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 ar afferents and evokes a series of cortical meningeal and brainstem events consistent with the devel

4 m, which is followed by a series of cortical meningeal and brainstem events that cause the migraine h

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

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

7 perivascular macrophages and populations of meningeal and choroid plexus macrophages in normal brain

8 In contrast, expression of meningeal and choroid plexus-associated P selectin was u

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

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

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

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

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

14 the CNS revealed a selective distribution of meningeal and parenchymal inflammatory lesions in the sp

15 metabotropic glutamate receptors (mGluRs) in meningeal and parenchymal microvasculature and in choroi

16 ion of TGF-beta1 in the brain increases both meningeal and parenchymal T lymphocyte number.

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

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

19 C3a/GFAP mice had massive meningeal and perivascular infiltration of macrophages a

20 eceptor pathway influences susceptibility to meningeal and pulmonary TB by different immune mechanism

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

22 may be superior in demonstrating perineural, meningeal, and skull base invasion.

23 lated leukocyte infiltrates in perivascular, meningeal, and ventricular regions of the brain that wer

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

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

26 some parenchymal invasion and abscesses, and meningeal arteritis.

27 tories: one that runs parallel to the middle meningeal artery (MMA), and another with a more or less

28 of the thinned cranium overlying the middle meningeal artery (MMA).

29 ow enhancement selectively within the middle meningeal artery dependent upon trigeminal and parasympa

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

31 The parietal dura above the middle meningeal artery was stimulated through a closed cranial

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

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

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

35 ssion, GCPs lose contact with laminin in the meningeal basement membrane, cease proliferating, and di

36 and TTR amyloid deposition was confirmed by meningeal biopsy.

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

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

39 lection for binding to the leptomeninges and meningeal blood vessels in human brain and not to the ce

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

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

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

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

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

45 Meningeal carcinomatosis (MC) is a rare complication ass

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

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

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

49 When meningeal cells are added to purified OECs there is a si

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

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

52 ain, hippocampal and neocortical neurons and meningeal cells had lysosomal storage.

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

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

55 Meningeal cells migrate into the lesion site after under

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

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

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

59 lso did not require adherence of bacteria to meningeal cells, but LPS was implicated.

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

61 Furthermore, the number of proliferating meningeal cells, which have been shown to be important f

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

63 and were distinct from other fibroblasts and meningeal cells.

64 sinusoidal lining of the spleen, neurons and meningeal cells.

65 following transplantation is the presence of meningeal cells.

66 al concentrations of LPS onto the surface of meningeal cells.

67 een the epithelial and mesenchymal states of meningeal cells.

68 ronal excitation modulates both the pial and meningeal circulation through a critical interaction wit

69 50% in resolved, and 83% in disseminated and meningeal coccidioidomycosis.

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

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

72 layer of neural crest cells that forms their meningeal covering.

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

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

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

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

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

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

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

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

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

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

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

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

85 ith Foxc1 mutations have cellular defects in meningeal development.

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

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

88 CNS disease included meningeal disease or CNS parenchymal masses with or with

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

90 formed in 62 patients (21 with proved SAS or meningeal disease) and 41 control patients.

91 detecting superficial abnormalities, such as meningeal disease, because they do not demonstrate contr

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

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

94 oconidia produced a chronic illness in which meningeal endarteritis obliterans was consistently obser

95 Magnetic resonance imaging (MRI) showed meningeal enhancement and single-photon emission compute

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

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

98 Cortical lesions, meningeal enhancement, and periventricular white-matter

99 Patients with meningeal enhancement, compared with patients without en

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

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

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

103 oneal disease, 2 pleural disease, and 1 each meningeal, enteric, paravertebral, bone, genital, and bl

104 Pharmacological blockade of meningeal ERK phosphorylation inhibited the development

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

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

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

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

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

110 This astroglial-meningeal fibroblast scar is fully developed by day 14 w

111 Activated meningeal fibroblastic stromal cells have the capacity t

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

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

114 amina; however, endoneurial, epineurial, and meningeal fibroblasts did not.

115 Unexpectedly, fak deletion specifically from meningeal fibroblasts elicited similar cortical ectopias

116 rganization of fibrillar laminin by isolated meningeal fibroblasts from double knockouts suggests tha

117 pment of the glial scar and the exclusion of meningeal fibroblasts from the injured spinal cord.

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

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

120 beta immunoreactivities through a network of meningeal fibroblasts in the three layers of meninges, p

121 phrin-B2 on reactive astrocytes and EphB2 on meningeal fibroblasts is an early event in the cellular

122 ith derivation from brain fibroblasts (e.g., meningeal fibroblasts).

123 2 and EphB2, are expressed by astrocytes and meningeal fibroblasts, respectively, in the adult spinal

124 B2-expressing astrocytes from EphB2-positive meningeal fibroblasts.

125 reactivity also was intense in the nuclei of meningeal fibroblasts.

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

127 Foxc1 mutant mice with defects in forebrain meningeal formation.

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

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

130 have shown variable efficacy in reducing the meningeal hypertrophy.

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

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

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

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

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

136 vasion-associated gene (iagA) contributes to meningeal infection and virulence by facilitating invasi

137 kpoints for some cephalosporins: one set for meningeal infection isolates and a new set for nonmening

138 analysis demonstrated a marked reduction in meningeal infiltrates at the same time point.

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

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

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

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

143 significantly less spinal cord pathology and meningeal inflammation and in reduced Th1 cellular respo

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

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

146 Meningeal inflammation correlated significantly with sma

147 GTN infusion (30 min) on the development of meningeal inflammation in a rat model using doses releva

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

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

150 Meningeal inflammation in the form of ectopic lymphoid-l

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

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

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

154 This observation may explain the vascular meningeal inflammation that developed in Alzheimer's dis

155 Meningeal inflammation was topographically associated wi

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

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

158 kocytosis, high protein accumulation, severe meningeal inflammation, persistent bacillary load, and p

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

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

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

162 sociation between cortical demyelination and meningeal inflammation.

163 , inflammatory, and strongly associated with meningeal inflammation.

164 ukocytosis, protein accumulation, and severe meningeal inflammation.

165 ivascular T2 lesions and signs suggestive of meningeal inflammation.

166 ine action, gammaHV68 induced a neutrophilic meningeal inflammatory infiltrate, while gammaHV68-M3.st

167 tracing from Sp5C areas that receive direct meningeal inputs.

168 t vimentin-ir through serial sections of the meningeal-intact adult rat brain revealed this network.

169 pping of Cx26 through serial sections of the meningeal-intact rat brain with four antibodies revealed

170 rcent of animals (n = 14) developed signs of meningeal irritation leading to death 30 to 63 days post

171 in Fos protein expression after generalised meningeal irritation.

172 A signal was also detected in the meningeal layers of the brain.

173 ive puncta was observed throughout the three meningeal layers, the perineurium of cranial nerves, and

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

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

176 breast, and one subcutaneous) or symptomatic meningeal leukemia (n = 1).

177 The infiltrating meningeal leukemia closely resembled the pathologic pres

178 An experimental animal model of meningeal leukemia was developed in the nude rat, rnu/rn

179 ma, subcutaneous nodules, leukemia cutis, or meningeal leukemia) at initial presentation.

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

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

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

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

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

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

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

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

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

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

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

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

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 In primates, meningeal lymphatics display a typical panel of lymphati

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

196 ctive inflammation, often granulomatous, and meningeal lymphocytosis.

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

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

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

200 y, circulating immune stimuli might activate meningeal macrophages and perivascular microglia along t

201 ascular microglia along blood vessels and in meningeal macrophages at the edge of the brain.

202 ings suggest that perivascular microglia and meningeal macrophages throughout the brain may be the ce

203 crovasculature or perivascular microglia and meningeal macrophages, and (2) direct transmission to th

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

205 tivity was expressed chiefly within resident meningeal macrophages.

206 in children >/= 3 years of age with advanced meningeal malignancies.

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

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

209 a, mGluR5, and mGluR7 were also expressed in meningeal microvasculature.

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

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

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

213 attenuated the proinflammatory character of meningeal myeloid cells.

214 = 358) who had either pulmonary (n = 183) or meningeal (n = 175) TB.

215 Meningeal nerves that infiltrate the periosteum through

216 bryos to retinoic acid at E10.0 reduces this meningeal neural crest and inhibits parietal ossificatio

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

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

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

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

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

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

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

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

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

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

227 ing pathway accounting for the activation of meningeal nociceptors by different migraine triggers?

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

229 ased from peripheral endings of perivascular meningeal nociceptors primary and to promote vasodilatat

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

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

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

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

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

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

236 n resulted in activation or sensitization of meningeal nociceptors.

237 ease of inflammatory molecules that activate meningeal nociceptors.

238 ation promote activation or sensitization of meningeal nociceptors.

239 are not sufficient to activate or sensitize meningeal nociceptors.

240 ization triggered by chemical stimulation of meningeal nociceptors.

241 siological correlate of migraine headache in meningeal nociceptors.

242 6 patients, the largest number to date, with meningeal or parenchymal CNS-HL confirmed by histopathol

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

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

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

246 the initial response of the BBB to the human meningeal pathogen group B Streptococcus (GBS) and the o

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

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

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

250 re no infectious complications caused by the meningeal pathogens.

251 chanism of BBB disruption and penetration by meningeal pathogens.

252 tial for additional protection against other meningeal pathogens.

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

254 of migraine involves not only irritation of meningeal perivascular pain fibers but also a transient

255 munoreactivity at the surface of the cortex (meningeal, pial layer, vasculature) and around the ventr

256 yers, the perineurium of cranial nerves, and meningeal projections into the brain, including sheaths

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

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

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

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

261 Isolated meningeal relapse in children with acute lymphoblastic l

262 mediating cortical development downstream of meningeal retinoic acid signaling.

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

264 dura mater, arachnoid, and pia mater of the meningeal sheath surrounding the optic nerve.

265 ly identified mast cells were present in the meningeal sheaths surrounding the cln3-/- nerve and in t

266 .5%), peripheral facial palsy (PFP) (36.4%), meningeal signs (19.5%), and pareses (7.8%).

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

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

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

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

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

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

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

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

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

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

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

278 eeks also had decreased neuronal, glial, and meningeal storage and averaged 2.5% of wild-type hGUS ac

279 eekly over 3 weeks had moderate reduction in meningeal storage but no change in neo-cortical neurons.

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

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

282 tertiary lymph follicles, along the cortical meningeal surface.

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

284 e strongly associated with susceptibility to meningeal TB (OR, 3.02; P < .001) than to pulmonary TB (

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

286 nd (ii) that its secretion from non-neuronal meningeal tissue is important for controlling the migrat

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

288 uberculosis and possibly against miliary and meningeal tuberculosis.

289 nary tuberculosis and 6 reporting miliary or meningeal tuberculosis.

290 ain reaction in a larger, independent set of meningeal tumors (n = 47).

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

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

293 ood flow (DBF), we examined whether CGRP and meningeal vasodilatation promote activation or sensitiza

294 uggests that peripheral CGRP and its related meningeal vasodilatation results in activation and sensi

295 that CGRP effects in the meninges, including meningeal vasodilatation, are not sufficient to activate

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

297 ected by immunocytochemistry in the walls of meningeal vessels and cells of the cerebrospinal fluid (

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

299 tomy (such as those of the frontal sinus and meningeal vessels) and neurophysiology (he was the first

300 atient with TBI showed amyloid angiopathy in meningeal vessels.