in stable relapsing-remitting (RR-MS) patients, whereas it was abs
293 e measured in 440 patients with MS (311 with relapsing-remitting [RR] MS, 92 with secondary-progressi
294 ical trial of AHSCT for patients with active relapsing remitting (RRMS) and secondary progressive MS
297 re aged 42-83 years and were referred with a relapsing remitting syndrome of fever (94%), constitutio
298 nical course of multiple sclerosis (MS) from relapsing-remitting to secondary progressive have not be
300 ohort of 18 MS patients (9 progressive and 9 relapsing-remitting) was compared to healthy controls an