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1 ravital microscopic observations in the mice cremaster muscle.
2 ctions in postcapillary venules of the mouse cremaster muscle.
3 ibroblast growth factor implanted on the rat cremaster muscle.
4 n in lung, skin and postcapillary venules of cremaster muscle.
5 tion to mCRP in inflamed but not noninflamed cremaster muscle.
6 of neutrophil arrest in venules of the mouse cremaster muscle.
7 heir firm adhesion to the endothelium in rat cremaster muscle.
8 d histamine-induced leukocyte rolling in the cremaster muscle.
9 easured in mice after arterial injury in the cremaster muscle.
10 as consistent with that reported for the rat cremaster muscle.
11 oth muscle cells (SMCs) compared to those of cremaster muscle.
12 mals in the peritonitis model but not in the cremaster muscle.
13  by using intravital microscopy of the mouse cremaster muscle.
14 died the permeability of microvessels in the cremaster muscle.
15 zed with a microcirculation model of exposed cremaster muscle.
16  50 V) in 2nd or 3rd order arterioles of the cremaster muscle.
17 ital confocal microscopy applied to inflamed cremaster muscles.
18      In response to field stimulation of the cremaster muscle (0.5, 1, 3 Hz), venular dilator and hyp
19 and transmigration in the TNF-alpha-inflamed cremaster muscle and a prolongation of chemokine-depende
20 o the endothelium in the vessels of lung and cremaster muscle and decreased the numbers of inflammato
21 t not of nonclassical monocytes in the mouse cremaster muscle and in in vitro flow chamber assays.
22 sis by 3D intravital video microscopy in the cremaster muscle and omentum, the major site of neutroph
23  vivo, LPS-induced inflammation in the mouse cremaster muscle and peritoneal cavity led to ICAM-1 exp
24 f experiments, the adhesion of leukocytes to cremaster muscle and the dynamics of thrombus formation
25 n venules of untreated and TNF-alpha-treated cremaster muscles and in Peyer's patch high endothelial
26 sinophil extravasation into CCL11-stimulated cremaster muscles and into the inflamed peritoneal cavit
27  for rolling in inflamed microvessels of the cremaster muscle are completely Core2GlcNAcT-I dependent
28 lower rolling, and increased adhesion in the cremaster muscle are dependent on L-selectin.
29     Isolated first-order arterioles from rat cremaster muscle are under dual regulation by insulin, w
30  rat vascular smooth muscle (VSM) cells from cremaster muscle arterioles and cerebral arteries.
31  FNIII-1-containing fibronectin fragments to cremaster muscle arterioles in situ, triggered a rapid,
32 Purkinje cell network in vitro and in ECs of cremaster muscle arterioles in vivo.
33 ion of function-blocking FNIII-1 peptides to cremaster muscle arterioles rapidly and specifically dec
34  myography to study rat isolated first-order cremaster muscle arterioles the AT1 R inhibitor candesar
35  and light/dye-induced thrombus formation in cremaster muscle arterioles were measured in wild-type (
36 ion, prior to laser-induced injury in murine cremaster muscle arterioles, resulted in formation of sm
37  in vivo thrombosis models in mesenterium or cremaster muscle arterioles, we demonstrate that Bambi-d
38 teric arterioles and laser-induced injury of cremaster muscle arterioles, we herein show that thrombi
39 vital microscopy and laser-induced injury to cremaster muscle arterioles, we show that thrombi formed
40 ned using microparticle image velocimetry in cremaster-muscle arterioles of wild-type mice.
41                       We have used the mouse cremaster muscle as a model of trauma- and cytokine-indu
42 ion in postcapillary venules of the inflamed cremaster muscle at sites of neutrophil extravasation, a
43 or macromolecules, RBCs, and WBCs in hamster cremaster muscle capillaries.
44 ation predominates (>/=90% of events) in the cremaster muscle circulation, but transcellular migratio
45 cruitment in untreated and TNF-alpha-treated cremaster muscles comparing ppGalNAcT-1-deficient mice (
46           Intravital microscopy of the mouse cremaster muscle confirmed the defect of CXCL1-induced l
47 hemic or tumor necrosis factor-alpha-treated cremaster muscle demonstrated that MAPCs migrate to peri
48          Immunohistochemical analysis of the cremaster muscle demonstrated that neovascularization in
49  of neutrophil migration in vitro and in the cremaster muscle demonstrated that stroke alone did not
50 ibrils in the extracellular matrix of intact cremaster muscle, demonstrating active polymerization of
51 l field stimulation was used to contract the cremaster muscle for 15 s at 30 Hz.
52            Surgical preparation of the mouse cremaster muscle for intravital microscopy induced P-sel
53      PAF increased permeability in wild-type cremaster muscle from a baseline of 2.4 +/- 2.2 to a pea
54   Topical application of fMLP onto the whole cremaster muscle generated the same number of adherent l
55  microscopy was performed on an exteriorized cremaster muscle in 11 wild-type mice to study the micro
56 al confocal microscopy of anesthetized mouse cremaster muscle in combination with immunofluorescence
57 was assessed by intravital microscopy of the cremaster muscle in mice treated for 4 days with sustain
58 firm neutrophil attachment to venules in the cremaster muscle in response to N-formyl- methionyl-leuc
59 sed adhesion of leukocytes to endothelium in cremaster muscle in vivo and with thrombosis in a mouse
60 m bovine heart endothelium) and in the mouse cremaster muscle in vivo.
61 mildly inflamed postcapillary venules of the cremaster muscle in vivo.
62 n E-selectin in TNF-alpha-treated venules of cremaster muscle in which P-selectin function was blocke
63   Intravital microscopy of TNFalpha-inflamed cremaster muscles in Myo1e-deficient mice revealed that
64 recruited more effectively in mouse inflamed cremaster muscles in vivo.
65 rosis factor-alpha (TNF-alpha)-treated mouse cremaster muscles in wild-type mice and gene-targeted mi
66                Functional studies in the rat cremaster muscle indicate that alpha1ARs predominate in
67        Using in vivo microscopy on the mouse cremaster muscle, intravascular adherence and subsequent
68 s mediated by P-selectin in the exteriorized cremaster muscle, is not further increased in response t
69 borated by intravital microscopy of inflamed cremaster muscle microcirculation in bone marrow chimera
70         We used intravital microscopy of rat cremaster muscle microcirculation to track intraarterial
71 mation following laser-induced injury in the cremaster muscle microcirculation.
72      Microvascular thrombosis was induced in cremaster muscle microvessels of normal and colitic mice
73 les, light/dye-induced thrombus formation in cremaster muscle microvessels, as well as disease activi
74 ed interactions with wild-type (WT) inflamed cremaster muscle microvessels.
75 intravital microscopic approach with a mouse cremaster muscle model.
76 gs indicate that for arterioles in the mouse cremaster muscle, nitric oxide and endothelial-derived h
77  arteries and downstream arterioles from the cremaster muscle of C57BL/6 mice.
78 n second-order arterioles (2A) supplying the cremaster muscle of C57BL6, PECAM-1-/-, and eNOS-/- mice
79 2.7 units, while the corresponding values in cremaster muscle of eNOS-/- mice were 1.0 +/- 0.3 and 15
80 l reconstructions were performed in skin and cremaster muscle of guinea-pigs, mice and rats injected
81 croscopy of postcapillary venules within the cremaster muscle of mice revealed that a significantly g
82 avital microscopy of inflamed vessels of the cremaster muscle of mice.
83                            Using the in situ cremaster muscle of obese Zucker rats (OZR; with lean Zu
84 sity and ultrastructure were assessed in the cremaster muscle of rats subjected to a 75% surgical red
85 applied directly to resistance arterioles in cremaster muscles of anaesthetized (pentobarbital sodium
86  fibres underlying a group of capillaries in cremaster muscles of anaesthetized hamsters were electri
87 tor-alpha (TNFalpha)-pretreated autoperfused cremaster muscles of C2GlcNAcT-I-deficient (core 2(-/-))
88                                          The cremaster muscles of these mice were treated with TNF-al
89                                          The cremaster muscles of these mice were treated with tumor
90 ere assessed by intravital microscopy of the cremaster muscles of wild-type mice following perivenula
91 onse to chemoattractants administered to the cremaster muscle or dorsal skin, but neutrophil-dependen
92 otor control in arterioles of the superfused cremaster muscle preparation of anesthetized C57Bl6 mice
93                                              Cremaster muscle preparations revealed endothelial dysfu
94  Vasopressin was superfused topically on the cremaster muscle resistance arterioles (15 to 25 microns
95       Complementary experiments in the mouse cremaster muscle revealed a pattern of alphaAR subtype d
96                 Intravital microscopy of the cremaster muscle revealed almost no rolling at times up
97     In vivo microscopy on the inflamed mouse cremaster muscle revealed that blockade of serine protea
98 t to a venule of the TNF-alpha-treated mouse cremaster muscle significantly increased the number of a
99        In the multiple tissues analyzed (eg, cremaster muscle, skin, mesenteric tissue), LERs were di
100 vated murine platelets and in venules of the cremaster muscle subjected to trauma.
101  a mouse model of microcirculation using the cremaster muscle that allows direct microscopic examinat
102 ls and intravital microscopy of the inflamed cremaster muscle that CD95 mediates leukocyte slow rolli
103      By using intravital microscopy of mouse cremaster muscle, the in vivo effects of several particu
104 ired in fMLP-induced transmigration into the cremaster muscle, thioglycollate-induced peritonitis, an
105 opy experiments were performed using the rat cremaster muscle to visually observe the formation of oc
106 rosis factor-alpha (TNF-alpha)-treated mouse cremaster muscles to quantitatively investigate the pote
107 ocyte adhesion and extravasation in inflamed cremaster muscle venules in comparison with control anim
108        We performed intravital microscopy of cremaster muscle venules in T-GFP mice, in which naive T
109 der flow conditions in vitro and in inflamed cremaster muscle venules in the situation in vivo.
110 investigated neutrophil adhesion in inflamed cremaster muscle venules in tumor necrosis factor (TNF)-
111 ge velocimetry (micro-PIV) was used in mouse cremaster muscle venules in vivo to measure velocity pro
112                     Intravital microscopy of cremaster muscle venules indicated that the leukocyte ro
113 e rolling was almost completely abolished in cremaster muscle venules of core2(-/-) mice, but not lit
114             These beads showed no rolling in cremaster muscle venules of core2(-/-) mice, but signifi
115                                  In inflamed cremaster muscle venules of St3gal6-null mice, we found
116 is of tumor necrosis factor-alpha-stimulated cremaster muscle venules revealed severely compromised l
117           TNF-alpha- treated CD18 null mouse cremaster muscle venules show increased leukocyte rollin
118 microscopy of untreated or TNF-alpha-treated cremaster muscle venules showed EGFP+ cells in vivo, but
119 ticle image velocimetry (micro-PIV) in mouse cremaster muscle venules to estimate the hydrodynamicall
120                                           In cremaster muscle venules treated with both TNF-alpha and
121              Leukocyte rolling velocities in cremaster muscle venules were increased significantly in
122  ligand, CCL19, triggered T cell sticking in cremaster muscle venules, but failed to induce extravasa
123 cient leukocytes is demonstrated in inflamed cremaster muscle venules, in a peritonitis model, and in
124  were unable to migrate into inflamed murine cremaster muscle venules, instead persisting between the
125 rotein transport following injuries to mouse cremaster muscle venules.
126 oss endothelium of initial lymphatics in rat cremaster muscle was investigated with micropipette mani
127               Intravital microscopy of mouse cremaster muscle was performed after intravenous injecti
128 copy of the microcirculation of exteriorized cremaster muscle was performed in 12 wild-type mice duri
129 y and simultaneous ultrasound imaging of the cremaster muscle was performed in 6 mice to determine wh
130                 Intravital microscopy of the cremaster muscle was performed in six wild-type mice and
131 copy of tissue necrosis factor-alpha-treated cremaster muscle was performed to assess the microvascul
132 l microscopy in postcapillary venules of the cremaster muscle, was markedly decreased 30 min after tr
133     Using intravital microscopy of the mouse cremaster muscle, we found that TNF-alpha and IL-17 also
134 al confocal microscopy of anesthetized mouse cremaster muscle, we separately examined the crawling an
135  confocal intravital microscopy to the mouse cremaster muscle, we show that neutrophils responding to
136 here to the endothelium in TNF-alpha-treated cremaster muscle, whereas PI3Kdelta was not required.
137 assessing experimental angiogenesis, the rat cremaster muscle, which permits live videomicroscopy and
138      Quantitative fluorescence microscopy of cremaster muscle whole mounts using rhodamine-labeled Gr

 
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