ライフサイエンスコーパス: meninges

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

2 ar malformations that remain adherent to the meninges.

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

4 , can diffuse into the neocortex through the meninges.

5 e on parasympathetic neurons innervating the meninges.

6 are localized primarily in the thalamus and meninges.

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

8 in white matter, periventricular zones, and meninges.

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

10 far the most common tumours arising from the meninges.

11 uclear cell infiltrates predominantly in the meninges.

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

13 located between the neuroepithelium and pia-meninges.

14 s invading the lesion site from the adjacent meninges.

15 uperficial layers of the cerebral cortex and meninges.

16 ng in the perivascular layer and through the meninges.

17 ranulomatous lesions along the ventricle and meninges.

18 rved surrounding the microinjection site and meninges.

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

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

21 s as well as in perivascular infiltrates and meninges.

22 was restricted to the anterior pituitary and meninges.

23 rising major surface-lying blood vessels and meninges.

24 tive giant cells in the brain parenchyma and meninges.

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

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

27 ain-sensitive structures of the intracranial meninges.

28 ic and nonneoplastic disorders affecting the meninges.

29 the brain, including the choroid plexus and meninges.

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

31 lence behavior of pneumococci that reach the meninges.

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

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

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

35 cerebral and cerebellar hemispheres and the meninges.

36 ogous in many respects to that of vertebrate meninges.

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

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

39 directed to the neural tissue instead of the meninges.

40 lation activity in neural tissue but not the meninges.

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

42 activation of nociceptors that innervate the meninges.

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

44 12.8 infected cells/mm(2), respectively) and meninges (133.0 versus 34.2 infected cells/mm(2), respec

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 63(+)BrdU(+) macrophages were present in the meninges and choroid plexus with AIDS.

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

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

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

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

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

65 functions by stimulating astrocytes from the meninges and hippocampus.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 8 T effector cells to exclusively target the meninges and vascular/perivascular space of the gray and

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

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

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

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

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

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

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

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

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

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

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

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

108 The meninges are not required for basement membrane establis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 The meninges forms a critical epithelial barrier, which prot

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 The meninges produce essential signaling molecules and major

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 Meninges, the connective tissue of the vertebrate centra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 0- and Raldh2-expressing cells in the dorsal meninges were either reduced or absent in the Foxc1 muta

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

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

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

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

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

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

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

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