ライフサイエンスコーパス: leptomeningeal

1 N-terminal sequence analysis of isolated leptomeningeal amyloid fibrils revealed homology to ABri

2 Clinical features attributed to her leptomeningeal amyloid included radiculopathy, central h

3 evere peripheral neuropathy with symptoms of leptomeningeal amyloid indicates that leptomeningeal amy

4 oms of leptomeningeal amyloid indicates that leptomeningeal amyloidosis should be considered part of

5 n HUV-EC cells but undetectable in cortical, leptomeningeal and bovine aortic endothelial cells.

6 myloid and amyloid-beta accumulation both in leptomeningeal and brain vessels when measured by intrav

7 ination revealed productive JCV infection of leptomeningeal and choroid plexus cells, and limited par

8 cts, (2) there was almost the same extent of leptomeningeal and cortical amyloid angiopathy in the no

9 redominantly amyloid-beta40) in the walls of leptomeningeal and cortical arterioles and is likely a c

10 nd hippocampus and was also prominent within leptomeningeal and cortical blood vessels of all APPsw A

11 ed derivatives were the predominant forms in leptomeningeal and cortical vessels.

12 ammation and necrosis (mesencephalon) and in leptomeningeal and white matter perivascular infiltrates

13 with parenchymal, 12.5% (1/8) for those with leptomeningeal, and 0/3 for patients with hydrocephalus.

14 were predominantly seen at perivascular and leptomeningeal, and not parenchymal, sites.

15 minent staining was in degenerating media of leptomeningeal arteries and sclerotic penetrating vessel

16 beta42 were abundant in VSMCs, especially in leptomeningeal arteries and their initial cortical branc

17 lammatory disorder affecting parenchymal and leptomeningeal arteries and veins.

18 to observe the earliest appearance of CAA in leptomeningeal arteries as multifocal deposits of band-l

19 In the leptomeningeal arteries the amyloid was deposited in mod

20 of vessels, including small and medium-sized leptomeningeal arteries, small penetrating white matter

21 Within leptomeningeal arteries, where we could define the three

22 paces and tunica media basement membranes of leptomeningeal arteries.

23 nt to a distinct subtype of PCNSV with small leptomeningeal artery vasculitis and rapid response to t

24 cerebrospinal fluid barrier and of the blood-leptomeningeal barrier, but not by endothelial cells of

25 meningitis and cranial neuropathies in whom leptomeningeal biopsy demonstrated Wegener's granulomato

26 erebral angiography followed by cortical and leptomeningeal biopsy for possible primary angiitis of t

27 tive CSF cytology, vitreous biopsy, or brain/leptomeningeal biopsy remain the current standard for di

28 m of the cerebral cortex is derived from the leptomeningeal blood vessels.

29 At this time point, leptomeningeal but not parenchymal CD4(+) T cells incorp

30 Although leptomeningeal carcinomatosis is a well-established clin

31 with metastatic breast cancer diagnosed with leptomeningeal carcinomatosis, CSF samples were subjecte

32 o facilitate and complement the diagnosis of leptomeningeal carcinomatosis.

33 abundance and distribution were examined in leptomeningeal cells and astrocytes infected with T. cru

34 of GFAP mRNA in the cultures of cortical and leptomeningeal cells and of protein in all cell types; V

35 Pores or stomata present on CSF-facing leptomeningeal cells ensheathing blood vessels in the su

36 ytes) or both connexin43 and connexin26 (for leptomeningeal cells) demonstrated that punctate gap jun

37 metastatic MYC amplified medulloblastoma or leptomeningeal cells, we were led to explore the bioacti

38 cing cells are identified as endothelial and leptomeningeal cells.

39 Seven pathologies-leptomeningeal cerebral amyloid angiopathy, large infarc

40 red model included moderate/severe occipital leptomeningeal cerebral amyloid angiopathy, moderate/sev

41 marrow involvement were more likely to have leptomeningeal (cerebrospinal fluid [CSF]) lymphoma than

42 Parenchymal and leptomeningeal CNS disease occurred in four and three pa

43 The adequacy of leptomeningeal collateral blood flow was rated as no or

44 p = 0.03) as independent predictors of poor leptomeningeal collateral status at baseline.

45 eruricemia, and age are associated with poor leptomeningeal collateral status in patients with acute

46 determinants associated with variability in leptomeningeal collateral status in patients with acute

47 , 0.73 [95% CI, 0.64-0.83]), and strength of leptomeningeal collaterals (odds ratio, 2.37 [95% CI, 1.

48 Two raters assessed leptomeningeal collaterals on baseline CTA by consensus,

49 or survival was noted for all mutations with leptomeningeal complications except for those with the T

50 agreed criteria were used for assessment of leptomeningeal, cortical and capillary cerebral amyloid

51 id peptides in the gray and white matter and leptomeningeal/cortical vessels of two AN-1792-vaccinate

52 ctron microscopy was used to show stomata on leptomeningeal coverings of blood vessels in the subarac

53 Leptomeningeal disease (LMD) significantly affects the p

54 Leptomeningeal disease (LMD) significantly affects the p

55 edulloblastoma at a young age with extensive leptomeningeal disease and metastasis to the spinal cord

56 For patients with leptomeningeal disease, inclusion of a separate cohort i

57 s at the time of study entry; and those with leptomeningeal disease.

58 Exclusion criteria were leptomeningeal disease; metastases in medulla, pons, or

59 Smo/Smo tumors also display leptomeningeal dissemination of neoplastic cells to the

60 nomas and one with mixed GCT) presented with leptomeningeal dissemination.

61 MRIs showed prominent leptomeningeal enhancement in 8 of 101 patients with PCN

62 Brain MRI showed a diffuse leptomeningeal enhancement in cortical sulcus.

63 e of magnetic resonance imaging to visualize leptomeningeal enhancement in patients with MS and place

64 magnetic resonance imaging (MRI) evidence of leptomeningeal enhancement in the cauda equina although

65 ce imaging correlation studies indicate that leptomeningeal enhancement is most common in patients wi

66 Leptomeningeal enhancement may prove a useful surrogate

67 Prominent gadolinium leptomeningeal enhancement on MRI may point to a distinc

68 s T2-weighted hyperintense lesions and focal leptomeningeal enhancement, consistent with the hypothes

69 Findings on MRI included ventriculitis, leptomeningeal enhancement, infarction, hemorrhage, and

70 m-enhanced contrast scans by the presence of leptomeningeal enhancement.

71 mount preparations, time-lapse microscopy of leptomeningeal explants, and in vitro proliferation assa

72 semaphorin 3A messenger RNA in cultured rat leptomeningeal fibroblasts compared with untreated cells

73 Cultured human leptomeningeal fibroblasts grafted into rat frontal cort

74 These data indicate that grafted leptomeningeal fibroblasts hyperexpress APP and A beta w

75 t cerebral cortex scar tissue and in primary leptomeningeal fibroblasts in vitro.

76 Furthermore, decorin treatment of leptomeningeal fibroblasts significantly increases their

77 n shown to be strongly expressed by invading leptomeningeal fibroblasts.

78 Leptomeningeal glioneuronal heterotopias are a focal typ

79 We report that leptomeningeal glioneuronal heterotopias form in Emx2(-/

80 es between the molecular layer and overlying leptomeningeal heterotopia and within the heterotopia it

81 n in regions of polymicrogyria and overlying leptomeningeal heterotopia suggest an association betwee

82 d in leukocytes traversing the ependyma from leptomeningeal infiltrates.

83 diating leukemia-cell entry into the CNS and leptomeningeal infiltration was further demonstrated by

84 matter demyelination, cortical atrophy, and leptomeningeal inflammation may be important components

85 ognosis due to AIDS-associated lymphoma with leptomeningeal involvement, advanced immunosuppression,

86 e imaging showed improvement in cochlear and leptomeningeal lesions as compared with baseline.

87 were identified in 16 patients and included leptomeningeal lesions in eight, parenchymal lesions in

88 Leptomeningeal lymphoma and intraocular lymphoma are top

89 onventional cytology for detection of occult leptomeningeal lymphoma; however, some FCM-negative pati

90 PPCA-expressing perivascular and leptomeningeal macrophages were detected throughout the

91 nce individually and separately for signs of leptomeningeal metastases and assigned a diagnostic rati

92 ic examination of VP shunt CSF for detecting leptomeningeal metastases in pediatric patients with pri

93 This is particularly true for cases in which leptomeningeal metastases manifest primarily or solely a

94 most common pediatric brain malignancy, with leptomeningeal metastases often present at diagnosis and

95 ib maintenance therapy, and subsequently had leptomeningeal metastases that responded to gefitinib.

96 Leptomeningeal metastases were depicted in 38 cases on c

97 In 20 cases, leptomeningeal metastases were detected by using only co

98 In three cases, leptomeningeal metastases were detected by using only FL

99 Radioimmunotherapy can effectively treat leptomeningeal metastases when radiolabeled antibodies a

100 tyrosine kinase inhibitor and patients with leptomeningeal metastases who had been pretreated with a

101 dministered to patients with either brain or leptomeningeal metastases who had never received an EGFR

102 titumor effect could be achieved in treating leptomeningeal metastases with i.t. administered 125IUdR

103 secondary to the treatment or prophylaxis of leptomeningeal metastases, and the cause of most deaths

104 ective against established CNS lymphoma with leptomeningeal metastases, sites that are usually consid

105 on other tumors, including brain metastases, leptomeningeal metastases, spine tumors, pediatric brain

106 delirium, spinal cord compression, brain or leptomeningeal metastases, within 3 months of advanced c

107 CNS metastases-including brain and leptomeningeal metastases-from epidermal growth factor r

108 metastases, and the cause of most deaths is leptomeningeal metastases.

109 s are better than FLAIR images for detecting leptomeningeal metastases.

110 sensitivity of 34% for cytologically proved leptomeningeal metastases.

111 patients with CNS GCT, including those with leptomeningeal metastases.

112 ine (125IUdR) was examined in a rat model of leptomeningeal metastases.

113 ients with ALK-rearranged NSCLC and brain or leptomeningeal metastases.

114 tients with EGFR-mutant NSCLC with brain and leptomeningeal metastases.

115 e systemic therapy may benefit patients with leptomeningeal metastasis and obviate the need for intra

116 e systemic therapy may benefit patients with leptomeningeal metastasis and obviate the need for intra

117 ts increasingly utilized in the treatment of leptomeningeal metastasis are targeted mAbs such as ritu

118 tilized intra-CSF agents in the treatment of leptomeningeal metastasis are targeted monoclonal antibo

119 ed therapeutically beneficial in suppressing leptomeningeal metastasis in these preclinical models.

120 Evaluation of leptomeningeal metastasis includes contrast-enhanced bra

121 single most important aspect to diagnosis of leptomeningeal metastasis is considering and pursuing th

122 Although treatment of leptomeningeal metastasis is palliative with median pati

123 Although treatment of leptomeningeal metastasis is palliative with median pati

124 Leptomeningeal metastasis occurs in approximately 3-5% o

125 Leptomeningeal metastasis occurs in approximately 5% of

126 Treatment of leptomeningeal metastasis often requires involved-field

127 Staging of leptomeningeal metastasis should include contrast-enhanc

128 survival of 2-3 months (15% of patients with leptomeningeal metastasis survive 1 year), treatment may

129 iew of methods of diagnosis and treatment of leptomeningeal metastasis was performed.

130 include central nervous system prophylaxis, leptomeningeal metastasis, and common hematologic compli

131 We molecularly dissected leptomeningeal metastasis, or spread of cancer to the ce

132 lide cerebrospinal fluid (CSF) flow study if leptomeningeal metastasis-directed therapy is being cons

133 F-liberating proteases that could facilitate leptomeningeal metastasis.

134 er neurologic deterioration in patients with leptomeningeal metastasis.

135 er neurologic deterioration in patients with leptomeningeal metastasis.

136 arding methods of diagnosis and treatment of leptomeningeal metastasis.

137 ent component 3 (C3) was upregulated in four leptomeningeal metastatic models and proved necessary fo

138 tions suggest that PGD2 may induce sleep via leptomeningeal PGD2 receptors with subsequent activation

139 ate T cells is not a general property of all leptomeningeal phagocytes, but varies between individual

140 pression in primary tumors was predictive of leptomeningeal relapse.

141 ensus, using a previously validated regional leptomeningeal score (rLMC).

142 duces pathologic responses in cultured human leptomeningeal smooth muscle cells including cellular de

143 logic form of the peptide for cultured human leptomeningeal smooth muscle cells.

144 he blood-brain barrier, the T cells scan the leptomeningeal space for autoantigen-presenting cells (A

145 lops when malignant cells gain access to the leptomeningeal space, producing several clinical symptom

146 n limited penetration of this agent into the leptomeningeal space.

147 roved necessary for cancer growth within the leptomeningeal space.

148 sseminate via the cerebrospinal fluid to the leptomeningeal spaces of the brain and spinal cord.

149 ated pattern in which tumor cells seeded the leptomeningeal spaces of the brain and spinal cord.

150 eral brain, and egressed at perivascular and leptomeningeal spaces.

151 ed gene expression profiles of nonneoplastic leptomeningeal specimens and human meningiomas of varyin

152 ugh the prognosis has improved considerably, leptomeningeal spread of the tumor remains a significant

153 oblastoma, which show greater propensity for leptomeningeal spread.

154 he first mouse medulloblastoma model to show leptomeningeal spread.

155 m cerebrospinal fluid and dissected cerebral leptomeningeal tissue from patients with multiple sclero

156 rated mGluR expression in both rat and human leptomeningeal tissues.

157 tion of amyloid beta (Abeta) in cortical and leptomeningeal vessel walls.

158 roll and crawl along the luminal surface of leptomeningeal vessels without showing calcium activity.

159 in the cerebral and cerebellar cortices, in leptomeningeal vessels, and in CWPs isolated by laser mi

160 present in the leptomeninges, especially the leptomeningeal vessels, and in the subependymal regions

161 was observed in the cortical neuropil and in leptomeningeal vessels.

162 using flow cytometry, confocal microscopy of leptomeningeal whole-mount preparations, time-lapse micr