ライフサイエンスコーパス: leptomeningeal

1 hymal (34.9%), focal-parenchymal (29.4%) and leptomeningeal (11.9%).

2 CNS relapses were early, predominantly leptomeningeal (73%), and co-occurred with systemic rela

3 ral pathogenesis, compounded by vascular and leptomeningeal abnormalities.

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

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

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

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

8 Leptomeningeal anastomoses or pial collateral vessels pl

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

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

11 , in particular in the presence of increased leptomeningeal and cerebrospinal fluid (CSF) inflammatio

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

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

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

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

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

17 However, whether leptomeningeal and dural macrophages play the same or di

18 evolution of BCLM and heterogeneity between leptomeningeal and extracranial metastatic sites.

19 ve vessel walls originating from Abeta-laden leptomeningeal and penetrating vessels.

20 Leptomeningeal and perivenular infiltrates are important

21 ice was at 22 to 24 months, first in frontal leptomeningeal and superficial cortical vessels followed

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

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

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

25 However, leptomeningeal angiomas were not associated, possibly be

26 but was not associated with upper eyelid or leptomeningeal angiomas, seizures, prior hemispherectomy

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

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

29 lammatory disorder affecting parenchymal and leptomeningeal arteries and veins.

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

31 Leptomeningeal arteries demonstrated substantially more

32 d CAA-induced cerebrovascular dysfunction in leptomeningeal arteries in vivo.

33 In the leptomeningeal arteries the amyloid was deposited in mod

34 ers that coalesce in variable patterns along leptomeningeal arteries, often merging around penetratin

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

36 Within leptomeningeal arteries, where we could define the three

37 paces and tunica media basement membranes of leptomeningeal arteries.

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

39 ine corpus callosum structure by influencing leptomeningeal-astroglial interactions at the IHF.

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

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

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

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

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

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

46 omeninges redistribute CLDN5 and PECAM1, and leptomeningeal capillaries exhibit foci with reduced blo

47 HER2(+) breast leptomeningeal carcinomatosis (HER2(+) LC) occurs when t

48 Leptomeningeal carcinomatosis (LC) occurs when tumor cel

49 izes molecular mechanisms that drive HER2(+) leptomeningeal carcinomatosis and demonstrates the effic

50 Although leptomeningeal carcinomatosis is a well-established clin

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

52 In models of TNBC leptomeningeal carcinomatosis, ICV dosing of hiNeuroS-TR

53 o facilitate and complement the diagnosis of leptomeningeal carcinomatosis.

54 oligodendrocyte precursor cell, and vascular leptomeningeal cell gene modules for both SSD and CHR-P

55 r study establishes a molecular map of human leptomeningeal cell types, providing significant insight

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

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

58 Indeed, when cultured, leptomeningeal cells display the signature of ex vivo AD

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

60 The exact nature of leptomeningeal cells has long been debated.

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

62 rophages, oligodendrocytes, and vascular and leptomeningeal cells, exhibit significant activation of

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

64 cing cells are identified as endothelial and leptomeningeal cells.

65 tributed primarily to brain perivascular and leptomeningeal cells.

66 Seven pathologies-leptomeningeal cerebral amyloid angiopathy, large infarc

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

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

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

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

71 infarct volume correlated with the grade of leptomeningeal collateral circulation (p=0.03) and with

72 the clot burden score to record the grade of leptomeningeal collateral circulation and the extension

73 s radiologic factors, including the grade of leptomeningeal collateral circulation, as well as the le

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

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

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

77 , 0.73 [95% CI, 0.64-0.83]), and strength of leptomeningeal collaterals (odds ratio, 2.37 [95% CI, 1.

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

79 ritical stroke outcomes due to a shutdown of leptomeningeal collaterals.

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

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

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

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

84 eir critical functions, our understanding of leptomeningeal development and maturation during human e

85 ful in identifying the molecular features of leptomeningeal development, injury, and repair that were

86 ing their coordinated roles in orchestrating leptomeningeal development.

87 rhage (38%); 3) scleral involvement (3%); 4) leptomeningeal disease (12%); 5) contrast enhancement (9

88 ations are noted, namely EGFR alterations in leptomeningeal disease (LMD) and MYC amplifications in m

89 Leptomeningeal disease (LMD) is a common complication fr

90 Leptomeningeal disease (LMD) is a devastating complicati

91 Leptomeningeal disease (LMD) is a devastating complicati

92 Leptomeningeal disease (LMD) is a subtype of central ner

93 Leptomeningeal disease (LMD) significantly affects the p

94 Leptomeningeal disease (LMD) significantly affects the p

95 ase, including parenchymal brain metastasis, leptomeningeal disease (LMD), or dural metastasis, who w

96 a critical need for effective treatments for leptomeningeal disease (LMD).

97 burtamab therapy in patients with metastatic leptomeningeal disease and compared it with the estimate

98 of overall survival, distant brain failure, leptomeningeal disease and local recurrence at 12-months

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

100 llowing for an improved therapeutic index to leptomeningeal disease and reduced systemic doses.

101 newer agents with enhanced CNS penetration, leptomeningeal disease and the need for intrathecal trea

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

103 h basilar meningitis, with or without spinal leptomeningeal disease.

104 ion cascade in the metastatic niche to treat leptomeningeal disease.

105 liver therapeutic absorbed doses to sites of leptomeningeal disease.

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

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

108 Leptomeningeal dissemination (LMD) is the primary cause

109 Leptomeningeal dissemination and less than 50% surgical

110 n of patients with metastatic cancer develop leptomeningeal dissemination of disease (LMD), and survi

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

112 iPSC-derived NES tumors develop quickly with leptomeningeal dissemination, whereas hbNES-derived cell

113 th lipopolysaccharide drives medulloblastoma leptomeningeal dissemination, whereas premedication with

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

115 single dose of radiation to the tumor drives leptomeningeal dissemination.

116 , had little or no effect on the response of leptomeningeal ECs to E. coli infection.

117 ll depletion therapies and identification of leptomeningeal ectopic lymphoid tissue (ELT) in patients

118 (n = 7, 37%) cortical T2 hyperintensity and leptomeningeal enhancement (n = 17, 89%).

119 d cortical and thalamic gray matter lesions, leptomeningeal enhancement (presence and foci number), d

120 Prominent involvement of gray matter and leptomeningeal enhancement are common in pediatric MOGAD

121 Leptomeningeal enhancement clinical correlates were anal

122 Leptomeningeal enhancement favoured MOGAD (27/59 (46%))

123 Leptomeningeal enhancement favours MOGAD over AQP4+NMOSD

124 Additionally, we demonstrated nodular leptomeningeal enhancement in 32.3% of participants, whi

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

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

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

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

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

130 Leptomeningeal enhancement may prove a useful surrogate

131 he meninges displayed focal and disseminated leptomeningeal enhancement on magnetic resonance imaging

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

133 Leptomeningeal enhancement was associated with higher le

134 The presence of leptomeningeal enhancement was highly suggestive for MOG

135 ssion of leukoencephalopathy and progressive leptomeningeal enhancement was observed in one patient e

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

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

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

139 in the acellular, protein, and cytokine-poor leptomeningeal environment remain elusive.

140 ess GMCSF-driven growth of HER2(+) LC in the leptomeningeal environment, providing a potential target

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

142 The VI functions as an extra-parenchymal leptomeningeal extension containing distinct myeloid cel

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

144 Cultured human leptomeningeal fibroblasts grafted into rat frontal cort

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

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

147 Furthermore, decorin treatment of leptomeningeal fibroblasts significantly increases their

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

149 Leptomeningeal glioneuronal heterotopias are a focal typ

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

151 ction or more than 4 microbleeds or areas of leptomeningeal hemosiderosis on magnetic resonance imagi

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

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

154 emyelinating activity in the initial stages, leptomeningeal immune cell infiltration, enriched in B c

155 These leptomeningeal infiltrates resembled tertiary lymphoid o

156 d in leukocytes traversing the ependyma from leptomeningeal infiltrates.

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

158 Leptomeningeal inflammation in multiple sclerosis is ass

159 Leptomeningeal inflammation is associated with greater e

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

161 with neurologic sequelae of COVID-19 harbor leptomeningeal inflammatory cytokines in the absence of

162 inflammation induces vasculocentric lesions, leptomeningeal involvement follows a subpial "surface-in

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

164 uating other pathological processes, such as leptomeningeal involvement, central vein and rim of lesi

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

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

167 sonance imaging, which correlated with heavy leptomeningeal lymphocytic infiltration.

168 Leptomeningeal lymphoma and intraocular lymphoma are top

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

170 th dural macrophages and MLVs had recovered, leptomeningeal macrophages and CSF drainage had not been

171 Perivascular and leptomeningeal macrophages reside near the central nervo

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

173 somes indicated a comprehensive depletion of leptomeningeal macrophages, a selective reduction in dur

174 The study suggests that leptomeningeal macrophages, distinct from the dural macr

175 ractant for monocytes, or acute depletion of leptomeningeal macrophages, following intracebroventricu

176 in, monoamine oxidase, calcifications, iron, leptomeningeal melanocytes, and microhemorrages.

177 ion characterized by the inflammation of the leptomeningeal membranes.

178 the mechanism by which cancer cells in these leptomeningeal metastases (LM) overcome these constraint

179 The cumulative incidence of brain (BrM) and leptomeningeal metastases (LM) was 39% and 2% at 1 year,

180 Leptomeningeal metastases (LMs) exhibit a high incidence

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

182 The biology of the leptomeningeal metastases and the local tumour microenvi

183 pediatric brain tumor often associated with leptomeningeal metastases and therapy resistance.

184 Leptomeningeal metastases are the major source of morbid

185 Leptomeningeal metastases are the most important source

186 r its receptor fail to control the growth of leptomeningeal metastases growth.

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

188 Presence of leptomeningeal metastases is indicative of poor prognosi

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

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

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

192 Leptomeningeal metastases were depicted in 38 cases on c

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

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

195 Radioimmunotherapy can effectively treat leptomeningeal metastases when radiolabeled antibodies a

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

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

198 eveal substantial inflammatory infiltrate in leptomeningeal metastases with enrichment of IFNgamma an

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

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

201 stoma, in particular in patients who develop leptomeningeal metastases, remains high in the absence o

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

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

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

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

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

207 sensitivity of 34% for cytologically proved leptomeningeal metastases.

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

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

210 on is both sufficient and necessary to drive leptomeningeal metastases.

211 eatment and/or prevention of medulloblastoma leptomeningeal metastases.

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

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

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

215 Breast cancer leptomeningeal metastasis (BCLM), where tumour cells gro

216 ndard-of-care radiotherapy for patients with leptomeningeal metastasis (LM) from solid tumors.

217 Leptomeningeal metastasis (LM) represents a devastating

218 Leptomeningeal metastasis (LM), or spread of cancer to t

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

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

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

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

223 Evaluation of leptomeningeal metastasis includes contrast-enhanced bra

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

225 Although treatment of leptomeningeal metastasis is palliative with median pati

226 Although treatment of leptomeningeal metastasis is palliative with median pati

227 Leptomeningeal metastasis occurs in approximately 3-5% o

228 Leptomeningeal metastasis occurs in approximately 5% of

229 Treatment of leptomeningeal metastasis often requires involved-field

230 Staging of leptomeningeal metastasis should include contrast-enhanc

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

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

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

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

235 cerebrospinal-fluid-filled leptomeninges, or leptomeningeal metastasis, represents a fatal complicati

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

237 er neurologic deterioration in patients with leptomeningeal metastasis.

238 arding methods of diagnosis and treatment of leptomeningeal metastasis.

239 ion, perivascular niche micrometastasis, and leptomeningeal metastasis.

240 upting the blood-brain barrier and promoting leptomeningeal metastasis.

241 nd patient-derived humanized mouse models of leptomeningeal metastasis.

242 F-liberating proteases that could facilitate leptomeningeal metastasis.

243 er neurologic deterioration in patients with leptomeningeal metastasis.

244 neic lung cancer, breast cancer and melanoma leptomeningeal-metastasis mouse models.

245 Leptomeningeal metastatic disease (LMD) represents a dev

246 Leptomeningeal metastatic disease (LMD), encompassing en

247 Enrolled participants who developed leptomeningeal metastatic dissemination before starting

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

249 cerebral blood flow pre-surgery, PcomA size, leptomeningeal microcollateral length and junction densi

250 lore ligand-receptor interactions within the leptomeningeal niche and computationally infer intercell

251 th additional reporter alleles for vascular, leptomeningeal or myeloid cells ensures precise localiza

252 Leptomeningeal overexpression of Ifng through a targeted

253 , we found various combinations of transient leptomeningeal, parenchymal and vessel wall enhancement;

254 ansfer occurring at sites of overlap between leptomeningeal perivascular (arteriovenous) spaces dispe

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

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

257 ations toward advancing the understanding of leptomeningeal physiology and pathology.

258 on in Draxin and misregulated astroglial and leptomeningeal proliferation as genetic and cellular fac

259 pression in primary tumors was predictive of leptomeningeal relapse.

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

261 and joint analyses with mouse and aged human leptomeningeal single-cell RNA sequencing (scRNA-seq) da

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

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

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

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

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

267 roved necessary for cancer growth within the leptomeningeal space.

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

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

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

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

272 erapy for tumor regression and prevention of leptomeningeal spread in xenograft mouse models of medul

273 liminary results, such as for meningioma and leptomeningeal spread of certain pediatric brain tumors.

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

275 lide acted on MYC to reduce tumor growth and leptomeningeal spread, which resulted in improved surviv

276 he first mouse medulloblastoma model to show leptomeningeal spread.

277 oblastoma, which show greater propensity for leptomeningeal spread.

278 , including parenchymal microhemorrhages and leptomeningeal superficial siderosis, were termed ARIA-H

279 ite of transgenic hosts, we demonstrate that leptomeningeal T cells generate IFNgamma to actively rec

280 apid/severe disease progression; presence of leptomeningeal tertiary lymphoid-like structures; large

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

282 e conducted single-nucleus RNA sequencing on leptomeningeal tissues from eight human embryos, capturi

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

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

285 yloid angiopathy-related vascular damage) in leptomeningeal vessels (P < 0.0001), but reduced cerebra

286 advanced cerebral amyloid angiopathy of the leptomeningeal vessels and may trigger secondary ischaem

287 rebral cortex, pia mater, and pia-ensheathed leptomeningeal vessels in two GBCA-exposed human brains

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

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

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

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

292 chronic bleeding events originating from the leptomeningeal vessels.

293 onic manifestation of bleeding episodes from leptomeningeal vessels.

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