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 ular annulus, which comprised post-capillary venules.

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

4 r, allowing rapid transit from arterioles to venules.

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

6 emodynamics were assessed in randomly chosen venules.

7 mean circulation time between arterioles and venules.

8 and in deep ascending cortical postcapillary venules.

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

10 alpha in KRIT1 deficient arterioles, but not venules.

11 necting terminal arterioles to postcapillary venules.

12 ndothelial cells in intestinal postcapillary venules.

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

14 all, hemostatically active thrombi formed in venules.

15 perfused unstimulated or TNF-alpha-activated venules.

16 of capillaries into vessels with features of venules.

17 vascular channels of thymic corticomedullary venules.

18 licular dendritic cells and high endothelial venules.

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

20 giogenesis, mother vessels, are derived from venules.

21 t pericytes and were more prevalent in small venules.

22 evels similar to that found in postcapillary venules.

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

24 nly in small vessels such as capillaries and venules.

25 ncreases leukocyte adhesion in postcapillary venules.

26 nt or sustained fashion, on high endothelial venules.

27 ic cells, stromal cells and high endothelial venules.

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

29 + B lymphocytes were dominant in bone marrow venules.

30 turing circulating red blood cells (RBCs) in venules.

31 ewis X L-selectin ligand in high endothelial venules.

32 d 6-sulfo sialyl Lewis X on high endothelial venules.

33 e leukocyte adherence receptor P-selectin in venules.

34 ng their passage through cytokine-stimulated venules.

35 semiautomated measurements of arterioles and venules.

36 n vivo crawling and TEM in the postcapillary venules.

37 was reduced in interleukin-1beta-stimulated venules.

38 icking of lymphocytes along high endothelial venules.

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

40 following injuries to mouse cremaster muscle venules.

41 ty at the level of individual arterioles and venules.

42 pre-capillary arterioles and post-capillary venules.

43 ries which connect peripheral arterioles and venules.

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

45 n-dependent adhesion in airway postcapillary venules.

46 al involvement in neutrophil emigration from venules.

47 l arrangement of arterioles, capillaries and venules.

48 ormation of lymph nodes and high endothelial venules.

49 but also from blood, across high endothelial venules.

50 of endogenous Tregs in dermal postcapillary venules.

51 and extensive induction of high endothelial venules.

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

53 of 96 +/- 18.3 microm, mean +/- S.E.M.) and venules (-14.4 +/- 4.0% from 249 +/- 25.8 microm; P < 0.

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

55 0+/-6 versus 32+/-5 bacteria) and collecting venules (48+/-5 versus 18+/-4 bacteria; P<0.05) of VWF k

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

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

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

59 hether optic disc size is related to retinal venule and arteriole diameters.

60 Narrower retinal venules and arterioles were found in the smaller optic d

61 to show that, after exiting high-endothelial venules and before entry into lymph node follicles, B ce

62 nt of diffusive shunting between arterioles, venules and capillaries and a decrease in hemoglobin's e

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

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

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

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

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

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

69 nvestigated in mouse cremaster postcapillary venules and in flow chambers coated with P-selectin, ICA

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

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

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

73 along the endothelial wall of postcapillary venules and integrin-mediated arrest.

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

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

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

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

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

79 esion and aggregation in histamine-activated venules and promoted thrombus dissolution in injured art

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

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

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

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

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

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

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

87 t mice failed to adhere firmly to stimulated venules and to migrate into sites of inflammation.

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

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

90 lows for clear identification of arterioles, venules, and capillaries, which is difficult using other

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

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

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

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

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

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

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

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

99 1.4 mum; P-trend = 0.03) and boys had wider venules ( approximately 2.3 mum; P-trend = 0.02).

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

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

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

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

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

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

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

107 lls and leukocytes adhered to arterioles and venules but did not affect overall blood flow, and there

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

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

110 leukocytes in capillaries and postcapillary venules, but no such adhesion in arterioles.

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

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

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

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

115 adherent leukocytes and platelets in colonic venules, caused gross and histologic injury, increased p

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

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

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

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

120 d sialyl 6-sulfo Lewis X in high endothelial venules, considerably reduced lymphocyte homing to perip

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

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

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

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

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

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

127 ability after r-FVIII infusion, the VWF(-/-) venules did not occlude.

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

129 node includes the growth of high endothelial venule endothelial cells and is functionally associated

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

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

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

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

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

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

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

137 n deposition, and increased high endothelial venule formation.

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

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

140 Venules had lost their cuboidal shape, showed reduced se

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

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

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

144 ec-6st is a highly specific high endothelial venule (HEV) gene that is crucial for regulating lymphoc

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

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

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

148 blood vessels develop from high endothelial venules (HEV), in which the proliferation rate of the en

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

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

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

152 of sialomucins displayed on high endothelial venules (HEVs) of lymph nodes.

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

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

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

156 1 chemokine, exclusively in high endothelial venules (HEVs) that are chief portals for the entry of b

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

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

159 peripheral lymph node (LN) high endothelial venules (HEVs), defined as MAdCAM-1(low) PNAd(high) LTbe

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

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

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

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

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

165 ognate T cells entering via high endothelial venules (HEVs).

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

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

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

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

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

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

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

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

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

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

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

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

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

179 carbohydrates restricted to high endothelial venules in lymph nodes.

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

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

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

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

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

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

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

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

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

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

193 he binding of L-selectin to high endothelial venules in vitro and contributed in vivo to O-glycan-ind

194 t attachment and rolling on high endothelial venules in vivo in both nonstimulated and inflamed PLNs.

195 sustain neutrophil adhesion in postcapillary venules in vivo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 es with sulfated ligands on high endothelial venules leads to rolling and is critical for recruitment

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

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

214 esion of leukocytes and platelets in colonic venules, light/dye-induced thrombus formation in cremast

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

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

217 of IL-12p40 protein around high endothelial venules located in close proximity to p40-expressing DC.

218 , CD40-positive endothelial cells in colonic venules may represent a major action of this signaling p

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

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

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

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

223 But, after a delay, all the injured venules occluded in these transgenic mice.

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

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

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

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

228 a-induced leukocyte responses in cremasteric venules of KO animals by intravital microscopy indicated

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

230 PSGL-1 was detected in venules of mesenteric lymph node and small intestine by

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

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

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

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

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

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

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

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

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

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

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

242 ter infusion (207% in arterioles and 238% in venules, p < .05 vs. baseline).

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

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

245 Superfusing CXCL1 over venules promoted neutrophil migration only after intrave

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

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

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

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

250 ilated (108 +/- 16 microm, P < 0.05) but the venules remained constricted (223 +/- 24 microm).

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

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

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

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

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

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

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

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

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

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

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

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

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

264 d more white blood cell adhesion in cerebral venules than their wild-type counterparts, and this was

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

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

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

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

269 intravital microscopy in parietal subsurface venules through a closed cranial window.

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

271 gulate neutrophil migration in postcapillary venules through the presentation of various adhesion lig

272 rtuosity indices of the arterioles (TIA) and venules (TIV) were calculated.

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

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

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

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

277 y and incidence and panretinal arteriole and venule tortuosity indexes (TI(a), TI(v)) were measured f

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

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

287 Wider venules were also associated with a dimensional measure

288 licles while lymphatics and high endothelial venules were found at the B cell/T cell interface.

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

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

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

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

293 the walls of unstimulated murine cremasteric venules where expression of key vascular basement membra

294 ffective, direct access to the postcapillary venules, where the target event (leukocyte-endothelial i

295 y recruited in surgery-activated cremasteric venules, whereas adherent CD45+ B220+ B lymphocytes were

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

297 leukocyte adhesion was assessed in cortical venules with intravital video microscopy.

298 scence intensity in submucosal postcapillary venules with the use of intravital microscopy.

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

300 eukocyte and platelet recruitment in colonic venules, with measurements obtained for tissue myelopero