ライフサイエンスコーパス: meninges

1 entral-to-dorsal maturation of telencephalic meninges.

2 ogous in many respects to that of vertebrate meninges.

3 f a soluble GDF5 inhibitor, Dan, made by the meninges.

4 r Pcdh8, Pcdh18, and Pcdh19 are found in the meninges.

5 directed to the neural tissue instead of the meninges.

6 lation activity in neural tissue but not the meninges.

7 ccumulation of IL-4-producing T cells in the meninges.

8 activation of nociceptors that innervate the meninges.

9 sia can be caused by cellular defects in the meninges.

10 s is also induced by surgical removal of the meninges.

11 ar malformations that remain adherent to the meninges.

12 rocytes, cells of the central canal, and the meninges.

13 , can diffuse into the neocortex through the meninges.

14 e on parasympathetic neurons innervating the meninges.

15 are localized primarily in the thalamus and meninges.

16 in storage in any area of the CNS except the meninges.

17 the repellent, but not the attractant in the meninges.

18 far the most common tumours arising from the meninges.

19 ingeal layers and show conservation in human meninges.

20 uclear cell infiltrates predominantly in the meninges.

21 noid space and in the arachnoid layer of the meninges.

22 located between the neuroepithelium and pia-meninges.

23 s invading the lesion site from the adjacent meninges.

24 uperficial layers of the cerebral cortex and meninges.

25 ng in the perivascular layer and through the meninges.

26 ranulomatous lesions along the ventricle and meninges.

27 rved surrounding the microinjection site and meninges.

28 elial cells of choroid plexus, ependyma, and meninges.

29 s as well as in perivascular infiltrates and meninges.

30 was restricted to the anterior pituitary and meninges.

31 rising major surface-lying blood vessels and meninges.

32 tive giant cells in the brain parenchyma and meninges.

33 with brain blood vessels and in cells in the meninges.

34 a, the external capsule, choroid plexus, and meninges.

35 ain-sensitive structures of the intracranial meninges.

36 ic and nonneoplastic disorders affecting the meninges.

37 aused by inflammation and hemorrhages in the meninges.

38 al cell proliferation and migration from the meninges.

39 yelopoiesis and egress of myeloid cells into meninges.

40 ciceptive neurons that innervate the cranial meninges.

41 e-1+ cells are also present in dura mater of meninges.

42 in white matter, periventricular zones, and meninges.

43 were able to increase CD4(+) T cells in the meninges.

44 the brain, including the choroid plexus and meninges.

45 n immune-competent stromal cell niche in the meninges.

46 lence behavior of pneumococci that reach the meninges.

47 hin, rather than simply transit through, the meninges.

48 lls do not circulate but are resident in the meninges.

49 mal transition (EMT) and repair the impaired meninges.

50 cerebral and cerebellar hemispheres and the meninges.

51 12.8 infected cells/mm(2), respectively) and meninges (133.0 versus 34.2 infected cells/mm(2), respec

52 include 20 grey matter specimens containing meninges, 26 inflammatory plaques, 19 areas of normal ap

53 on of nociceptive neurons that innervate the meninges, a process thought to be involved in the pathop

54 ts in the attachment of RGC processes at the meninges, a reduction in cortical size, and enhanced apo

55 The meninges, a triple layer of membranes-the pia mater, ara

56 In the meninges, a unique subset of tissue-resident macrophages

57 te that peripheral monocytes can engraft the meninges after an inflammatory challenge, imprinting the

58 is that a similar response develops in human meninges after GTN challenge.

59 igrate from the small intestine to brain and meninges after stroke.

60 s containing tubercle bacilli throughout the meninges, all of which were absent in wild-type mice.

61 activation of nociceptors that innervate the meninges--an event believed to set off migraine headache

62 bet-dependent NKp46(+) ILCs localized in the meninges and acted as chief coordinators of meningeal in

63 Lymphangiogenesis in the meninges and altered glymphatic fluid transport after el

64 Intracranial mast cells first appear in the meninges and are located perivascularly close to neurons

65 Herniation of meninges and atretic brain parenchyma was also seen thro

66 t multiple parts of the entire neuraxis from meninges and brain to the spinal cord and peripheral ner

67 extra-axial inflammatory signal was found in meninges and calvarial bone overlying the occipital lobe

68 be traced to the common origin of forebrain meninges and cardiac outflow tract from the TRAF7-expres

69 is causes life-threatening infections of the meninges and central nervous system, affecting more than

70 in) and intracranial structures (such as the meninges and cerebral blood vessels) suggests that senso

71 t and in provoking structural changes in the meninges and cerebral cortex of male and female mice.

72 (BAMs) residing in the dura mater, subdural meninges and choroid plexus consisted of distinct subset

73 MAC387(+) macrophages accumulated in the meninges and choroid plexus in early inflammation and in

74 ize the features of authentic DCs within the meninges and choroid plexus in healthy mouse brains.

75 Therefore, the meninges and choroid plexus of a steady-state brain cont

76 63(+)BrdU(+) macrophages were present in the meninges and choroid plexus with AIDS.

77 l these genes are highly expressed in rodent meninges and choroid plexus, anatomical regions relevant

78 Because retina lacks tissue equivalents of meninges and choroid plexus, rich sources of dendritic c

79 endymal cells, microglia, and cells from the meninges and choroid were infected.

80 phase, innate immune cells invade brain and meninges and contribute to ischemic damage, but may also

81 I showed a marked enhancement throughout her meninges and ependyma, and TTR amyloid deposition was co

82 and CD8+ T cells and CD79+ B cells) into the meninges and extensive subpial demyelination.

83 functions by stimulating astrocytes from the meninges and hippocampus.

84 beta-expressing macrophages increased in the meninges and IL-1beta-expressing microglia were induced

85 in fibroblasts in dorsal root ganglia (DRG) meninges and in the epi/perineurium of the sciatic nerve

86 erneurons in the cortex, is expressed in the meninges and IPCs.

87 c drainage from the brain to its surrounding meninges and its draining cervical lymph nodes.

88 layer VI, whereas IL-34 was expressed in the meninges and layers II-V.

89 through connective tissue of the optic nerve meninges and lining the anterior lacerated foramen.

90 Thus, the meninges and medial neocortex use a cascade of signals t

91 compare the transcriptomes of nonneoplastic meninges and meningiomas of all malignancy grades.

92 genase-2 (RALDH2) present in the surrounding meninges and mesenchyme by embryonic day 13.

93 MMP-9 was present in the meninges and neurons of the uninjured cord.

94 (Part I) is the MR appearance of the normal meninges and nonneoplastic causes of meningeal disease.

95 teristics of the typical cells of vertebrate meninges and of their peripheral nervous system (PNS) co

96 s as adult mice but are also observed in the meninges and parenchyma of the brain.

97 that included B cell infiltration within the meninges and parenchymal B cell aggregates, were examine

98 Although the trigeminal nerve innervates the meninges and participates in the genesis of migraine hea

99 found that although T cells could reach the meninges and perivascular space in the absence of TNFR1,

100 on of EAE led to inflammatory changes in the meninges and perivascular spaces of both wild-type and c

101 uman blood-borne macrophages repopulated the meninges and perivascular spaces of chimeric animals.

102 es are present, Tregs were restricted to the meninges and perivascular spaces.

103 ncreased the number of CD4(+) T cells in the meninges and production of IL-13, whereas neither Morris

104 s related to the inflammatory process in the meninges and pronounced in actively demyelinating cortic

105 erefore, the higher evolutionary rate in the meninges and temporal lobe could be due to an enhanced i

106 l-molecular-clock analysis showed that HIV-1 meninges and temporal lobe subpopulations evolve about 3

107 r primordia involved in the formation of the meninges and the bones of the skull.

108 refore, we assessed viral populations in the meninges and the brain parenchyma by laser capture micro

109 -skull cranial window avoids exposure of the meninges and the cortex, thus providing a minimally inva

110 ntalization of viral populations between the meninges and the parenchyma.

111 se of the disease, infiltrating cells in the meninges and the ventricles were found to express C5aR m

112 this network consists of fibroblasts in the meninges and the walls of large blood vessels, of pericy

113 Cx26 and vimentin immunoreactivities in the meninges and their projections into the brain.

114 of basal laminae (BL) and connective tissue (meninges and their projections) in the adult brain is un

115 , calls for a reconsideration of the role of meninges and vascular tissues, and appears to reflect th

116 8 T effector cells to exclusively target the meninges and vascular/perivascular space of the gray and

117 ciated with extracellular matrix components, meninges and vasculature due to the heparin binding prop

118 a1(+) macrophages were prominent in the pial meninges and ventricle lining, mainly at P1-P5.

119 Interestingly, POMT2 deletion in the meninges (and blood vessels) did not disrupt the develop

120 dization was observed in the choroid plexus, meninges, and also surrounding blood vessels.

121 arily expressed in the endothelial cells and meninges, and because the meninges play a critical role

122 ents, and proteomic analysis of human skull, meninges, and brain samples revealed dysregulated inflam

123 LT-1, is expressed by specific layers of the meninges, and by satellite cells in the dorsal root gang

124 g cortical neurons, astrocytes, capillaries, meninges, and cerebrospinal fluid.

125 f myeloid cells that inhabit the parenchyma, meninges, and choroid plexus and discuss their roles in

126 r organs; ependymal cells of the ventricles, meninges, and choroid plexus; and the arcuate nucleus of

127 ition of embryonic skin and bone structures, meninges, and cortex lamination in situ enables a better

128 inges, the vasculature of both the brain and meninges, and extends into the brain parenchyma.

129 antigen in the stroma of the choroid plexus, meninges, and external granular layer of the cerebellum

130 ircumventricular organs of the brain, in the meninges, and in the dorsal root ganglion.

131 the appearance of follicular B cells in the meninges, and of immunoglobulin class switching in the c

132 ells colocalized with collagen fibers in the meninges, and some of Lyve-1+ cells had intracellular co

133 The meninges are a multilayered structure composed of fibrob

134 luded that not all vascular responses in the meninges are born alike and, consequently, that drugs th

135 when nociceptive signals originating in the meninges are conveyed to the somatosensory cortex throug

136 ns as in migraine, and the brain, blood, and meninges are likely sources of headache triggers.

137 The meninges are not required for basement membrane establis

138 from arachnoidal cells associated with brain meninges, are usually benign, and are frequently associa

139 were implanted between the pia and arachnoid meninges as well as in the sciatic nerve to mimic centra

140 m and the bone, and between the bone and the meninges; as well as fibers that run inside the diploe i

141 frequently observed but were present in the meninges at 8 h, reached a maximum in the dorsal funicul

142 phoid tissue containing B cells forms in the meninges at late stages of human multiple sclerosis (MS)

143 CSF entered initial lymphatics in the meninges at the skull base and continued through extracr

144 Third, cells of the meninges became activated at 2 hr and persisted until 12

145 lso considered drug penetration indices into meninges, bone, and peritoneum.

146 eveal networks of microvessels linking brain-meninges-bone marrow.

147 CXCL12 is expressed by the meninges bordering the optic pathway, and CXCR4 by both

148 rain, cells cultured from P1 mouse cortex or meninges, bovine aortic endothelial cells and human umbi

149 re isolated from representative areas of the meninges, brain parenchyma, terminal plasma, and cerebro

150 otype (83 patients; 81%) was inflammation of meninges, brain, spinal cord, or all 3 (meningoencephalo

151 ek for 13 weeks showed clearance not only in meninges but also in parietal neocortical and hippocampa

152 is not distributed uniformly throughout the meninges but is restricted to territories over the devel

153 sitively with mast cell degranulation in the meninges but not in the thalamus.

154 eability of vessels to serum proteins in the meninges, but no increase in vascular permeability was o

155 ospinal fluid barrier and of the spinal cord meninges, but not by the endothelium of the blood-spinal

156 Necrotic injury in the meninges, but not the brain parenchyma, recruited GFP+ c

157 obulins have been speculated to occur in the meninges, but the exact cellular composition and underly

158 loping brain and in the developing and adult meninges, but there is no clear evidence for the presenc

159 observed the dynamics of immune cells in the meninges by two-photon microscopy.

160 at muscimol administered through the cranial meninges can prevent focal neocortical seizures.

161 here that application of CGRP to the cranial meninges causes behavioral responses consistent with hea

162 tion of the distinct anatomical sites (i.e., meninges, cerebrospinal fluid, and parenchyma) associate

163 eptors localized in nonneuronal cells in the meninges, choroid plexus, and blood vessels may be invol

164 imals displayed weak COX-2 expression in the meninges, choroid plexus, and larger blood vessels.

165 h lesser extent, CD4(+) lymphocytes into the meninges, choroid plexus, ventricles, and parenchyma of

166 ata, in primary cultures of murine embryonic meninges, cilia length was significantly reduced in hete

167 udy we demonstrate that the dorsal forebrain meninges communicate with the adjacent radial glial endf

168 Emerging evidence shows that the meninges conduct essential immune surveillance and immun

169 ructural and cellular details of human skull-meninges connections (SMCs) compared with veins.

170 en measured shortly after the removal of the meninges, consistent with an intact blood-brain barrier,

171 Unlike the adjacent brain parenchyma, the meninges contain a wide repertoire of immune cells.

172 hat, during homeostasis, the mouse and human meninges contain IgA-secreting plasma cells.

173 Gross spinal cord anatomy, spinal meninges, contrast agent-enhanced spinal vasculature, an

174 lowed by BMT reduced lysosomal distension in meninges, corneal fibroblasts, and bone when compared wi

175 Foxc1 dosage and loss of meninges correlated with a dramatic reduction in both ne

176 and yielding insights into the mechanisms of meninges development and function.

177 that the prominent phenotypes appear as the meninges differentiate into pia, arachnoid, and dura.

178 Lymphatic vessels in meninges drain interstitial fluid into the deep-cervical

179 tes in CNS parenchyma, pia-enriched subdural meninges, dura mater, choroid plexus and cerebrospinal f

180 rvous system lymphatics develop in the mouse meninges during early postnatal periods and display rema

181 located between radial glial endfeet and the meninges during embryonic cerebellar development.

182 A-4-dependent B cell accumulation within the meninges during neuroinflammation, a key early step in t

183 ndrogenic mesenchyme, periocular mesenchyme, meninges, endothelial cells, and kidney.

184 cell types, including neurons, glial cells, meninges, ependymal cells, and cells of cerebral vessels

185 The meninges forms a critical epithelial barrier, which prot

186 lls in brain parenchyma, choroid plexus, and meninges from 17 macaques that developed acquired immune

187 B cells reach the meninges from the calvaria through specialized vascular

188 ue, and in some cases, leukocytes within the meninges, gray, and white matter, of both controls and M

189 Inflammation in the spinal cord meninges has been associated with axonal loss, a patholo

190 This neurogenic inflammation within the meninges has been suggested as a model to explain the pa

191 ers of the stomach, lung, kidney, brain, and meninges; however, the totality of the evidence is incon

192 ntigen-experienced B cells that populate the meninges in aging mice are blood-borne.

193 was detected in the brain parenchyma and the meninges in all cases.

194 Besides revealing the signaling role of meninges in cortical development, our study suggests tha

195 Using high-resolution optical imaging of the meninges in living animals, we show that zebrafish posse

196 nce regarding the embryogenesis of the human meninges in the context of meningioma pathogenesis and a

197 n about T lymphocyte immune reactions in the meninges in the human cases.

198 this study suggest that CGRP effects in the meninges, including meningeal vasodilatation, are not su

199 4), and those that did were primarily in the meninges, injection site, ventricles, and perivascular s

200 pocalin secreted from the choroid plexus and meninges into cerebrospinal fluid.

201 hat (1) [(3)H] muscimol diffused through the meninges into the cortical tissue underlying the epidura

202 essed close to these migration sites, in the meninges investing the hippocampal primordium and the pr

203 erentiation of arachnoid cells in the mutant meninges is also abnormal.

204 rate that attachment of RGC processes at the meninges is important for RGC survival and the control o

205 To test whether the behavior of Tregs in the meninges is influenced by interactions with CD11c(+) cel

206 Cell proliferation in the meninges is reduced, causing loss of arachnoid fibroblas

207 that a gene active in the choroid plexus and meninges is responsive to T3.

208 In AD, increased deposition of Abeta in the meninges leads to greater resistance to CSF outflow.

209 minin subunits demonstrated that loss of the meninges led to changes in basement membrane composition

210 Among nonneuronal cells, ependyma and meninges lining the ventricular and subarachnoid spaces

211 by c-fos mRNA labeling of cells of the outer meninges (mainly arachnoid), blood vessels (arteries, ve

212 -inflammatory cytokine production within the meninges may be a key to this process.

213 the cranial nerves (vestibular schwannomas), meninges (meningiomas), and spinal cord (ependymomas).

214 The recent discovery in the meninges of a lymphatic network that drains the CNS call

215 eta deposition in cerebral blood vessels and meninges of aged transgenic mice overexpressing this cyt

216 factor and interferon gamma was found in the meninges of cases with secondary progressive multiple sc

217 were detected in lymphoid tissues and in the meninges of infected animals.

218 ic lesions, and stronger immune responses in meninges of mice infected with ste12alpha cells than tho

219 ation of mast cells in both the thalamus and meninges of mice.

220 ctive monocytic inflammatory response in the meninges of mucoid variant-infected rats.

221 oid tissues (TLTs) have been observed in the meninges of multiple sclerosis (MS) patients, but the st

222 Here, we report that the meninges of perinatal mice contain a population of neuro

223 he lymphatic and nonlymphatic regions in the meninges of rats.

224 ressed in the choroid plexus, microglia, and meninges of the brain and in the ovary.

225 The meninges of the central nervous system (CNS) are populat

226 icular significance, neurons, microglia, and meninges of the central nervous system were virtually cl

227 ult in meningiomas in the mesodermal-derived meninges of the midline and paramedian anterior, central

228 axons enter the brain, the laminin-positive meninges on the surface of the olfactory bulb primordium

229 ogenitor cell proliferation, deficits in the meninges or basement membrane, or cell autonomous defect

230 y of quinolinic acid into the brain from the meninges or blood.

231 cells and cortical plate neurons, passed the meninges or terminated their migration prematurely.

232 te of infection can involve the bloodstream, meninges, or urinary tract, but disease is frequently di

233 and .003, respectively), their corresponding meninges (P = .086 and .006, respectively), and the drai

234 uced increases in vessel permeability in the meninges, parenchyma, and choroid plexus were polymorpho

235 meningeal fibroblasts in the three layers of meninges, perivascular cells, and ependymocytes and in a

236 othelial cells and meninges, and because the meninges play a critical role in interneuron development

237 t pro-inflammatory molecules produced in the meninges play a major role in cortical demyelination in

238 VR]) in 4 regions of interest comprising the meninges plus the adjacent overlying skull bone (paramen

239 CXCL12 or ventral diencephalon meninges potently promoted axon outgrowth from both ipsi

240 tanding of the embryological origins for the meninges prior to proposing next steps for this work.

241 The meninges produce BMP7, an inhibitor of callosal axon out

242 The meninges produce essential signaling molecules and major

243 le sclerosis, B cell aggregates populate the meninges, raising the central question as to whether the

244 Our data reveal that the meninges regulate the development of the skull and cereb

245 he build-up of immune cell aggregates in the meninges represents a rational target for therapeutic in

246 els of the chemokine receptor CXCR6 and seed meninges shortly after birth.

247 nse population of resident mast cells in the meninges, structures surrounding the brain and spinal co

248 did leukocytes accumulate in the ventricles, meninges, sub-arachnoid spaces, and injection site.

249 regions included the ethmoid sinus, clivus, meninges, substantia nigra, but not the basal ganglia or

250 erficial white matter structures adjacent to meninges suggested initial recruitment of effector T cel

251 ivity and the mast cell degranulation in the meninges suggests that these parameters are linked.

252 ved in areas surrounding the injection site, meninges surrounding the brain and perivascular cells an

253 al and spinal nerves to various parts of the meninges surrounding the central nervous system (CNS).

254 gioma is a frequently occurring tumor of the meninges surrounding the central nervous system.

255 However, the meninges surrounding the CNS host diverse populations of

256 as a novel cell type resident in the healthy meninges that are activated after CNS injury.

257 te-dominant inflammation in the brain and/or meninges that clearly was morphologically distinct from

258 erived radial glia-like cells present in the meninges that migrate and differentiate into functional

259 cade of morphogenic signals initiated by the meninges that regulates corpus callosum development.

260 teraction of Neisseria meningitidis with the meninges that surround and protect the brain is a pivota

261 ) cells induced robust TLTs within the brain meninges that were associated with local demyelination d

262 Meninges, the connective tissue of the vertebrate centra

263 indicate a novel role for mast cells in the meninges, the membranes that envelop the brain, as poten

264 ey respond to a diffusible attractant in the meninges, the nonneural tissues covering the nervous sys

265 channels also directly provide leukocytes to meninges, the privileged sampling of brain-derived dange

266 r network that courses through all layers of meninges, the vasculature of both the brain and meninges

267 ed site, but recent data have shown that the meninges-the membranes that surround the brain and spina

268 ILC2s are present throughout the naive mouse meninges, though are concentrated around the dural sinus

269 Myelin-specific T cells infiltrate the meninges throughout the CNS, regardless of the T(H)17:T(

270 transmission of nociceptive signals from the meninges to the cortex.

271 molecules, and immune cells from the CNS and meninges to the peripheral (CNS-draining) lymph nodes.

272 ve pathways that carry pain signals from the meninges to the spinal cord, and if so, to what extent a

273 nal cord injury and shift the focus from the meninges to the vasculature during scar formation.

274 ta1 and retinoic acid (RA) released from the meninges, together with oxygen tension, could constitute

275 routes taken by immune cells that patrol the meninges under healthy conditions and invade the parench

276 ells associated with CNS border regions (the meninges, vasculature, and choroid plexus), in addition

277 on of TLR4 transcripts in mouse brain in the meninges, ventricular ependyma, circumventricular organs

278 hat originates in neurons and spreads to the meninges via astrocytes.

279 CSD promotes neutrophil trafficking to meninges via vascular channels originating from skull bo

280 hing for T-cell gateways into and out of the meninges, we discovered functional lymphatic vessels lin

281 th meningeal overgrowth or selective loss of meninges, we have identified a cascade of morphogenic si

282 ad entered the CNS and were infiltrating the meninges were characterized by high expression of vascul

283 n one of these animals, viral populations in meninges were closely related to those from CSF and shar

284 0- and Raldh2-expressing cells in the dorsal meninges were either reduced or absent in the Foxc1 muta

285 Two models of the human meninges were established in vitro, using (i) sections o

286 led that activated CD4(+) T cells within the meninges were highly migratory, whereas Tregs moved more

287 Concurrently, the meninges were infiltrated by inflammatory monocytes that

288 With this in mind, cultures of the P1 mouse meninges were used as a comparative cell type in order t

289 close to the neocortical surface and in the meninges, were left unaffected, hence leaving PGE2 synth

290 pace, known as the glymphatic system, to the meninges, where meningeal lymphatic vessels (MLVs) remov

291 quires interaction with neural crest-derived meninges, whereas ossification of the neural crest-deriv

292 s related to inflammatory infiltrates in the meninges, which was pronounced in invaginations of the b

293 r connections between skull marrow and brain meninges, which were filled with immune cells upon strok

294 ain receptors suppresses host defense in the meninges while, later, taste receptors amplify inflammat

295 in meningiomas in neural-crest cell-derived meninges, while variants affecting Hedgehog signaling, P

296 parenchymal infiltration (14/14), present in meninges, white and grey matter, associated with variabl

297 ith (18)F-flortaucipir and most often in the meninges with (18)F-MK-6240.

298 iate tumorigenesis in the cranial nerves and meninges with typical histological features and molecula

299 l intestine, bacteremia, and invasion of the meninges, with animals frequently succumbing to lethal i

300 ansion of lymphocytes within the spinal cord meninges, with preferential expansion of regulatory T-ce