ライフサイエンスコーパス: meningeal

1 lymphatic (28%), disseminated (23%), and CNS/meningeal (22%) disease.

2 tigen-experienced B cell clones derived from meningeal aggregates were also present in the parenchyma

3 e purification of Abeta amyloid fibrils from meningeal Alzheimer's brain tissue and their structural

4 ion established a close relationship between meningeal and choroid plexus DCs (m/chDCs) and spleen DC

5 Perivascular, subdural meningeal and choroid plexus macrophages are non-parench

6 Notably, although both meningeal and dermal vessels were affected, intracerebra

7 low CD4 counts were more likely to have CNS/meningeal and disseminated disease.

8 Patients with central nervous system (CNS)/meningeal and disseminated EPTB and those with human imm

9 of AR-42 on cell-cycle progression of normal meningeal and meningioma cells may have implications for

10 Protection against meningeal and miliary tuberculosis was also high in infa

11 conducted for CrAg+ patients to distinguish meningeal and nonmeningeal cryptococcosis and to identif

12 lyses indicated that CD4 T cells entered the meningeal and perivascular areas of VIP-deficient mice,

13 sclerosis were examined for the presence of meningeal and perivascular immune cell infiltrates in ti

14 ore likely to have severe forms of EPTB (CNS/meningeal and/or disseminated) (AOR 1.6; 95% CI, 1.0, 2.

15 es of B cells in blood, cerebrospinal fluid, meningeal, and brain tissues of MS patients (n = 10).

16 nation revealed a common pattern associating meningeal arterial calcifications, necrotic and calcifie

17 rterial supply of the AVM, particularly from meningeal arteries, en-passant arteries or perforating f

18 al-regulated kinase (ERK) phosphorylation in meningeal arteries.

19 the A11 significantly inhibited peri-middle meningeal artery dural and noxious pinch evoked firing o

20 ature along the dural sinuses and the middle meningeal artery.

21 e characterized the repertoires derived from meningeal B cell aggregates and the corresponding parenc

22 Neutrophils preceded the accumulation of meningeal B cell clusters, and inhibition of CXCR2-media

23 us system (CNS) inflammation, elimination of meningeal B cells, and reduction of MOG-specific Th1 and

24 ta1-deficient RGCs processes detach from the meningeal basement membrane (BM) followed by apoptotic d

25 e imaging, cerebrospinal fluid analysis, and meningeal biopsy.

26 transmission in dorsal horn neurons, reduced meningeal blood flow, reduced nocifensive behavior induc

27 ous spread of virus-infected leukocytes from meningeal blood vessels into the subarachnoid space.

28 nfected central nervous system as well as in meningeal blood vessels.

29 These results suggest that Acvr1-mediated meningeal Bmp signaling regulates Lef1 expression in the

30 nt or with selective conditional deletion of meningeal Bmp7 also have dentate developmental defects.

31 in pial basement membrane disrupt the neural-meningeal boundary, resulting in ectopia of meningeal fi

32 Meningeal carcinomatosis (MC) is a rare complication ass

33 acute brain injury induces vascular damage, meningeal cell death, and the generation of reactive oxy

34 These data characterize ILC2s as a novel meningeal cell type that responds to SCI and could lead

35 in A are restricted to endothelial cells and meningeal cells and are absent in neurons and glia.

36 d proliferation of both Ben-Men-1 and normal meningeal cells by increasing expression of p16(INK4A),

37 type, possibly representing radial glia-like meningeal cells differentiating to neuronal cells.

38 c1 protein expression in all three layers of meningeal cells in Foxc1(hith/hith) mice contributes to

39 tor of this mechanism, and its expression in meningeal cells is regulated by integrated upstream sign

40 Meningeal cells migrate into the lesion site after under

41 cellular matrix is thought to originate from meningeal cells surrounding the CNS.

42 A, and proliferating cell nuclear antigen in meningeal cells while significantly reducing the express

43 Single-cell RNA sequencing identified meningeal cells with distinct transcriptome signatures c

44 roglia, macrophages and other myeloid cells, meningeal cells, proliferating oligodendrocyte precursor

45 een the epithelial and mesenchymal states of meningeal cells.

46 reas it induced cell-cycle arrest at G(1) in meningeal cells.

47 Acute responses to meningeal CGRP are female-specific and sensitization to

48 50% in resolved, and 83% in disseminated and meningeal coccidioidomycosis.

49 une surveillance that takes place within the meningeal compartment, the mechanisms governing the entr

50 ects, TUS also induced signal changes in the meningeal compartment.

51 of para-arterial, parasinus, and paravenous meningeal contrast enrichment using high-resolution 3D i

52 B disruption, while paravenous and parasinus meningeal contrast enrichment was evident in both groups

53 We identified LLC in meningeal, cortical and neurogenic brain regions.

54 The central nervous system (CNS) and its meningeal coverings accommodate a diverse myeloid compar

55 ervous system tumors that originate from the meningeal coverings of the brain and spinal cord.

56 howing that Cxcl12 ablation in IPCs, leaving meningeal Cxcl12 intact, attenuates intracortical TCA gr

57 ur study raises the possibility that primary meningeal defects may cortical dysplasia in some cases.

58 null alleles of Foxc1 to study the effect of meningeal defects on neocortical organization.

59 terotopia formation, neuronal overmigration, meningeal defects, and changes in basement membrane comp

60 These results establish RA as a potent, meningeal-derived cue required for successful corticogen

61 a congenital lesion developed as a result of meningeal development abnormalities or a lesion acquired

62 topia formation, neuronal overmigration, and meningeal development appeared earlier in gestation and

63 ilized Foxc1-mutant mice in which defects in meningeal development lead to alterations in cortical de

64 tive loss of Bmp expression due to defective meningeal development or with selective conditional dele

65 evelopment in the face of severe deficits in meningeal development.

66 ith Foxc1 mutations have cellular defects in meningeal development.

67 hermore, we provide evidence that defects in meningeal differentiation can lead to severe cortical dy

68 Systemic (extra-CNS) and/or meningeal disease did not affect outcome.

69 s to the Group for Enteric, Respiratory, and Meningeal Disease Surveillance in South Africa (GERMS-SA

70 Functionally, AKAP12 modulates meningeal EMT by regulating the TGF-beta1-non-Smad-SNAI1

71 However, the molecular mechanisms of meningeal EMT remain largely undefined.

72 ancement, paraspinal and epidural abscesses, meningeal enhancement at the affected spine level.

73 CNSV who presented with prominent gadolinium meningeal enhancement on magnetic resonance imaging (MRI

74 Patients with meningeal enhancement, compared with patients without en

75 In cases of nerve-root or meningeal enhancement, Lyme disease should be considered

76 edema, and three demonstrated nerve-root or meningeal enhancement.

77 ponse to therapy, with resolution of the MRI meningeal enhancement.

78 Pharmacological blockade of meningeal ERK phosphorylation inhibited the development

79 ist muscimol into PVN inhibit both basal and meningeal-evoked activities of Sp5C neurons.

80 t gabazine infusions into the PVN facilitate meningeal-evoked responses of Sp5C neurons.

81 Ins and S1 cortices, enhancing or inhibiting meningeal-evoked responses of Sp5C, without affecting cu

82 nd S1 induced facilitation and inhibition of meningeal-evoked responses, respectively.

83 confined to the PVN depresses both basal and meningeal-evoked Sp5C activities.

84 Activated meningeal fibroblastic stromal cells have the capacity t

85 t (DKO) mice display disorganized laminin in meningeal fibroblasts and a cobblestone lissencephaly-li

86 We find that embryonic meningeal fibroblasts are transcriptionally distinct bet

87 aphorins that are expressed by GFAP-negative meningeal fibroblasts at the injury site, we analyzed mi

88 s, providing molecular profiles of embryonic meningeal fibroblasts by layer and yielding insights int

89 view the critical immune-stimulating role of meningeal fibroblasts in promoting recruitment and reten

90 -meningeal boundary, resulting in ectopia of meningeal fibroblasts in the cerebral cortex and reactiv

91 Meningeal fibroblasts secrete a variety of factors that

92 udies have generated an unparalleled view of meningeal fibroblasts, providing molecular profiles of e

93 Spontaneous opticospinal EAE and meningeal follicle-like structures were observed in IgH(

94 Foxc1 mutant mice with defects in forebrain meningeal formation.

95 Meningeal gammadelta T cells express high levels of the

96 r findings suggest that IL-17a production by meningeal gammadelta17 T cells represents an evolutionar

97 a cellular and molecular characterization of meningeal gammadelta17 T cells, we defined the nearest c

98 to enlarge in the presence of post-traumatic meningeal hemorrhages or deformities of the vertebral ca

99 he subarachnoid space with or without brain/ meningeal herniation on magnetic resonance [MR] cisterno

100 but have not included a detailed analysis of meningeal humoral immunity.

101 have shown variable efficacy in reducing the meningeal hypertrophy.

102 LR2A mutant tumors show dysregulation of key meningeal identity genes, including WNT6 and ZIC1/ZIC4.

103 ollowing intravenous challenge, showing that meningeal IgA is essential for defending the central ner

104 B cell receptor sequencing confirmed that meningeal IgA(+) cells originated in the intestine.

105 is and an impact of the intestinal flora and meningeal IL-17(+) gammadelta T cells on ischemic injury

106 After spinal cord injury (SCI), meningeal ILC2s are activated in an IL-33-dependent mann

107 rogressive multiple sclerosis with extensive meningeal immune cell infiltration exhibited a more seve

108 A variable extent of meningeal immune cell infiltration was detected and more

109 uid process mobilizes CNS-derived Ags toward meningeal immune cells and subsequently the peripheral i

110 Meningeal immunity along with its associated lymphatic v

111 ew the current state of our understanding of meningeal immunity and its effects on healthy and diseas

112 Meningeal immunity has recently come under the spotlight

113 Convention may imply that meningeal immunity is an ominous threat to brain functio

114 This review addresses meningeal immunity, a less-studied aspect of neuroimmune

115 These constitute meningeal immunity, which is primarily concerned with im

116 Our findings suggest that meningeal infiltrates may play a contributory role in th

117 d acute neuropathological changes, including meningeal infiltrates, encephalitis, particularly of the

118 ulated clinical and pathological features of meningeal infiltration seen in patients with ALL.

119 utant bacteria also induced markedly reduced meningeal inflammation and brain pathology compared with

120 Our findings are reminiscent of CSD-induced meningeal inflammation and provide the first imaging evi

121 Our data suggest that generalized diffuse meningeal inflammation and the associated inflammatory m

122 meninges and acted as chief coordinators of meningeal inflammation by inducing the expression of pro

123 Meningeal inflammation correlated significantly with sma

124 eatures are reproduced in a model of chronic meningeal inflammation generated by the injection of len

125 o investigate the extent of perivascular and meningeal inflammation in primary progressive multiple s

126 es in multiple sclerosis have suggested that meningeal inflammation in the brain may be linked to dis

127 Meningeal inflammation in the form of ectopic lymphoid-l

128 outside the brain parenchyma, in particular meningeal inflammation or through cerebrospinal fluid me

129 ronal survival and recovery, but the role of meningeal inflammation remains poorly understood.

130 ccompanying quantitative increase in diffuse meningeal inflammation that correlated with the degree o

131 Meningeal inflammation was topographically associated wi

132 y, inflammatory infiltrates, the presence of meningeal inflammation, and a topographic association be

133 ing of infection, a lower risk of associated meningeal inflammation, and reduced bacterial densities

134 d to determine their relationship to diffuse meningeal inflammation, white matter perivascular infilt

135 ical demyelination, gray matter atrophy, and meningeal inflammation.

136 ivascular T2 lesions and signs suggestive of meningeal inflammation.

137 nd in cases exhibiting an increased level of meningeal inflammation.

138 sociation between cortical demyelination and meningeal inflammation.

139 , inflammatory, and strongly associated with meningeal inflammation.

140 neurons in upper-cortical layers underlying meningeal inflammation; such MS neuron populations exhib

141 ates the trigeminovascular system, evoking a meningeal inflammatory response.

142 and sensitisation of trigeminal afferents by meningeal inflammatory stimuli and upstream role of inte

143 tracing from Sp5C areas that receive direct meningeal inputs.

144 eningiomas (MNs), arising from the arachnoid/meningeal layer, are nonresponsive to chemotherapies, wi

145 We define new markers for meningeal layers and show conservation in human meninges

146 d to be worse with parenchymal compared with meningeal lesions or hydrocephalus.

147 Despite a higher antigen titer with meningeal lesions, outcomes tended to be worse with pare

148 s the often tight investment of axons by the meningeal-like cells, with an intercalated basement memb

149 rstudied but important factor is the role of meningeal-located immune cells in modulating brain patho

150 Therefore, vertebral LVs add to skull meningeal LVs as gatekeepers of CNS immunity and may be

151 We show here that meningeal LVs develop postnatally, appearing first aroun

152 The plasticity and regenerative potential of meningeal LVs should allow manipulation of cerebrospinal

153 AV8-VEGF-C injection significantly increased meningeal lymphangiogenesis (P = .035) and tracer dye up

154 Manipulation of meningeal lymphangiogenesis could be a new therapeutic s

155 rtex underlying the electrodes and extensive meningeal lymphangiogenesis in the surrounding dura.

156 Meningeal lymphangiogenesis was also evident in mice pre

157 nial implants, which include glial scarring, meningeal lymphangiogenesis, and increased glymphatic ac

158 plantation of extradural electrodes provokes meningeal lymphangiogenesis, enhanced glymphatic influx

159 Conversely, an excess of VEGF-C induced meningeal lymphangiogenesis.

160 gna of HE rats 1 day after surgery to induce meningeal lymphangiogenesis.

161 ter headache patients, suggesting that these meningeal lymphatic channels were universal anatomical s

162 rtant new model for experimental analysis of meningeal lymphatic development and opens up new avenues

163 Promoting meningeal lymphatic drainage and enhancing waste clearan

164 We tested our hypothesis that enhancement of meningeal lymphatic drainage could decrease neuroinflamm

165 Finally, we report that rejuvenation of meningeal lymphatic drainage function in aged mice can a

166 rms of brain trauma cause severe deficits in meningeal lymphatic drainage that begin within hours and

167 hts into both the causes and consequences of meningeal lymphatic dysfunction in TBI and suggest that

168 nstrate that increased ICP can contribute to meningeal lymphatic dysfunction.

169 Recent studies of brain meningeal lymphatic endothelial cells in mouse and zebra

170 lopment and opens up new avenues for probing meningeal lymphatic function in health and disease.

171 ng animals, we show that zebrafish possess a meningeal lymphatic network comparable to that found in

172 However, the characterization of the meningeal lymphatic network has shed light on previously

173 e clearly delineated with the discovery of a meningeal lymphatic system capable of carrying fluid, im

174 Very little is known about the role of the meningeal lymphatic system in HE.

175 and suggest that therapeutics targeting the meningeal lymphatic system may offer strategies to treat

176 side dural venous sinuses, recapitulates the meningeal lymphatic system of rodents.

177 ervous system, and the recent studies on the meningeal lymphatic system represent an emblematic examp

178 gs and recent studies revealing a functional meningeal lymphatic system that drains cerebrospinal flu

179 ding of the development and structure of the meningeal lymphatic system, the contribution of this net

180 which cerebrospinal fluid drains through the meningeal lymphatic system.

181 e, sympathetic, parasympathetic, sensory and meningeal lymphatic systems.

182 However, the exact localization of the meningeal lymphatic vasculature and the path of drainage

183 ouse model of glioblastoma, we show that the meningeal lymphatic vasculature can be manipulated to mo

184 published a pioneering paper showing how the meningeal lymphatic vasculature can be manipulated with

185 ociation between glymphatic activity and the meningeal lymphatic vasculature.

186 The recent discovery of meningeal lymphatic vessels (LVs) has raised interest in

187 Recent work has shown that meningeal lymphatic vessels (mLVs), mainly in the dorsal

188 We also describe the recently characterized meningeal lymphatic vessels and their role in drainage o

189 e spotlight owing to the characterization of meningeal lymphatic vessels draining the CNS.

190 discoveries of the glymphatic system and of meningeal lymphatic vessels have generated a lot of exci

191 ymphatic concept along with the discovery of meningeal lymphatic vessels have, in recent years, highl

192 Here, we report the existence of meningeal lymphatic vessels in human and nonhuman primat

193 ipheral organs with the proposed function of meningeal lymphatic vessels in neurological disorders, s

194 re accumulated in the lymphatics of CLNs and meningeal lymphatics after SAH.

195 When the meningeal lymphatics are depleted in a mouse model of SA

196 However, whether meningeal lymphatics are involved in clearing extravasat

197 Recent advances in understanding the role of meningeal lymphatics as a communicator between the brain

198 uman para-arterial glymphatic transports and meningeal lymphatics by clear depiction of para-arterial

199 In primates, meningeal lymphatics display a typical panel of lymphati

200 In contrast, meningeal lymphatics do not undergo lymphangiogenesis du

201 en together, this work demonstrates that the meningeal lymphatics drain extravasated erythrocytes fro

202 scuss here, elucidates the importance of the meningeal lymphatics for the drainage of macromolecules

203 ying lymphatic development, the existence of meningeal lymphatics has not yet been reported in this s

204 Meningeal lymphatics have been reported to drain macromo

205 unications between the glymphatic system and meningeal lymphatics in CNS disorders and develop new th

206 The recent discovery of meningeal lymphatics in mammals is reshaping our underst

207 ce machine to study cerebral glymphatics and meningeal lymphatics in patients with reversible cerebra

208 ss novel strategies for targeting microglia, meningeal lymphatics, and the peripheral immune system t

209 d intracranial pressure (ICP) influences the meningeal lymphatics.

210 mmune cell trafficking and transmigration in meningeal lymphatics.

211 cerebrospinal fluid, and presence of EBV in meningeal lymphoid follicles and perivenular infiltrates

212 While the formation and persistence of meningeal lymphoid follicles suggest persistence of anti

213 High RNA levels of Pim-2 and FoxP1 in meningeal lymphoma cells were associated with disease re

214 Surprisingly, the thoracolumbal meningeal Lyve-1+ cells were predominantly round in morp

215 c choriomeningitis virus infection, resident meningeal macrophages (MMs) acquired viral antigen and i

216 Immunol., 2019) investigated meningeal macrophages (MMs) in the context of viral infe

217 A recent report shows that when murine meningeal macrophages are killed by viruses, circulating

218 macrophages (CAMs), such as perivascular and meningeal macrophages, are implicated in virtually all d

219 r macrophages, as well as choroid plexus and meningeal macrophages, dendritic cells, and granulocytes

220 roaches in mice, we identified evidence that meningeal mast cells can importantly contribute to the k

221 ling around capillaries, arteries and in the meningeal membranes.

222 the regulation of cognitive function through meningeal myeloid cell phenotype and brain-derived neuro

223 -/-) mice exhibited a skewed proinflammatory meningeal myeloid cell phenotype and cognitive deficits.

224 tion of T cells from meningeal spaces skewed meningeal myeloid cells toward a proinflammatory phenoty

225 attenuated the proinflammatory character of meningeal myeloid cells.

226 Meningeal nerves that infiltrate the periosteum through

227 ndent inflammatory response characterized by meningeal neutrophil swarming and microglial reconstitut

228 by inflammatory monocytes that engrafted the meningeal niche and remained in situ for months after vi

229 G4-positive plasma cells within inflammatory meningeal niches strongly suggests a specific response a

230 orticofugal networks that directly influence meningeal nociception in the brainstem trigeminocervical

231 cortical areas to test the effects of CSD on meningeal nociception.

232 se trials, CSD induced a twofold increase in meningeal nociceptor firing rate that persisted for 37.0

233 NTG-evoked delayed meningeal nociceptor sensitization was associated with a

234 ibited the development of NTG-evoked delayed meningeal nociceptor sensitization.

235 teum through suture branches of intracranial meningeal nociceptors and/or somatic branches of the occ

236 These findings identify Adelta meningeal nociceptors as a likely site of action of frem

237 vent the activation of Adelta but not C-type meningeal nociceptors by CSD.

238 entral neurons) depends on activation of the meningeal nociceptors from their receptors in the dura.

239 es in the activity and mechanosensitivity of meningeal nociceptors in response to administration of t

240 ivation of mechanosensitive primary afferent meningeal nociceptors that innervate the cranial dura, u

241 occipital headache may involve activation of meningeal nociceptors that innervate the posterior 1/3 o

242 a, we sought to map the origin and course of meningeal nociceptors that innervate the posterior dura

243 ular signaling in mediating the responses of meningeal nociceptors to NO.

244 , pin prick, or KCl; single-unit activity of meningeal nociceptors was monitored in vivo in the rat b

245 e phase of migraine depends on activation of meningeal nociceptors, and that for selected patients, a

246 robust increase in the mechanosensitivity of meningeal nociceptors, with a time course resembling the

247 f CSD can trigger long-lasting activation of meningeal nociceptors--the first-order neurons of the tr

248 siological correlate of migraine headache in meningeal nociceptors.

249 ese headaches are initiated by activation of meningeal nociceptors.

250 6 patients, the largest number to date, with meningeal or parenchymal CNS-HL confirmed by histopathol

251 ibrils of collagen in copepods conforms to a meningeal organization.

252 Ins and S1 selectively affect interoceptive (meningeal) over exteroceptive (cutaneous) nociceptive in

253 By using mice either with meningeal overgrowth or selective loss of meninges, we h

254 GBS from a commensal organism to a virulent meningeal pathogen.

255 mine the distribution of serotypes/groups of meningeal pathogens across Nigeria and help inform and s

256 K, Medical Research Council: Respiratory and Meningeal Pathogens Research Unit.

257 ndothelial cells (hBMECs) with GBS and other meningeal pathogens results in the induction of host tra

258 chanism of BBB disruption and penetration by meningeal pathogens.

259 tial for additional protection against other meningeal pathogens.

260 nd spread in a limited fashion, close to the meningeal penetration site.

261 acrophage subtypes include border-associated meningeal, perivascular and choroid plexus macrophages.

262 Specific depletion of meningeal plasma cells or IgA deficiency resulted in red

263 a (LTalphabeta) on Th17 cells and LTbetaR on meningeal radio-resistant cells were necessary for the p

264 change in AKAP12 expression, causing prompt meningeal reconstruction after CNS injury by regulating

265 on, could constitute the mechanism for rapid meningeal reconstruction.

266 it fails to completely eliminate the risk of meningeal recurrence, likely due to minimal CNS penetrat

267 mediating cortical development downstream of meningeal retinoic acid signaling.

268 CGRP-mAb fremanezumab (TEV-48125) modulates meningeal sensory pathways.

269 .5%), peripheral facial palsy (PFP) (36.4%), meningeal signs (19.5%), and pareses (7.8%).

270 radicular pain and more often presented with meningeal signs but less frequently complained of malais

271 For 2 cases, fever and meningeal signs were absent at presentation.

272 Severe headache, altered mental status, meningeal signs, and other neurological signs at present

273 The meningeal space is occupied by a diverse repertoire of i

274 ion of wild-type lung-derived ILC2s into the meningeal space of IL-33R(-/-) animals partially improve

275 NS; microglia), as well as around it (in the meningeal spaces and choroid plexus) has been shown to b

276 perivascular macrophages and microglia, the meningeal spaces are supplied with a diverse immune repe

277 The algorithm unfolded the meningeal spaces into four images per patient.

278 Curved MIPs of the meningeal spaces may shorten detection time for epidural

279 Depletion of T cells from meningeal spaces skewed meningeal myeloid cells toward a

280 rt of learning and memory takes place in the meningeal spaces.

281 n occurring between the brain parenchyma and meningeal spaces.

282 evels in only 2 of the 12 multiple sclerosis meningeal specimens examined.

283 phalopathy, some of the 21 monkeys exhibited meningeal, subpial neocortical, and periventricular viru

284 nic zone intimately associated with the pial meningeal surface lining the outer edge of the forming d

285 tertiary lymph follicles, along the cortical meningeal surface.

286 ntial diagnosis of a patient presenting with meningeal symptoms, paraesthesia or hyperaesthesia, and

287 lammation in the pathophysiology of migraine meningeal symptoms.

288 ting to the diversity and specificity of the meningeal T cell repertoire; the routes taken by immune

289 n use, is effective against disseminated and meningeal TB in young children but is not effective agai

290 demyelination in patients who had sufficient meningeal tissue for study.

291 role of neuropeptides and their release from meningeal trigeminal nerve endings in the mechanism of m

292 CG efficacy against pulmonary and miliary or meningeal tuberculosis by conducting a systematic review

293 uberculosis and possibly against miliary and meningeal tuberculosis.

294 nary tuberculosis and 6 reporting miliary or meningeal tuberculosis.

295 ere used to investigate the possible role of meningeal vascular signaling in mediating the responses

296 an important, yet unappreciated, role of the meningeal vasculature in the genesis of migraine pain.

297 spinal fluid antigen titers were higher with meningeal versus parenchymal lesions, and hydrocephalus

298 hough different immune cells traffic through meningeal vessels en route to the brain, mature mast cel

299 s in vascular barrier function in dermal and meningeal vessels were measured in real time in mouse mo

300 atient with TBI showed amyloid angiopathy in meningeal vessels.