ライフサイエンスコーパス: secondary progressive

1 n be preceded by a relapsing disease course (secondary progressive).

2 benign, 14 with relapsing-remitting, 10 with secondary progressive, 16 with primary progressive and t

3 6 +/- 2.89 versus 47.44 +/- 2.70, P < 0.01), secondary-progressive (46.33 +/- 2.84 versus 44.75 +/- 3

4 was observed in T(1) hypointense lesions in secondary-progressive (49.0 +/- 7.0 mM) and primary-prog

5 psing/remitting disease (EDSS > 3), 13 (24%) secondary progressive and 21 (39%) benign (relapsing/rem

6 6+/-10 years; 67.8% relapsing-remitting, 28% secondary progressive and 4.2% primary progressive MS) a

7 from 54 patients (17 primary progressive, 30 secondary progressive and 7 controls).

8 s and were divided into relapsing-remitting, secondary progressive and primary progressive subgroups.

9 aging and compares the abnormalities between secondary progressive and relapsing remitting multiple s

10 7 patients with relapsing-remitting, 23 with secondary-progressive and 20 with primary-progressive mu

11 ndrome, 29 with relapsing-remitting, 28 with secondary-progressive and 28 with primary-progressive mu

12 tients with MS (27 relapsing-remitting, nine secondary progressive) and in 20 control subjects to qua

13 ient may prevent recurrence, reoperation and secondary progressive aortic valve disease.

14 A phase 3 trial [the International MS Secondary Progressive Avonex Controlled Trial (IMPACT)]

15 e Sclerosis [SENTINEL], and International MS Secondary Progressive Avonex Controlled Trial [IMPACT])

16 g-remitting (coefficient = -0.48, P < 0.01), secondary-progressive (coefficient = -0.51, P < 0.01) an

17 ent = -0.28, P = 0.02), and both primary and secondary-progressive compared to relapsing-remitting mu

18 Sodium concentrations were higher in secondary-progressive compared with relapsing-remitting

19 a relapsing-remitting clinical course into a secondary progressive course.

20 , one a primary progressive course and one a secondary progressive course.

21 rse and 58 of 66 (87.8%) patients who became secondary progressive (cross-validated error rate = 7.2%

22 POMS patients also took longer to develop secondary progressive disease (32 vs 18 years, p=0.0001)

23 patients with multiple sclerosis (seven with secondary progressive disease and 14 with a relapsing re

24 m MRI natural history in a large cohort with secondary progressive disease and to ascertain its relat

25 is associated with greater brain atrophy in secondary progressive disease over a period of short ter

26 cumulation of disability in MS patients with secondary progressive disease regardless of the severity

27 d WM abnormalities was weaker in primary and secondary progressive disease than in relapsing-remittin

28 short-term MRI activity is generally high in secondary progressive disease, confirming a useful role

29 ent outcome in early relapsing-remitting and secondary progressive disease.

30 The cohort had clinical features typical of secondary progressive disease: thus, all had moderate or

31 5-HC) in patients with SPMS and in mice with secondary progressive experimental autoimmune encephalom

32 ctor H levels were capable of distinguishing secondary progressive from relapsing remitting disease (

33 or disability in the primary progressive and secondary progressive groups was similar preceding death

34 e sclerosis (MS) from relapsing-remitting to secondary progressive have not been clarified yet.

35 en men, 21 women; 18 relapsing remitting, 10 secondary progressive; mean age 42 years).

36 ssion, relapse, and chronic progression in a secondary progressive model of demyelinating disease.

37 gnificantly higher in the caudate nucleus in secondary progressive MS (12.9/s vs 10.9/s, p=0.03).

38 -remitting MS (P < 0.01), only marginally in secondary progressive MS (P < 0.05), and not at all in p

39 y Status Scale (EDSS) score in patients with secondary progressive MS (r = -0.69, P = .004) and no co

40 Among secondary progressive MS (SPMS) cases with attacks, all

41 y and mtDNA deletions in single neurons from secondary progressive MS (SPMS) cases.

42 y and mtDNA deletions in single neurons from secondary progressive MS (SPMS) cases.

43 volumes in relapsing remitting MS (RRMS) and secondary progressive MS (SPMS) patients and controls.

44 10 relapsing-remitting MS (RRMS) patients, 9 secondary progressive MS (SPMS) patients, and 9 healthy

45 ng-remitting MS (RRMS), and 27 patients with secondary progressive MS (SPMS).

46 I = 13.5-22.5%) evolved from relapsing MS to secondary progressive MS (SPMS).

47 se, these therapies show limited efficacy in secondary progressive MS (SPMS).

48 ary progressive MS multiple sclerosis ( SPMS secondary progressive MS ) patients provided written inf

49 Thirty-four MS patients (7 with secondary progressive MS [SPMS], 27 with relapsing remit

50 AM/TSP, 74 relapsing-remitting MS [RRMS], 17 secondary progressive MS [SPMS], and 40 primary progress

51 retina, and by inference the optic nerve, in secondary progressive MS and primary progressive MS.

52 could differentiate primary progressive from secondary progressive MS better than random guessing.

53 Forty-eight ROIs from 4 secondary progressive MS brains were analyzed.

54 Two-thirds of patients with secondary progressive MS had elevated anti-SNO-cysteine

55 duals suffering from relapsing-remitting and secondary progressive MS had significantly higher prothr

56 Increased caudate R(2)' in patients with secondary progressive MS is consistent with increased ir

57 RMS relaxing-remitting MS ) patients, and 12 secondary progressive MS multiple sclerosis ( SPMS secon

58 that memory and naive B cells from RRMS and secondary progressive MS patients exhibited a significan

59 s in RNFLT and macular volume in the eyes of secondary progressive MS patients not previously affecte

60 hfield phase imaging of highly active and of secondary progressive MS patients.

61 y and EDSS score was better in patients with secondary progressive MS than in those with relapsing-re

62 MPF macromolecular proton fraction in SPMS secondary progressive MS was reduced relative to RRMS re

63 Within each gender, men and women with secondary progressive MS were more depressed than men or

64 no disability and a half will have developed secondary progressive MS with increasing disability.

65 th secondary progressive multiple sclerosis (secondary progressive MS) (8 male; 19 female; mean age 5

66 essive MS, and intravenous immunoglobulin in secondary progressive MS).

67 Of the patients with secondary progressive MS, 14 had clinical history of opt

68 macular volume were significantly reduced in secondary progressive MS, but not in primary progressive

69 ppear to be at increased risk for developing secondary progressive MS.

70 rate a partial effect on disease activity in secondary progressive MS.

71 itting MS and 23.6 mL per year in those with secondary progressive MS.

72 mulation of new inflammatory disease foci in secondary progressive MS.

73 pairments were most prevalent in people with secondary progressive MS.

74 in patients with active relapsing than with secondary progressive MS.

75 nts with relapsing-remitting MS (n = 123) or secondary-progressive MS (n = 28) (mean age, 36 years; r

76 Fifteen secondary-progressive MS (SPMS) patients, 12 relapsing-r

77 and EDSS <4 or <6, and time to conversion to secondary-progressive MS (SPMS).

78 Patients had secondary-progressive MS and an Expanded Disability Stat

79 This analysis also determined that secondary-progressive MS patients are immunologically cl

80 ignificantly more GM, but not WM atrophy, in secondary-progressive MS versus relapsing-remitting MS (

81 ch as multiple sclerosis (MS), especially in secondary-progressive MS which follows relapsing-remitti

82 ith relapsing-remitting MS and 16 (28%) with secondary-progressive MS, and 21 HC subjects were imaged

83 whom developed relapsing-remitting MS and 11 secondary-progressive MS, with the rest experiencing no

84 ase duration 11 years), and 27 patients with secondary progressive multiple sclerosis (secondary prog

85 rferon beta-1b (IFNbeta-1b) in patients with secondary progressive multiple sclerosis (SP multiple sc

86 te that grossly unaffected white matter from secondary progressive multiple sclerosis (SP-MS) patient

87 Patients with secondary progressive multiple sclerosis (SPMS) are lack

88 rate of whole brain atrophy in patients with secondary progressive multiple sclerosis (SPMS).

89 psing-remitting multiple sclerosis (RRMS) or secondary progressive multiple sclerosis (SPMS).

90 Thirty patients with secondary progressive multiple sclerosis and 17 healthy

91 nges has been identified as a key feature of secondary progressive multiple sclerosis and may contrib

92 Significantly, analysis of secondary progressive multiple sclerosis brain tissue al

93 cid levels (i) are abnormal in patients with secondary progressive multiple sclerosis compared with h

94 etization transfer ratio were greater in the secondary progressive multiple sclerosis compared with r

95 otrigine on cerebral volume of patients with secondary progressive multiple sclerosis did not differ

96 amma was found in the meninges of cases with secondary progressive multiple sclerosis exhibiting tert

97 ed patients aged 18-65 years with primary or secondary progressive multiple sclerosis from 27 UK neur

98 s was equally low in primary progressive and secondary progressive multiple sclerosis groups versus c

99 ntricles in both the relapsing remitting and secondary progressive multiple sclerosis groups.

100 A substantial proportion of cases with secondary progressive multiple sclerosis have extensive

101 xonal damage between primary progressive and secondary progressive multiple sclerosis have not been r

102 tem cells were safely given to patients with secondary progressive multiple sclerosis in our study.

103 Patients with secondary progressive multiple sclerosis involving the v

104 Secondary progressive multiple sclerosis patients showed

105 e and efficacious in relapsing-remitting and secondary progressive multiple sclerosis patients.

106 ients with primary progressive compared with secondary progressive multiple sclerosis raise the quest

107 tients with relapsing-remitting or relapsing secondary progressive multiple sclerosis to receive 3 mg

108 One hundred and twenty three cases with secondary progressive multiple sclerosis were examined f

109 Patients aged 18-65 years with secondary progressive multiple sclerosis were randomly a

110 Twenty-four patients with secondary progressive multiple sclerosis were studied ps

111 Patients with secondary progressive multiple sclerosis who attended th

112 We report the findings in 60 patients with secondary progressive multiple sclerosis who had monthly

113 e disability in both primary progressive and secondary progressive multiple sclerosis with a common p

114 res in an extensive collection of cases with secondary progressive multiple sclerosis with a wide age

115 on-beta1b was performed on 718 patients with secondary progressive multiple sclerosis with follow-up

116 se, and 2.89 cm3/year in those who developed secondary progressive multiple sclerosis, a difference o

117 from 23 patients with relapsing-remitting or secondary progressive multiple sclerosis, all of whom we

118 atients with relapsing remitting and 28 with secondary progressive multiple sclerosis, and 38 healthy

119 4 years disease duration), 13 subjects with secondary progressive multiple sclerosis, and in 17 age-

120 ) stimulation was lower in the patients with secondary progressive multiple sclerosis, compared with

121 Secondary progressive multiple sclerosis, for which no s

122 In secondary progressive multiple sclerosis, T2* in normal-

123 We conclude that for relapsing-remitting and secondary progressive multiple sclerosis, the combinatio

124 EAE) and in brain samples from patients with secondary progressive multiple sclerosis.

125 ications for the axonal loss associated with secondary progressive multiple sclerosis.

126 ng tissue loss in both arms of this study of secondary progressive multiple sclerosis.

127 ing-remitting multiple sclerosis and 20 with secondary progressive multiple sclerosis.

128 -beta-1b was also shown to be efficacious in secondary progressive multiple sclerosis.

129 carried out in 20 patients with primary and secondary progressive multiple sclerosis.

130 n appealing candidate drug for patients with secondary progressive multiple sclerosis.

131 as a potential neuroprotective treatment for secondary progressive multiple sclerosis.

132 ferent pathogenetic mechanisms compared with secondary progressive multiple sclerosis.

133 ine is also neuroprotective in patients with secondary progressive multiple sclerosis.

134 cal spinal cord in patients with primary and secondary progressive multiple sclerosis.

135 tic neuritis, and chronically in primary and secondary progressive multiple sclerosis.

136 esion development in relapsing-remitting and secondary progressive multiple, sclerosis, and this usua

137 clerosis, with higher concentrations seen in secondary-progressive multiple sclerosis and in patients

138 um concentrations were higher in primary and secondary-progressive multiple sclerosis.

139 n heterozytgotes was significantly higher in secondary progressive (P < 0.01) and primary progressive

140 more extensive in primary progressive versus secondary progressive patients (33% reduction versus 16%

141 m and putamen, and this was most apparent in secondary progressive patients with MS.

142 By contrast, in the subgroup of secondary progressive patients, microglial activation at

143 The secondary progressive phase is due to neurodegeneration

144 course during the study and entered into the secondary progressive phase.

145 e sclerosis [20 relapsing remitting (RR), 21 secondary progressive (SP) and 10 primary progressive (P

146 s and remissions and typically followed by a secondary progressive (SP) course.

147 ses with relapsing-remitting (RR)-MS (n=81), secondary progressive (SP) MS (n=13) and primary progres

148 -remitting (RR), 17 with benign, and 23 with secondary progressive (SP) MS and 18 healthy control sub

149 syndrome (CIS), relapsing remitting (RR) and secondary progressive (SP) MS.

150 in people with relapsing-remitting (RR) and secondary progressive (SP) MS.

151 10 relapsing remitting (RR) and 11 secondary progressive (SP) patients with multiple sclero

152 relapsing-remitting (RR) stage followed by a secondary progressive (SP) phase.

153 iple sclerosis, primary progressive (PP) and secondary progressive (SP) versus relapsing-remitting (R

154 ients had relapsing-remitting (RR) (n=92) or secondary-progressive (SP) (n=49) MS; clinical course wa

155 11 with relapsing-remitting [RR] MS, 92 with secondary-progressive [SP] MS, and 37 with primary-progr

156 sera with no significant difference between secondary progressive (SPMS) and relapsing-remitting (RR

157 toantibody patterns that distinguished RRMS, secondary progressive (SPMS), and primary progressive (P

158 lerosis determines when a patient enters the secondary progressive stage of the disease.

159 ffectively treat patients in the primary and secondary progressive stages of the disease.

160 h is three times higher in those who develop secondary progressive than in those who remain relapsing

161 ople with multiple sclerosis, and more so in secondary progressive than relapsing remitting multiple

162 e range 1.5-6.5; 35 relapsing remitting, two secondary-progressive) underwent 3 T MRI including high-