ライフサイエンスコーパス: perivascular

1 Perivascular access and distribution of full-length IgG

2 Osmolyte co-infusion significantly enhanced perivascular access of the larger antibody from the CSF,

3 Perivascular access to smooth muscle basement membrane c

4 had patchy accumulations of neutrophils and perivascular accumulations of lymphocytes.

5 Adrb1 activation stimulates WAT resident perivascular (Acta2+) cells to form cold-induced beige a

6 internal mammary arteries (IMAs) with their perivascular adipose tissue (PVAT) and thoracic adipose

7 ACT: Previous studies have demonstrated that perivascular adipose tissue (PVAT) causes vasoconstricti

8 ertension was associated with an increase in perivascular adipose tissue expression of the chemokine

9 Y POINTS: The fat surrounding blood vessels (perivascular adipose tissue or PVAT) releases vasoactive

10 -induced T-cell activation in the spleen and perivascular adipose tissue was blunted in Tcrdelta(-/-)

11 1 and M2 macrophages, and dendritic cells in perivascular adipose tissue.

12 We identified a niche of CXCL13(+) perivascular and CXCL12(+)LTB(+) and PD-L1(+) epithelial

13 nucleic acid rescued angiotensin II-induced perivascular and interstitial fibrosis.

14 They are also enriched in perivascular and necrotic regions.

15 rved pronounced histologic evidence for both perivascular and peribronchial inflammation in the lungs

16 lation of versican and HA, especially in the perivascular and peribronchial regions, which were enric

17 us production, airway epithelial thickening, perivascular and peribronchiolar inflammation, and struc

18 itions form sprouts composed of endothelial, perivascular, and other proliferative cells.

19 Two weeks after perivascular application to balloon-injured rat common c

20 er alterations in AQP4 expression or loss of perivascular AQP4 localization are features of the aging

21 of AQP4 protein, AQP4 immunoreactivity, and perivascular AQP4 localization in the frontal cortex wer

22 Loss of perivascular AQP4 localization may be a factor that rend

23 When controlling for age, loss of perivascular AQP4 localization was associated with incre

24 Perivascular AQP4 localization was significantly associa

25 phin (alpha-Syn) that demonstrate diminished perivascular aquaporin-4 pool but retain the non-endfoot

26 ttenuates blood-brain barrier disruption via perivascular aquaporin-4 pool.

27 activated mast cells and neutrophils in the perivascular area of atherosclerotic plaques.

28 of oxidative stress, was also upregulated in perivascular areas after chemotherapy.

29 localization of Kir4.1 with AQP4 clusters in perivascular areas but not in parenchyma.

30 , CCR2 was required for iMO trafficking from perivascular areas to sites of virus infection within th

31 tion, where they localized preferentially to perivascular areas.

32 ificantly increased intracellular calcium in perivascular astrocyte processes, the onset of astrocyte

33 und hematoma at 24 hrs after ICH, along with perivascular astrocytes and endothelial cells.

34 Here, we show that AQP4 polarization in the perivascular astrocytic end feet was impaired after TBI,

35 Neutrophils need to penetrate the perivascular basement membrane for successful extravasat

36 yte process detachment and disruption of the perivascular basement membrane surrounding the VECs.

37 spatiotemporal and regional contributions of perivascular BMDCs (pBMDC) to GBM development.

38 EdU pulse-chase experiments demonstrated a perivascular cancer stem cell population in Pten/Trp53 d

39 We measured the accumulation of brain perivascular (CD163(+)) and inflammatory (MAC387(+)) mac

40 oglial activation, reduced neuronal density, perivascular CD3-positive T-lymphocyte clustering, and f

41 ortem human brain tissue, IL-21 localized to perivascular CD4(+) T cells in the area surrounding acut

42 rchitecture, and cell survival and decreased perivascular CD68(+) cell infiltration in the ischemic h

43 ent is the reduction of both endothelial and perivascular cell populations.

44 We used perivascular-cell-specific and pericyte-specific lineage

45 We show that a Nestin-Cre transgene targets perivascular cells (adventitial cells and pericyte-like

46 malian cardiomyocytes, is sharply induced in perivascular cells after injury to the adult zebrafish h

47 helium through co-seeding of endothelial and perivascular cells and a two-phase culture protocol.

48 ocyte survival or proliferation; a supply of perivascular cells and possibly other cell types such as

49 eport a mechanism of the interaction between perivascular cells and tumour-associated macrophages (TA

50 lete loss of mature osteoblastic cells while perivascular cells are maintained.

51 These results identify perivascular cells as fibro/adipogenic progenitors in WA

52 Activation of PDGFRalpha signaling in perivascular cells causes them to transition into ECM-sy

53 Genetic inactivation of Klf4 in perivascular cells decreased formation of a pre-metastat

54 with human cells, including endothelial and perivascular cells derived from induced pluripotent stem

55 The origin of these scars is thought to be perivascular cells entering lesions on ingrowing blood v

56 discussion, and current consensus holds that perivascular cells form mesenchymal stem cells in most t

57 uted throughout the BM, and on pericytes and perivascular cells in multiple organs.

58 revealed a previously unidentified role for perivascular cells in pre-metastatic niche formation and

59 Cell, Kramann et al. (2016) show that Gli1+ perivascular cells in the outermost vessel layer are pro

60 lineage-tracing models to trace the fate of perivascular cells in the pre-metastatic and metastatic

61 we use a developmental model to investigate perivascular cells in white adipose tissue (WAT) and the

62 Pericytes, perivascular cells involved in microvascular function, e

63 Pericytes are perivascular cells localized to capillaries that promote

64 We show that perivascular cells lose the expression of traditional vS

65 y gene Klf4 in these phenotypically switched perivascular cells promoted a less differentiated state,

66 of perivascular cells, we hypothesized that perivascular cells similarly regulate tumor cell fate at

67 Perivascular cells such as macrophages and mast cells th

68 his study was to examine the contribution of perivascular cells to odontoblasts during the developmen

69 Sox10(+) stem cells could differentiate into perivascular cells to stabilize newly formed microvessel

70 g bone remodeling originate from bone marrow perivascular cells, bone remodeling compartment canopy c

71 Perivascular cells, however, quickly resumed proliferati

72 Perivascular cells, including vascular smooth muscle cel

73 Given the well-described plasticity of perivascular cells, we hypothesized that perivascular ce

74 in the kidney detected evident expression in perivascular cells, with negligible expression in the en

75 deletion from vascular endothelial, but not perivascular, cells impeded tumor growth, suggesting a v

76 ognized role for Th1 cells as integrators of perivascular CF and cardiac dysfunction in nonischemic H

77 ables RGS protein binding accumulated in the perivascular channels of thymic corticomedullary venules

78 We highlight recent data suggesting that perivascular chemokine CXC ligand (CXCL)12-expressing me

79 pithelium, the presence of a thin choroid, a perivascular choroidal inflammatory infiltrate, and atro

80 These CD11c(+) cells are organized in perivascular clusters, targeted by T cells, and strongly

81 side in a vascular niche, located within the perivascular compartment of adipose tissue blood vessels

82 mber that was restricted to the interstitial/perivascular compartment, without recruitment of macroph

83 dothelial cells (ECs) and tightly associated perivascular constituents that regulate haematopoiesis t

84 clei were localized to CD163+ macrophages in perivascular cuffs and lesions.

85 ty to spread systemically, PA14::hepP formed perivascular cuffs around the blood vessels within the s

86 had prominent representation of inflammatory perivascular cuffs, inflammatory molecules and EMMPRIN,

87 ve in preventing intimal hyperplasia through perivascular delivery of rapamycin.

88 d SAMHD1 was localized to endothelial cells, perivascular dendritic cells, and macrophages, and SAMHD

89 ical features with epithelioid cells along a perivascular distribution and characteristic immunohisto

90 tic liver, COL15A1-expressing PMFs adopted a perivascular distribution outlining vascular capillaries

91 ectively), followed by new T2 lesions with a perivascular distribution pattern (34.6%).

92 Contrast-enhancing lesions with a perivascular distribution pattern outside of the PML les

93 de gliomas, in which they exhibited a unique perivascular distribution.

94 he absence of CLU, Abeta clearance shifts to perivascular drainage pathways, resulting in fewer paren

95 from an increased focus on mouse models and perivascular drainage.

96 de useful scaffolding for devising effective perivascular drug delivery particularly suited for preve

97 s showing widespread microvascular collapse, perivascular edema, and microthrombosis associated with

98 in bronchoalveolar lavage, lung weight gain, perivascular edema, as well as reduced static compliance

99 multifocal moderate to severe hepatitis, and perivascular edema.

100 cytes, while, in contrast, AQP4 localized to perivascular end feet in the CD44- protoplasmic astrocyt

101 d capillary permeability, and re-established perivascular end-feet astrocytes in symptomatic ALS mice

102 ced astrogliosis, microgliosis, and enhanced perivascular end-feet astrocytes were also determined in

103 eleasing vasoactive agents (e.g., K(+)) from perivascular endfeet surrounding parenchymal arterioles.

104 glutamate receptors, and form aquaporin-4(+) perivascular endfeet.

105 rete clusters of GLT-1 were also detected at perivascular endfeet.

106 CHEST cells are a primary cell line with perivascular endothelial properties that expand hematopo

107 an in vitro platform to study the biology of perivascular-endothelial interactions.

108 agnetic resonance imaging findings of linear perivascular enhancement in patients.

109 hronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPER

110 nal mesenchymal lesions recapitulating human perivascular epithelioid cell tumors (PEComas) from pati

111 ed blood vessels, and usually named PEComas (perivascular epithelioid cell tumors).

112 This study has also documented the perivascular expression of Serpin B2 by angiotropic mela

113 equency of interaction of particles with the perivascular extracellular matrix for smaller nanopartic

114 Renal sinus fat (RSF) is a perivascular fat compartment located around renal arteri

115 ng of lipid-laden atherosclerotic plaque and perivascular fat was demonstrated, where a lab-built 500

116 na also showed increased vascularization and perivascular fibers containing NPY.

117 turn stimulates exuberant Notch signaling in perivascular fibroblasts and enhances fibrosis.

118 cular niche, in which macrophages, PCECs and perivascular fibroblasts interact, may help to develop t

119 , resulted in approximately 50% reduction of perivascular fibrosis after transverse aortic constricti

120 nase kinase 6-p38 developed interstitial and perivascular fibrosis in the heart, lung, and kidney as

121 old (n = 5 to 7; p < 0.01), respectively, in perivascular fibrotic areas after transverse aortic cons

122 We report for the first time in HFpEF perivascular fluid cuff formation around extra-alveolar

123 ternalization resulted in the formation of a perivascular fluorescent coating around blood vessels.

124 On tissue analysis, we also identified small perivascular foci of microglia and T cells without blood

125 vaporation occurs from the vascular bundles (perivascular), from the photosynthetic mesophyll cells,

126 CLIPPERS patients had brainstem predominant perivascular gadolinium enhancing lesions on magnetic re

127 These cells form the perivascular gastric stem cell niche, and Wnt5a produced

128 These findings implicate perivascular Gli1(+) MSC-like cells as a major cellular

129 Aquaporin 4 (AQP4) is highly expressed at perivascular glia end-feet in the mammalian brain and ma

130 Coalescing and mostly perivascular granuloma-like accumulations of storage-lad

131 Proneural, perivascular GSCs activated EZH2, whereas mesenchymal GS

132 microaneurysms, perivascular space dilation, perivascular haemosiderin leakage, and myelin loss.

133 Its filamentous pial, subventricular, and perivascular immunostaining pattern on mouse tissue rese

134 scular rejection (Banff ACR grade III) and a perivascular infiltrate mostly consisting of T cells.

135 lagen tissue, inflammatory infiltrate cells, perivascular infiltrate, angiogenesis, spongy change, an

136 In brain, abundant mononuclear cells in perivascular infiltrates and scattered intraparenchymal

137 dermal dysmaturation, neutrophil exocytosis, perivascular infiltration of lymphocytes and neutrophils

138 patient samples revealed that a significant perivascular infiltration of M1, but not M2, macrophages

139 Peribronchial and perivascular inflammation and mucus production were larg

140 ncluding increased vascular permeability and perivascular inflammation associated with decreased PEC

141 Recent studies have emphasized the role of perivascular inflammation in cardiovascular disease.

142 ole of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vasc

143 71% of biopsies demonstrated epineurial perivascular inflammation.

144 f vascular dysfunction through modulation of perivascular inflammation.

145 is) exert protective effects in DN improving perivascular inflammation.

146 ent muscularization, medial hypertrophy, and perivascular inflammatory cell infiltration, associated

147 were most severe in regions of extravasated perivascular inflammatory cells.

148 entiated nuclear layers of the retina, and a perivascular inflammatory infiltrate within the choroid.

149 istomorphology of the muscle showed a mainly perivascular inflammatory infiltrate, fibrotic degenerat

150 oma-endothelial cell interactions leading to perivascular invasion, a phenomenon originally described

151 Here, we show that ephrin-B2 mediates GSC perivascular invasion.

152 We studied mechanisms of perivascular leukocyte infiltration in angiotensin II (A

153 Perivascular-like cells as an eventual target in NSCLC w

154 Together, our data show that perivascular-like cells present in NSCLC retain function

155 Perivascular localization of aquaporin-4 (AQP4) facilita

156 ogenous CD16(+) monocytes were detected in a perivascular location within active MS lesions, and CD16

157 ger and distributed in both interstitial and perivascular locations.

158 encephalitis, characterized predominantly by perivascular lymphohistiocytic infiltrates.

159 Circulating autoantibodies, lung perivascular lymphoid tissue, and elevated cytokines hav

160 A similar perivascular, M2-related TAM subset was present in human

161 Instead, perivascular macrophage-like myeloid cells populate the

162 Brain perivascular macrophages (PVM) located in the perivascul

163 The proliferative capacity of Ki-67+ perivascular macrophages (PVM) was confirmed by their nu

164 ons of neurovascular unit coupling caused by perivascular macrophages (PVMs) as a cause of hypertensi

165 Perivascular macrophages (PVMs) represent a distinct pop

166 us system and observed highest expression in perivascular macrophages (which are characterized by abu

167 chemokine CCL2, a ligand for CCR2, included perivascular macrophages and microglia.

168 a-induced PAH, in association with increased perivascular macrophages and muscularized distal arterie

169 We report that perivascular macrophages are critical for neutrophil mig

170 Most perivascular macrophages that comprise SIVE lesions and

171 we describe a novel subset of murine dermal perivascular macrophages that extend protrusions across

172 ment that includes parenchymal microglia and perivascular macrophages, as well as choroid plexus and

173 nary capillary endothelial cells (PCECs) and perivascular macrophages, impeding alveolar repair and p

174 alpha-hemolysin produced by S. aureus lyses perivascular macrophages, which leads to decreased neutr

175 growth factor receptor 1 (VEGFR1)-expressing perivascular macrophages.

176 Intravascular and perivascular markers such as Evans blue (EB), isolectin

177 zed vascular support cells termed podocytes, perivascular mesangial cells, and parietal epithelial ce

178 e rise to marrow reticular stromal cells and perivascular mesenchymal progenitors suggesting they fun

179 Perivascular mesenchymal stem and progenitor cells (MSPC

180 ology have implicated diverse organ-resident perivascular mesenchymal stem cell (MSC)-like cells and

181 In particular, perivascular microenvironments in the bone marrow confer

182 of the same ephrin-B2 ligand in GSC enabled perivascular migration through homotypic forward signall

183 Here, we demonstrate that Gli1 marks perivascular MSC-like cells that substantially contribut

184 Pericytes are perivascular mural cells of brain capillaries.

185 these mouse strains, only those that marked perivascular mural cells tracked the cold-induced beige

186 sortilin was highly expressed by infiltrated perivascular myeloid cells, mainly in vessel cuffs, in t

187 ations known to occur in some of soft tissue perivascular myoid cell neoplasms were also absent in SN

188 , low-grade mesenchymal neoplasm of probable perivascular myoid cell origin.

189 (to inhibit sympathetic neurotransmission), perivascular nerve stimulation (PNS) evoked dilatation i

190 sed in the tumor cell niches compared to the perivascular niche across multiple regions in GBM patien

191 s within skin injuries, where they home to a perivascular niche and generate alternatively activated,

192 ling axis as crucial for exploitation of the perivascular niche and identify potential therapeutic ta

193 Haematopoietic stem cells (HSCs) reside in a perivascular niche but the specific location of this nic

194 Here, we report that SCC cells within the perivascular niche have undergone epithelial to mesenchy

195 oietic stem cells (HSCs) are maintained by a perivascular niche in bone marrow but it is unclear whet

196 Mesenchymal stem cells (MSCs) reside in the perivascular niche of many organs, including kidney, lun

197 Evidence has emerged for macrophages in the perivascular niche of tumors regulating important proces

198 reby enriching for deposition of MSLC in the perivascular niche through an HIF1alpha-dependent proces

199 (MSCs) are recruited from the endosteal and perivascular niche to become fibrosis-driving myofibrobl

200 When an HSPC arrives in the perivascular niche, a group of endothelial cells remodel

201 netrant medulloblastoma originating from the perivascular niche, which exhibited abnormal blood vesse

202 ma stem-like cells (MSLC) accumulated in the perivascular niche.

203 Some adult animals presented perivascular niches outside the V-SVZ.

204 ming abilities, with the majority located in perivascular niches where GSCs are found.

205 cancer cells (GSCs) that home to specialized perivascular niches.

206 rospinal fluid along a brain-wide network of perivascular pathways recently termed the glymphatic sys

207 yloid-beta, through the brainwide network of perivascular pathways termed the glymphatic system, whic

208 pathway existed in adipose tissues including perivascular, perirenal, epididymal, subcutaneous and br

209 rvival monkeys of which two, newly described perivascular phenotypes (Pldv and Elu) and a small perce

210 contained significantly more NIK(+) ECs and perivascular platelet-derived growth factor receptor bet

211 FDCs arise from perivascular platelet-derived growth factor receptor bet

212 cial for the treatment of cerebral edema; 2) perivascular pool of aquaporin-4 plays a critical role i

213 resuscitation by exerting its effect via the perivascular pool of aquaporin-4.

214 eration, are recruited to a Nestin-GFP(high) perivascular population, and contribute to cartilage rep

215 te and moderate macrophage infiltrates, with perivascular predominance as well as diffuse parenchymal

216 cal 0.75 m mannitol increasing the number of perivascular profiles per slice area accessed by IgG by

217 We have thus identified a self-renewing perivascular progenitor cell line that lacks osteogenic,

218 We identified a highly scalable, perivascular progenitor cell line that we termed PC-A, w

219 The hESC-derived perivascular progenitors described here have potential a

220 quality protocols for deriving self-renewing perivascular progenitors from the human embryonic stem c

221 s were capable of further differentiation to perivascular progenitors with limited differentiation ca

222 Pten inactivation created an abnormal perivascular proliferative niche in the cerebellum that

223 Among patients, striking perivascular radial enhancement was found on brain magne

224 cell (HSPC) proliferation and homing to the perivascular region.

225 like T cells that infiltrate the kidney and perivascular regions of both large arteries and arteriol

226 es adjacent to microcapillaries; clusters in perivascular regions of the cortex were larger than in p

227 s along with persistent fungal debris in the perivascular regions of the lungs.

228 on is upregulated in cancer cells, mainly at perivascular regions of tumors.

229 ing collectively invading tumor cells and in perivascular regions.

230 eutic efficacy by selectively targeting this perivascular, relapse-promoting M2-related TAM cell popu

231 In the gut, blood flow is governed by perivascular sensory and sympathetic nerves but little i

232 With perivascular sensory nerve stimulation, dilatation and i

233 loss of dilatory signalling mediated through perivascular sensory nerves may compromise perfusion of

234 properties leading to a stable yet flexible perivascular sheath and steady and prolonged release kin

235 CR4 ligand, CXCL12, was upregulated in these perivascular sites after chemotherapy, where it was sele

236 Kupffer cells in the hepatic parenchyma and perivascular sites and absence of TLR4, IFN-gamma, or de

237 ity that allowed angiotensin II to enter the perivascular space and activate angiotensin type 1 recep

238 ancer cells were specifically located in the perivascular space and closely associated with blood ves

239 ouble-negative CD3(+)CD4(-)CD8(-) T cells in perivascular space and reduced vascular oxidative stress

240 roid plexus in early inflammation and in the perivascular space and SIV encephalitis (SIVE) lesions l

241 CD163(+) macrophages accumulated in the perivascular space and SIVE lesions with late inflammati

242 s not required for monocyte migration to the perivascular space and that vascular remodeling followin

243 hed to VE-cadherin(+) cells, implicating the perivascular space as a near-homogenous location of LT-H

244 infarcts, microinfarcts, arteriolosclerosis, perivascular space dilation and myelin loss-predicted co

245 orrhage, fibrinoid necrosis, microaneurysms, perivascular space dilation, perivascular haemosiderin l

246 mas are highly invasive tumours that use the perivascular space for invasion and co-opt existing vess

247 Using MRI-visible perivascular space location and severity together with o

248 find that glioma cells, as they populate the perivascular space of preexisting vessels, displace astr

249 MRI-visible perivascular space severity in either location did not p

250 genesis, the migration of monocytes into the perivascular space surrounding collateral arteries and t

251 erivascular macrophages (PVM) located in the perivascular space, a major site of brain Abeta collecti

252 Rac in the Nestin(+) cells would perturb the perivascular space, altering HSC localization and hemato

253 lexity of regulation of hematopoiesis in the perivascular space.

254 s play an important role in the integrity of perivascular space.

255 al stromal cells (MSCs) are important in the perivascular space.

256 allowing substances in the CSF to enter the perivascular space.

257 ject-based morphologic estimates of enlarged perivascular spaces (ePVSs) in clinical-field-strength (

258 However, whether large perivascular spaces (L-PVSs) (>3 mm in diameter) visible

259 ite matter lesion load, frequency of dilated perivascular spaces (PVS) and abnormalities in cerebral

260 MRI-visible perivascular spaces (PVS) are potential neuroimaging mar

261 Perivascular spaces (PVSs) in brain have a close relatio

262 th advancing age, an increased visibility of perivascular spaces (PVSs) on magnetic resonance imaging

263 acytic inflammation, with a predilection for perivascular spaces and collagenous tissues, was observe

264 lation of mature thymocytes within medullary perivascular spaces and reduced numbers of recent thymic

265 odies exhibited size-dependent access to the perivascular spaces and tunica media basement membranes

266 pace may provide unique entry sites into the perivascular spaces from the CSF.

267 grade), whereas the severity of MRI-visible perivascular spaces in the basal ganglia was associated

268 justed analyses, the severity of MRI-visible perivascular spaces in the centrum semi-ovale was indepe

269 We also hypothesized that MRI-visible perivascular spaces in the centrum semi-ovale would be a

270 's disease, we hypothesized that MRI-visible perivascular spaces in the centrum semi-ovale would be a

271 t the anatomical distribution of MRI-visible perivascular spaces may reflect the underlying cerebral

272 distribution to deep brain regions along the perivascular spaces of all vessel types, with sdAb acces

273 fluid, although convective transport in the perivascular spaces of cerebral blood vessels was also e

274 he brain surface and convective transport in perivascular spaces of cerebral blood vessels.

275 Perivascular spaces that are visible on magnetic resonan

276 MRI-visible perivascular spaces were rated using a validated 4-point

277 method for multimodal autoidentification of perivascular spaces yields individual whole-brain morpho

278 cal superficial siderosis, centrum semiovale perivascular spaces, and white matter hyperintensities.

279 cal superficial siderosis, centrum semiovale perivascular spaces, and white matter hyperintensities.

280 ensity - WMH, microbleeds, lacunes, enlarged perivascular spaces, brain atrophy) as seen on structura

281 ild inflammatory exudates, in endomysial and perivascular spaces, consisted of lymphocytes, histiocyt

282 ter confinement of CD4(+) lymphocytes to CNS perivascular spaces.

283 matrix and reduces NP confinement within the perivascular spaces.

284 t, Tregs were restricted to the meninges and perivascular spaces.

285 nly sustained by a subpopulation of ICAM1(+) perivascular stromal cells.

286 s with an apparent increase in the choroidal perivascular stromal tissue and minimal effect on the ov

287 The ratio between the perivascular stromal tissue and the subfoveal choroidal

288 Perivascular, subdural meningeal and choroid plexus macr

289 ATP, released from perivascular sympathetic nerves, causes vasoconstriction

290 es of grade II to III VCA rejection, namely, perivascular T cell infiltrates, but not with vascular C

291 effect, swelling, contrast enhancement, new perivascular T2 lesions and signs suggestive of meningea

292 can modulate neutrophil functions within the perivascular tissue space.

293 fects of vascular dilation and tortuosity on perivascular tissue.

294 ite for neutrophil arrest and migration into perivascular tissues.

295 kinetics of PGZ from fat depots transplanted perivascular to jugular vein were assessed by HPLC/MS/MS

296 Fat explants placed perivascular to the external jugular vein were retained,

297 Perivascular transport involved blood vessels of all cal

298 Notably, perivascular tumor cells expressed hepatic stem cell mar

299 nized endothelium and a robust multicellular perivascular tunica media.

300 PW1(+) progenitor cells are present in the perivascular zone in rodent and human control lungs.