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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
7 perivascular macrophages and populations of meningeal and choroid plexus macrophages in normal brain
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
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
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
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.
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
27 tories: one that runs parallel to the middle meningeal artery (MMA), and another with a more or less
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
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
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.
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
46 acute brain injury induces vascular damage, meningeal cell death, and the generation of reactive oxy
50 d proliferation of both Ben-Men-1 and normal meningeal cells by increasing expression of p16(INK4A),
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
57 A, and proliferating cell nuclear antigen in meningeal cells while significantly reducing the express
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
68 ronal excitation modulates both the pial and meningeal circulation through a critical interaction wit
70 une surveillance that takes place within the meningeal compartment, the mechanisms governing the entr
73 The central nervous system (CNS) and its meningeal coverings accommodate a diverse myeloid compar
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.
78 terotopia formation, neuronal overmigration, meningeal defects, and changes in basement membrane comp
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
86 hermore, we provide evidence that defects in meningeal differentiation can lead to severe cortical dy
89 s to the Group for Enteric, Respiratory, and Meningeal Disease Surveillance in South Africa (GERMS-SA
91 detecting superficial abnormalities, such as meningeal disease, because they do not demonstrate contr
94 oconidia produced a chronic illness in which meningeal endarteritis obliterans was consistently obser
97 CNSV who presented with prominent gadolinium meningeal enhancement on magnetic resonance imaging (MRI
103 oneal disease, 2 pleural disease, and 1 each meningeal, enteric, paravertebral, bone, genital, and bl
107 Ins and S1 cortices, enhancing or inhibiting meningeal-evoked responses of Sp5C, without affecting cu
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
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
123 2 and EphB2, are expressed by astrocytes and meningeal fibroblasts, respectively, in the adult spinal
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
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
134 rogressive multiple sclerosis with extensive meningeal immune cell infiltration exhibited a more seve
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
140 d acute neuropathological changes, including meningeal infiltrates, encephalitis, particularly of the
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
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
151 outside the brain parenchyma, in particular meningeal inflammation or through cerebrospinal fluid me
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
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
166 ine action, gammaHV68 induced a neutrophilic meningeal inflammatory infiltrate, while gammaHV68-M3.st
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
173 ive puncta was observed throughout the three meningeal layers, the perineurium of cranial nerves, and
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
183 The plasticity and regenerative potential of meningeal LVs should allow manipulation of cerebrospinal
185 e clearly delineated with the discovery of a meningeal lymphatic system capable of carrying fluid, im
187 gs and recent studies revealing a functional meningeal lymphatic system that drains cerebrospinal flu
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
193 ipheral organs with the proposed function of meningeal lymphatic vessels in neurological disorders, s
195 unications between the glymphatic system and meningeal lymphatics in CNS disorders and develop new th
197 cerebrospinal fluid, and presence of EBV in meningeal lymphoid follicles and perivenular infiltrates
200 y, circulating immune stimuli might activate meningeal macrophages and perivascular microglia along t
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
207 roaches in mice, we identified evidence that meningeal mast cells can importantly contribute to the k
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
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
221 se trials, CSD induced a twofold increase in meningeal nociceptor firing rate that persisted for 37.0
224 teum through suture branches of intracranial meningeal nociceptors and/or somatic branches of the occ
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
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
242 6 patients, the largest number to date, with meningeal or parenchymal CNS-HL confirmed by histopathol
244 Ins and S1 selectively affect interoceptive (meningeal) over exteroceptive (cutaneous) nociceptive in
246 the initial response of the BBB to the human meningeal pathogen group B Streptococcus (GBS) and the o
249 ndothelial cells (hBMECs) with GBS and other meningeal pathogens results in the induction of host tra
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
260 it fails to completely eliminate the risk of meningeal recurrence, likely due to minimal CNS penetrat
265 ly identified mast cells were present in the meningeal sheaths surrounding the cln3-/- nerve and in t
267 radicular pain and more often presented with meningeal signs but less frequently complained of malais
269 Severe headache, altered mental status, meningeal signs, and other neurological signs at present
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
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
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 (
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
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
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