ライフサイエンスコーパス: venule

1 (5.0% versus 3.4% for wider versus narrower venules).

2 mmation and nuclear debris in post capillary venules.

3 ty at the level of individual arterioles and venules.

4 pre-capillary arterioles and post-capillary venules.

5 ries which connect peripheral arterioles and venules.

6 ly low-oxygen and low-velocity postcapillary venules.

7 n-dependent adhesion in airway postcapillary venules.

8 al involvement in neutrophil emigration from venules.

9 l arrangement of arterioles, capillaries and venules.

10 ormation of lymph nodes and high endothelial venules.

11 but also from blood, across high endothelial venules.

12 of endogenous Tregs in dermal postcapillary venules.

13 and extensive induction of high endothelial venules.

14 ular annulus, which comprised post-capillary venules.

15 , despite their role during B-cell arrest in venules.

16 r, allowing rapid transit from arterioles to venules.

17 to 92%), with a more pronounced increase in venules.

18 emodynamics were assessed in randomly chosen venules.

19 mean circulation time between arterioles and venules.

20 and in deep ascending cortical postcapillary venules.

21 sion of effector T cells and Tregs in dermal venules.

22 oll and integrins to arrest in postcapillary venules.

23 necting terminal arterioles to postcapillary venules.

24 ndothelial cells in intestinal postcapillary venules.

25 in both unstimulated and TNF-alpha-activated venules.

26 all, hemostatically active thrombi formed in venules.

27 perfused unstimulated or TNF-alpha-activated venules.

28 of capillaries into vessels with features of venules.

29 licular dendritic cells and high endothelial venules.

30 essels (MV), that originate from preexisting venules.

31 giogenesis, mother vessels, are derived from venules.

32 t pericytes and were more prevalent in small venules.

33 evels similar to that found in postcapillary venules.

34 tefin A and cystatins B and C, by these same venules.

35 nly in small vessels such as capillaries and venules.

36 ncreases leukocyte adhesion in postcapillary venules.

37 nt or sustained fashion, on high endothelial venules.

38 ic cells, stromal cells and high endothelial venules.

39 tes leukocyte entry through high endothelial venules.

40 lar tree, including arteries, arterioles and venules.

41 ascular FRCs and associated high endothelial venules.

42 eases in velocity and flow in arterioles and venules.

43 ferric chloride-induced injury of mesenteric venules.

44 vascular channels of thymic corticomedullary venules.

45 al node addressin (PNAd) on high endothelial venules.

46 alpha in KRIT1 deficient arterioles, but not venules.

47 PCs) that form the wall of the postcapillary venules.

48 n vivo crawling and TEM in the postcapillary venules.

49 following injuries to mouse cremaster muscle venules.

50 rosion casts were composed of interconnected venules (10-50 mum) forming a hexagonal meshwork.

51 idence interval [CI] -4.4 mum, -1.9 mum) and venules (-2.7 mum; 95% CI -4.9 mum, -0.5 mum) were assoc

52 iously observed in arterioles also occurs in venules, (2) plasma leakage persists well beyond red cel

53 0+/-6 versus 32+/-5 bacteria) and collecting venules (48+/-5 versus 18+/-4 bacteria; P<0.05) of VWF k

54 ls are neutrophils; however, in unstimulated venules, a greater percentage of the total monocyte popu

55 by endothelial cells that line postcapillary venules, a primary site of leukocyte recruitment during

56 ialized blood vessels named high endothelial venules, a process that increases markedly during immune

57 ghly specialized, featuring high endothelial venules across which most of the resident lymphocytes cr

58 both blood and tissues via high endothelial venules and afferent lymphatics, respectively, and forme

59 bral-blood-volume (CBV)-fMRI from individual venules and arterioles.

60 ar endothelial cells (ECs) in post-capillary venules and circulating leukocytes.

61 sted the hypothesis that as a consequence of venules and collecting lymphatics sharing a common embry

62 ng B- and T-cell areas with high endothelial venules and dendritic cells.

63 ulation through MAdCAM-1(+) high endothelial venules and efferent lymphatics, and had immune profiles

64 uorescent microparticle image velocimetry in venules and endothelialized cylindrical collagen microch

65 addressin (PNAd)-expressing high endothelial venules and enriched in B and Foxp3(+) T cells, is impor

66 ) T cells adhered poorly to high endothelial venules and exhibited defects in lymph node entrance and

67 tissue (ST), often contain high endothelial venules and follicular dendritic cells (FDCs).

68 e in lymphocyte sticking to high endothelial venules and in recruitment of resident dendritic cells t

69 o increased leukocyte adhesion in mesenteric venules and increased the frequency of neutrophils in tu

70 ced rolling in thrombin-activated mesenteric venules and inflamed brain microcirculation.

71 s through and migrate along high endothelial venules and later disperse and integrate into the DC net

72 g, including enlargement of capillaries into venules and lymphangiogenesis.

73 and stromal cells including high endothelial venules and lymphatic vessels that resemble secondary ly

74 omes were higher in those with wider retinal venules and narrower retinal arterioles.

75 s in areas of ischemia, and predilection for venules and peripheral involvement.

76 Episodic flow within the SVP arterioles and venules and poor visualization of flow in capillaries wa

77 ovascular membranes that arise from inflamed venules and postcapillary venules, increase in size as t

78 ced by ionophore treatment of the mesenteric venules and reduced plasma vWF multimers.

79 ocyte extravasation through high endothelial venules and reduced subsequent parenchymal motility.

80 aster than across conventional postcapillary venules and requires a unique set of adhesion receptors

81 high shear forces exist in high endothelial venules and sinusoids, respectively.

82 t inflammation were identified within portal venules and stained with insulin.

83 brand factor)-platelet strings in mesenteric venules and that this is dependent on PAD4 enzymatic act

84 hrough EC junctions within mouse cremasteric venules and that this response is elicited following red

85 rmined by the distribution of arterioles and venules and their respective relative flow rates.

86 cularized by aquaporin-1(+) high endothelial venules and vascular cell adhesion molecule-positive ves

87 with increased interendothelial cell gaps in venules and was reversed by transfusion with wild-type e

88 the microvasculature (capillaries and small venules) and the macrovasculature (large veins), respect

89 stress (WSS) were measured in arterioles and venules, and compared between DR and C subjects using ge

90 sed adhesion and a reduced occlusion time in venules, and displayed a higher aggregation rate after t

91 r content and organization, high endothelial venules, and lymphatic vessels (LVs).

92 hesion molecule 1 on the DLN high endothelia venules, and production of IL-6 and CC chemokines, all c

93 es are situated adjacent to high endothelial venules, and some lymphocytes access these sinuses withi

94 The BOLD signal originated primarily from venules, and the CBV signal from arterioles.

95 by engaging selectins as leukocytes roll in venules, and they move to the raft-enriched uropods of p

96 ymphatics have barrier properties similar to venules, and thus participate in exchange.

97 1.4 mum; P-trend = 0.03) and boys had wider venules ( approximately 2.3 mum; P-trend = 0.02).

98 thin the perivascular cuff of post-capillary venules are highly glycolytic as manifested by strong ex

99 alth conditions suggested that wider retinal venules are not simply an artifact of co-occurring healt

100 t lymphocyte exit sites in deeper lymph node venules, as dogma dictates, has a dominant function in a

101 mild leukocyte adhesion occurred in mCMV-ND venules at 7 and 21 weeks p.i. HC alone caused temporary

102 rives the transformation of capillaries into venules at an early stage of the sustained inflammatory

103 Most leukocytes can roll along the walls of venules at low shear stress (1 dyn cm-2), but neutrophil

104 erns of laminin proteins in high endothelial venule basement membranes and the cortical ridge that co

105 the LFA-1-dependent crawling in unstimulated venules becomes Mac-1 dependent upon inflammation, likel

106 ch neutrophils adhered to the endothelium of venules but did not extravasate into the tissue.

107 a dextran from capillaries and postcapillary venules but had no effect on extravasation of 70-kDa dex

108 bited increased firm adhesion to Peyer patch venules but reduced homing to the gut.

109 pha4beta7 enhanced adhesion to Peyer's patch venules, but suppressed lymphocyte homing to the gut, di

110 lated in the endothelium of high endothelial venules by the inflammatory cytokine tumor necrosis fact

111 igands CD34 and CD54 on the high endothelial venule can be enhanced during inflammation.

112 work needs to be highly organized, including venules, capillaries, and arterioles, to supply all of t

113 e, characterized by leukocyte recruitment in venules, capture of circulating red blood cells, reducti

114 composite models of the human postcapillary venule, combining ECs with PCs or PC-deposited BM, to be

115 surements with a magnified effect in retinal venules compared with arteries.

116 er amplify leukocytes adhesion to intestinal venules compared with either hypoxemia or hemorrhagic sh

117 arrower retinal arterioles and wider retinal venules conferred long-term risk of mortality and ischem

118 ge diameter of retinal arterioles (CRAE) and venules (CRVE), and summarized as the arteriovenous rati

119 In venules, D was higher in NDR and NPDR (P </= 0.03), whil

120 rved aberrant organization of arterioles and venules, decreased secondary branching, and dilated vess

121 Intravital microscopy of mouse mesenteric venules demonstrated that PD1n-3 DPA and RvD5n-3 DPA dec

122 Mean arteriole and venule diameter in the inner and outer zones.

123 significant difference between the baseline venule diameter of the diabetic and the control groups (

124 The control group showed no change in the venule diameter.

125 In contrast, venules dilate only in response to prolonged stimulation

126 zed exclusively to perivenular cells, not to venule endothelial cells.

127 eriole equivalent [CRAE] and central retinal venule equivalent [CRVE]) from digitized visual field on

128 iameters, referred to as the central retinal venule equivalent and the central retinal arteriole equi

129 t 4 new loci associated with central retinal venule equivalent, one of which is also associated with

130 on with both tortuosity and width of retinal venules, even among people without clinical diabetes, wh

131 ith dexamethasone, capillaries enlarged into venules expressing leukocyte adhesion molecules, sprouti

132 alization, the formation of high endothelial venules, follicular dendritic cell networks, functional

133 mphatic vessels, as well as high endothelial venules, form within these lymphoid aggregates, but the

134 n deposition, and increased high endothelial venule formation.

135 In all, 279 802 arterioles and 285 791 venules from 5947 participants (mean age, 67.6 years; st

136 de flow, venous valves spare capillaries and venules from being subjected to damaging elevations in p

137 Constrictions of venules from euglycemic pigs to endothelin-1 (ET-1), thr

138 ntegrin-dependent adhesion of neutrophils in venules, generated tissue factor-bearing microparticles,

139 Venules had lost their cuboidal shape, showed reduced se

140 arrower retinal arterioles and wider retinal venules have been associated with negative cardiovascula

141 ner (p = 0.03) than that found previously in venules having a similar diameter range and under simila

142 Subjects with wider retinal venules (hazard ratio [HR], 1.13; 95% confidence interva

143 f lymphocytes by binding to high endothelial venule (HEV)-expressed ligands during recirculation.

144 cells (DC), associated with high endothelial venules (HEV) and clusters of T cells and mature DCs, in

145 rom AMP and is expressed on high endothelial venules (HEV) and subsets of lymphocytes.

146 rolling and firm arrest on high endothelium venules (HEV), thereby attributing their inefficient tra

147 c cell location relative to high endothelial venules (HEV).

148 ration, and the presence of high endothelial venules (HEV).

149 zed by greater expansion of high endothelial venules (HEVs) and lymphatic vessels in comparison to th

150 High endothelial venules (HEVs) are specialised postcapillary venules tha

151 oss vascular portals termed high endothelial venules (HEVs) because of lack of expression of the CCR7

152 ymphocyte interactions with high endothelial venules (HEVs) of lymphoid organs through binding to lig

153 Here, we demonstrate that high endothelial venules (HEVs) of the greater omentum constitute a main

154 How high endothelial venules (HEVs) permit lymphocyte transmigration while ma

155 , little is known about how high endothelial venules (HEVs) within Peyer's patches (PPs) are patterne

156 e vessels, designated tumor high endothelial venules (HEVs), appear to facilitate tumor destruction b

157 LNs, their interaction with high endothelial venules (HEVs), specialized blood vessels for lymphocyte

158 tical ridge (CR) and around high endothelial venules (HEVs).

159 are recruited from blood by high-endothelial venules (HEVs).

160 howed impaired formation of high endothelial venules (HEVs).

161 teracting with and crossing high endothelial venules (HEVs).

162 CCR7 signaling to adhere to high endothelial venules (HEVs).

163 n to the luminal surface of high endothelial venules (HEVs).

164 on direct contact with the high endothelial venule in inflamed lymph node.

165 us visualization of LVs and high endothelial venules in a lymph node of a living mouse for the first

166 We found that SS cells rolled along dermal venules in a P-selectin- and E-selectin-dependent manner

167 ype 2 (VEGFR2) in the regulation of gingival venules in a rat model of experimental diabetes are exam

168 r in close association with high endothelial venules in adult lymph nodes.

169 erefore flow in arterioles, capillaries, and venules in all nine subjects.

170 M) endothelium and to inflamed postcapillary venules in an E-selectin-dependent manner.

171 jugular vein, and cremasteric arterioles and venules in Apoe(-/-)and CatG-deficient mice (Apoe(-/-)Ct

172 neutrophils extravasate from inflamed dermal venules in close proximity to perivascular macrophages,

173 d extravasation in inflamed cremaster muscle venules in comparison with control animals.

174 rk of arterioles, bona fide capillaries, and venules in FGF9-expressing tumors.

175 aser injury in both cremaster arterioles and venules in FVIII(null) mice either infused with FVIII or

176 phocytes via L-selectin and high endothelial venules in lymph nodes and demonstrates how the presence

177 ly a few tissues, including high endothelial venules in lymph nodes, but inflammatory signals can upr

178 driving force for capillary remodeling into venules in M. pulmonis-infected mouse airways.

179 ates parasite sequestration in postcapillary venules in P. falciparum malaria.

180 d marginalized in the lumen of postcapillary venules in postmortem brain tissue derived from cases of

181 ions of individual penetrating arterioles or venules in rat cortex.

182 ct the external lamina with high endothelial venules in T-cell areas and also extend into germinal ce

183 required for remodeling of capillaries into venules in the airways of mice with Mycoplasma infection

184 ssageways around arterioles, capillaries and venules in the brain, along which a range of substances

185 lerated thrombus formation in arterioles and venules in the cerebral vasculature of mice that express

186 EGFR2 expression in the mast cells along the venules in the diabetic group, whereas mast cells were r

187 increased presence of small capillaries and venules in the infarcted zones by CD31 staining.

188 are essential for endothelial homeostasis in venules in the lung and that perturbation in ERG-APLNR s

189 il rolling and adhesion to the postcapillary venules in the mouse ears is significantly attenuated ev

190 ns in vitro and in inflamed cremaster muscle venules in the situation in vivo.

191 from pulmonary arterioles to capillaries and venules in two-dimensional oxygen saturation maps.

192 sustain neutrophil adhesion in postcapillary venules in vivo.

193 kness is well established in capillaries and venules in vivo.

194 d (>60%) leukocyte adhesion to postcapillary venules in wild type and Fpr1(-/-), but not Fpr2/Alx(-/-

195 is demonstrated in inflamed cremaster muscle venules, in a peritonitis model, and in an in vitro chem

196 rise from inflamed venules and postcapillary venules, increase in size as the disease progresses, and

197 eeding model and a cremaster laser arteriole/venule injury model, there were limitations to platelet-

198 igrate into inflamed murine cremaster muscle venules, instead persisting between the endothelium and

199 , and prevented homing from high endothelial venules into murine LNs.

200 induced neutrophil emigration from cremaster venules into the tissues of P2X1(-/-) mice.

201 al migration of neutrophils in postcapillary venules is a key event in the inflammatory response agai

202 ectin binding to lymph node high endothelial venules is reduced in the absence of ST3Gal-VI and to a

203 previously known as NF from high endothelial venules) is an IL-1 family cytokine that signals through

204 thelial injury/thrombosis in the cremasteric venules, lactadherin-deficient mice had significantly sh

205 g sickle red blood cells (sRBCs) in inflamed venules, leading to critical reduction in blood flow and

206 s the normal cathepsin-CPI balance in nearby venules, leading to degradation of their basement membra

207 sis, which obliterate the lumen of pulmonary venules, leading to pulmonary hypertension, right ventri

208 including overadherence to high-endothelial venules, less interstitial migration and inefficient com

209 In inflamed venules, leukocytes use P-selectin glycoprotein ligand-1

210 sed of aberrant clusters of malformed dermal venule-like channels underlying hyperkeratotic skin.

211 low chamber experiments, under postcapillary venule-like flow conditions, the pretreatment of HUVECs,

212 completely stopped in all the arterioles and venules (median RBC velocity in first-order arterioles,

213 es (adjacent arterioles minus DH [DeltaA] or venules minus DH [DeltaV]).

214 width of arterioles (MWa) and mean width of venules (MWv).

215 In inflamed venules, neutrophils roll on P- or E-selectin, engage P-

216 In inflamed venules, neutrophils rolling on E-selectin induce integr

217 helial growth factor (VEGF)-A occurs through venules, not capillaries, and particularly through the v

218 Bleeding-observed mostly from venules-occurred as early as 20 minutes after challenge,

219 VWF-platelet strings that form on venules of Adamts13(-/-) mice were immediately cleared a

220 esion and platelet-neutrophil aggregation in venules of Berkeley (SCD) mice challenged with tumor nec

221 ificant vasoconstriction was observed in the venules of diabetic rats compared with the baseline (81.

222 mesenteric collecting lymphatic vessels and venules of juvenile male rats.

223 had high expression in the high endothelial venules of lymphoid organs and was secreted.

224 performed intravital microscopy in cremaster venules of mice reconstituted with bone marrow from LysM

225 ced leukocyte rolling (approximately 40%) in venules of mice.

226 -Woods et al. tracked neutrophils in vivo in venules of mouse striated muscle and revealed how endoth

227 re slowly on P-selectin in trauma-stimulated venules of Selp(KI) (/) (KI) mice.

228 Arterioles and venules of smaller diameters (20-35.5 mum) showed better

229 In inflamed cremaster muscle venules of St3gal6-null mice, we found impaired P-select

230 flowing within mildly inflamed postcapillary venules of the cremaster muscle in vivo.

231 electin on activated murine platelets and in venules of the cremaster muscle subjected to trauma.

232 2 results in leak formation in postcapillary venules of the inflamed cremaster muscle at sites of neu

233 alved the efficiency of neutrophil arrest in venules of the mouse cremaster muscle.

234 d leukocyte rolling and adhesion in cerebral venules of wild-type (WT) mice, which were further exace

235 as might occur to connect capillary beds to venules or lymphatics.

236 nt physiological (capillaries vs. arterioles/venules) or pathological (ischemia, inflammation) levels

237 ar pulsation amplitude (arterioles P = .028; venules P < .0001).

238 Interrogation of an arteriole-venule pair revealed that 92+/-7% (n=6) of MSCs arrest a

239 e, there are 11 muscle fibers, 0.4 arteriole/venule pairs, and 0.2 IL vessels per fascicle.

240 Superfusing CXCL1 over venules promoted neutrophil migration only after intrave

241 of 27 to 76 Ws (arterioles' range: 85%-92%; venules' range: 45%-53%).

242 nal vein equivalent (CRVE), and arteriole-to-venule ratio (AVR) at baseline.

243 nal vein equivalent (CRVE), and arteriole-to-venule ratio (AVR) at baseline.

244 the control group, whereas the arteriole to venule ratio and vascular tortuosity were significantly

245 nal vein equivalent (CRVE), the arteriole to venule ratio, tortuosity, and fractal dimension were mea

246 e higher hydrostatic pressure experienced by venules relative to collecting lymphatics in vivo.

247 Arrest of rapidly flowing neutrophils in venules relies on capturing through selectins and chemok

248 ice, whereas transcytosis in capillaries and venules remained unchanged.

249 sis factor-alpha-stimulated cremaster muscle venules revealed severely compromised leukocyte adhesion

250 dothelial cell interactions in postcapillary venules revealed that CXCL1-induced neutrophil adhesion

251 strated as one-way flow from arteriole(s) to venule(s) with no integration of the capillary network b

252 hat neutrophil polarization within activated venules served to organize a protruding domain that enga

253 aries varied drastically (from 4-20 min) and venules showed relatively slower recovery (~12 min).

254 Intravital microscopy of mesenteric venules showed that leukocyte rolling time was decreased

255 ntravital microscopy of live mouse cremaster venules showed that these vesicles can selectively bind

256 However, TNF increased murine P-selectin in venules, slowing rolling and increasing adhesion, wherea

257 llaries enlarge and acquire the phenotype of venules specialized for plasma leakage and leukocyte rec

258 of either Erg or Aplnr results in pulmonary venule-specific endothelial proliferation in vitro.

259 n amplitude of retinal arterioles (SRAP) and venules (SRVP).

260 il extravasation occurs across postcapillary venules, structures composed of endothelial cells (ECs),

261 retinal vein occlusions or adjacent retinal venules, suggesting an arterial source.

262 ophrenia were distinguished by wider retinal venules, suggesting microvascular abnormality reflective

263 lar in magnitude to adjacent arterioles than venules, supporting an arterial origin for DH.

264 macrophages, plasma cells, high endothelial venules, supporting follicular dendritic cells network,

265 anced intratumor content of high endothelial venules surrounded by high CD8(+) T-cell density.

266 tion during which capillaries transform into venules that expand the region of the vasculature in whi

267 eferentially recruited to a unique subset of venules that express high levels of intercellular adhesi

268 venules (HEVs) are specialised postcapillary venules that specifically serve this function and are fo

269 d the remodeling of mucosal capillaries into venules, the amount of leukocyte influx, and disease sev

270 esidential macrophages near high endothelial venules, the results highlight critical roles of innate/

271 Neutrophils roll on E-selectin in inflamed venules through interactions with cell-surface glycoconj

272 he functional adaptation of high endothelial venules to accelerate naive T cell recruitment to the ly

273 imetry (micro-PIV) in mouse cremaster muscle venules to estimate the hydrodynamically relevant glycoc

274 he functional adaptation of high endothelial venules to increase naive T cell trafficking to the lymp

275 as histamine and bradykinin act directly on venules to increase the permeability of endothelial cell

276 s was effectively drained by the penetrating venules to limit lateral perfusion.

277 Neutrophils emigrate from venules to sites of infection or injury in response to c

278 ll proliferation, increased high endothelial venule trafficking efficiency and VCAM-1 expression, and

279 increased activity of cathepsins (B>S>L) in venules transitioning into MV, as well as from a recipro

280 e interactions within inflamed postcapillary venules under conditions of blood flow by intravital mic

281 he basement membrane of dermal postcapillary venules undergoes changes in structure and composition.

282 in both retinal arterioles (up to 110%) and venules (up to 92%), with a more pronounced increase in

283 As with venules, vasoactive agents can alter both the permeabili

284 Leukocyte adherence to cortical venules was attenuated in response to stroke, as well as

285 No reperfusion of arterioles or venules was observed at M3 on FA or SS-WF OCTA.

286 ha-challenged mouse cremaster post-capillary venules, we demonstrate that fluorescently tagged albumi

287 Changes in diameter of the selected gingival venule were measured by vital microscopy combined with d

288 Wider venules were also associated with a dimensional measure

289 Less tortuous retinal arterioles and venules were associated with all glaucomas, but only sig

290 Thinner venules were associated with high-density lipoprotein (H

291 2 diabetes (6.5%; 95% CI, 2.8%-10.4%); wider venules were associated with older age (2.6 mum; 95% CI,

292 Retinal venules were isolated from pigs with streptozocin-induce

293 Retinal pigment and dipping venules were present in 100% of eyes.

294 nute flows down to 0.3 mm/s in arterioles or venules were readily detectable at depths down to 3.2 mm

295 ic conductivity of collecting lymphatics and venules were similar, the contribution of convective cou

296 slower onset (0.97 s), whereas dilations in venules were smaller (1.0%) and slower (1.06 s) still.

297 aggregates associated with high endothelial venules) were detectable in 9 of 13 heart allografts stu

298 CXCR4 to get access across high endothelial venules, whereas macrophage-1 Ag, LFA-1, and CXCR4 were

299 ts originated from capillaries (and possibly venules), with the earliest detectable morphological abn

300 elopment of PNAd-expressing high endothelial venules within intragraft lymphoid follicles and the rec