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1 d severalfold in the omentum, but not in the cremaster.
2  increased in the interleukin-1beta inflamed cremaster.
3                                   Studies in cremaster and cerebral VSMCs show heterogeneity of BKCa
4 impairs neutrophil recruitment into inflamed cremaster and peritoneum.
5 l3-induced carotid thrombosis, laser-induced cremaster arteriolar injury, and inferior vena cava (IVC
6 ckout mice have reduced laser injury-induced cremaster arteriolar thrombus formation and prolonged Fe
7 (a major source of RGD sequences) also cause cremaster arteriolar vasodilation through the alpha v be
8 ormation following laser injury in two mouse cremaster arteriole injury model data: one wild-type mou
9 n and platelet accumulation in laser-induced cremaster arteriole injury, and PDI(ss-oo) mice had atte
10  FVa and FXa after laser injury in the mouse cremaster arteriole.
11 amined clot response to laser injury in both cremaster arterioles and venules in FVIII(null) mice eit
12 t and a decrease in the beta1:alpha ratio in cremaster arterioles compared to cerebral vessels.
13 brin formation after laser-induced injury of cremaster arterioles compared with control mice but with
14 ant delay in time to thrombotic occlusion in cremaster arterioles compared with wild-type littermates
15   DSS colitis enhanced thrombus formation in cremaster arterioles of wild-type mice.
16                                   Similarly, cremaster arterioles showed a decrease in total BKCa pro
17 effect on basal vascular tone or response of cremaster arterioles to vasoactive compounds.
18  and induced potent dilation of isolated rat cremaster arterioles, both of which were specifically bl
19 ed vasodilation when applied to isolated rat cremaster arterioles.
20                                   In a mouse cremaster artery laser injury model, a single intravenou
21                                              Cremaster BKCa channels thus demonstrated an approximate
22 e produced within the vasculature in the rat cremaster, effectively occluding blood flow.
23 llowing injection, the number of MSCs in the cremaster further decreased to 14% of the initial number
24                              Transplanted WT cremaster in p75-/- mice showed a robust leukocyte rolli
25                              However, in the cremaster injury model, only pcBF8 was more effective, m
26 er, in both a cuticular bleeding model and a cremaster laser arteriole/venule injury model, there wer
27 nesis, we mated activin transgenic mice with CreMaster mice, which are characterized by Cre recombina
28 gfr2-deficient mice with mast cell-deficient CreMaster mice.
29 od vessels of the isolated retina and in the cremaster microcirculation of anesthetized mice.
30 , intravital microscopy studies of the mouse cremaster microcirculation showed that tumor necrosis fa
31 eposited in the postcapillary venules of the cremaster microcirculation, secondary to increased vascu
32  delayed thrombosis after carotid artery and cremaster microvascular injury without affecting paramet
33                           We used an in vivo cremaster model (hamster and mouse) in which circulating
34 y intravital microscopic studies in a murine cremaster model of inflammation.
35 y roll slower and adhere more readily in the cremaster model than wild-type neutrophils.
36 s identified by intravital microscopy in the cremaster model.
37      In response to field stimulation of the cremaster muscle (0.5, 1, 3 Hz), venular dilator and hyp
38 and transmigration in the TNF-alpha-inflamed cremaster muscle and a prolongation of chemokine-depende
39 o the endothelium in the vessels of lung and cremaster muscle and decreased the numbers of inflammato
40 t not of nonclassical monocytes in the mouse cremaster muscle and in in vitro flow chamber assays.
41 sis by 3D intravital video microscopy in the cremaster muscle and omentum, the major site of neutroph
42  vivo, LPS-induced inflammation in the mouse cremaster muscle and peritoneal cavity led to ICAM-1 exp
43 f experiments, the adhesion of leukocytes to cremaster muscle and the dynamics of thrombus formation
44  for rolling in inflamed microvessels of the cremaster muscle are completely Core2GlcNAcT-I dependent
45 lower rolling, and increased adhesion in the cremaster muscle are dependent on L-selectin.
46     Isolated first-order arterioles from rat cremaster muscle are under dual regulation by insulin, w
47  rat vascular smooth muscle (VSM) cells from cremaster muscle arterioles and cerebral arteries.
48  FNIII-1-containing fibronectin fragments to cremaster muscle arterioles in situ, triggered a rapid,
49 Purkinje cell network in vitro and in ECs of cremaster muscle arterioles in vivo.
50 ion of function-blocking FNIII-1 peptides to cremaster muscle arterioles rapidly and specifically dec
51  myography to study rat isolated first-order cremaster muscle arterioles the AT1 R inhibitor candesar
52  and light/dye-induced thrombus formation in cremaster muscle arterioles were measured in wild-type (
53 ion, prior to laser-induced injury in murine cremaster muscle arterioles, resulted in formation of sm
54  in vivo thrombosis models in mesenterium or cremaster muscle arterioles, we demonstrate that Bambi-d
55 teric arterioles and laser-induced injury of cremaster muscle arterioles, we herein show that thrombi
56 vital microscopy and laser-induced injury to cremaster muscle arterioles, we show that thrombi formed
57                       We have used the mouse cremaster muscle as a model of trauma- and cytokine-indu
58 ion in postcapillary venules of the inflamed cremaster muscle at sites of neutrophil extravasation, a
59 or macromolecules, RBCs, and WBCs in hamster cremaster muscle capillaries.
60 ation predominates (>/=90% of events) in the cremaster muscle circulation, but transcellular migratio
61           Intravital microscopy of the mouse cremaster muscle confirmed the defect of CXCL1-induced l
62 hemic or tumor necrosis factor-alpha-treated cremaster muscle demonstrated that MAPCs migrate to peri
63          Immunohistochemical analysis of the cremaster muscle demonstrated that neovascularization in
64  of neutrophil migration in vitro and in the cremaster muscle demonstrated that stroke alone did not
65 l field stimulation was used to contract the cremaster muscle for 15 s at 30 Hz.
66            Surgical preparation of the mouse cremaster muscle for intravital microscopy induced P-sel
67      PAF increased permeability in wild-type cremaster muscle from a baseline of 2.4 +/- 2.2 to a pea
68   Topical application of fMLP onto the whole cremaster muscle generated the same number of adherent l
69  microscopy was performed on an exteriorized cremaster muscle in 11 wild-type mice to study the micro
70 al confocal microscopy of anesthetized mouse cremaster muscle in combination with immunofluorescence
71 was assessed by intravital microscopy of the cremaster muscle in mice treated for 4 days with sustain
72 firm neutrophil attachment to venules in the cremaster muscle in response to N-formyl- methionyl-leuc
73 sed adhesion of leukocytes to endothelium in cremaster muscle in vivo and with thrombosis in a mouse
74 m bovine heart endothelium) and in the mouse cremaster muscle in vivo.
75 mildly inflamed postcapillary venules of the cremaster muscle in vivo.
76 n E-selectin in TNF-alpha-treated venules of cremaster muscle in which P-selectin function was blocke
77                Functional studies in the rat cremaster muscle indicate that alpha1ARs predominate in
78 borated by intravital microscopy of inflamed cremaster muscle microcirculation in bone marrow chimera
79         We used intravital microscopy of rat cremaster muscle microcirculation to track intraarterial
80 mation following laser-induced injury in the cremaster muscle microcirculation.
81      Microvascular thrombosis was induced in cremaster muscle microvessels of normal and colitic mice
82 les, light/dye-induced thrombus formation in cremaster muscle microvessels, as well as disease activi
83 ed interactions with wild-type (WT) inflamed cremaster muscle microvessels.
84 intravital microscopic approach with a mouse cremaster muscle model.
85  arteries and downstream arterioles from the cremaster muscle of C57BL/6 mice.
86 n second-order arterioles (2A) supplying the cremaster muscle of C57BL6, PECAM-1-/-, and eNOS-/- mice
87 2.7 units, while the corresponding values in cremaster muscle of eNOS-/- mice were 1.0 +/- 0.3 and 15
88 l reconstructions were performed in skin and cremaster muscle of guinea-pigs, mice and rats injected
89 croscopy of postcapillary venules within the cremaster muscle of mice revealed that a significantly g
90 avital microscopy of inflamed vessels of the cremaster muscle of mice.
91                            Using the in situ cremaster muscle of obese Zucker rats (OZR; with lean Zu
92 sity and ultrastructure were assessed in the cremaster muscle of rats subjected to a 75% surgical red
93 onse to chemoattractants administered to the cremaster muscle or dorsal skin, but neutrophil-dependen
94 otor control in arterioles of the superfused cremaster muscle preparation of anesthetized C57Bl6 mice
95                                              Cremaster muscle preparations revealed endothelial dysfu
96  Vasopressin was superfused topically on the cremaster muscle resistance arterioles (15 to 25 microns
97       Complementary experiments in the mouse cremaster muscle revealed a pattern of alphaAR subtype d
98                 Intravital microscopy of the cremaster muscle revealed almost no rolling at times up
99     In vivo microscopy on the inflamed mouse cremaster muscle revealed that blockade of serine protea
100 t to a venule of the TNF-alpha-treated mouse cremaster muscle significantly increased the number of a
101 vated murine platelets and in venules of the cremaster muscle subjected to trauma.
102  a mouse model of microcirculation using the cremaster muscle that allows direct microscopic examinat
103 ls and intravital microscopy of the inflamed cremaster muscle that CD95 mediates leukocyte slow rolli
104 opy experiments were performed using the rat cremaster muscle to visually observe the formation of oc
105 ocyte adhesion and extravasation in inflamed cremaster muscle venules in comparison with control anim
106        We performed intravital microscopy of cremaster muscle venules in T-GFP mice, in which naive T
107 der flow conditions in vitro and in inflamed cremaster muscle venules in the situation in vivo.
108 investigated neutrophil adhesion in inflamed cremaster muscle venules in tumor necrosis factor (TNF)-
109 ge velocimetry (micro-PIV) was used in mouse cremaster muscle venules in vivo to measure velocity pro
110                     Intravital microscopy of cremaster muscle venules indicated that the leukocyte ro
111 e rolling was almost completely abolished in cremaster muscle venules of core2(-/-) mice, but not lit
112             These beads showed no rolling in cremaster muscle venules of core2(-/-) mice, but signifi
113                                  In inflamed cremaster muscle venules of St3gal6-null mice, we found
114 is of tumor necrosis factor-alpha-stimulated cremaster muscle venules revealed severely compromised l
115           TNF-alpha- treated CD18 null mouse cremaster muscle venules show increased leukocyte rollin
116 microscopy of untreated or TNF-alpha-treated cremaster muscle venules showed EGFP+ cells in vivo, but
117 ticle image velocimetry (micro-PIV) in mouse cremaster muscle venules to estimate the hydrodynamicall
118                                           In cremaster muscle venules treated with both TNF-alpha and
119              Leukocyte rolling velocities in cremaster muscle venules were increased significantly in
120  ligand, CCL19, triggered T cell sticking in cremaster muscle venules, but failed to induce extravasa
121 cient leukocytes is demonstrated in inflamed cremaster muscle venules, in a peritonitis model, and in
122  were unable to migrate into inflamed murine cremaster muscle venules, instead persisting between the
123 rotein transport following injuries to mouse cremaster muscle venules.
124 oss endothelium of initial lymphatics in rat cremaster muscle was investigated with micropipette mani
125               Intravital microscopy of mouse cremaster muscle was performed after intravenous injecti
126 copy of the microcirculation of exteriorized cremaster muscle was performed in 12 wild-type mice duri
127 y and simultaneous ultrasound imaging of the cremaster muscle was performed in 6 mice to determine wh
128                 Intravital microscopy of the cremaster muscle was performed in six wild-type mice and
129 copy of tissue necrosis factor-alpha-treated cremaster muscle was performed to assess the microvascul
130      Quantitative fluorescence microscopy of cremaster muscle whole mounts using rhodamine-labeled Gr
131 ibrils in the extracellular matrix of intact cremaster muscle, demonstrating active polymerization of
132        Using in vivo microscopy on the mouse cremaster muscle, intravascular adherence and subsequent
133 s mediated by P-selectin in the exteriorized cremaster muscle, is not further increased in response t
134 gs indicate that for arterioles in the mouse cremaster muscle, nitric oxide and endothelial-derived h
135        In the multiple tissues analyzed (eg, cremaster muscle, skin, mesenteric tissue), LERs were di
136      By using intravital microscopy of mouse cremaster muscle, the in vivo effects of several particu
137 ired in fMLP-induced transmigration into the cremaster muscle, thioglycollate-induced peritonitis, an
138 l microscopy in postcapillary venules of the cremaster muscle, was markedly decreased 30 min after tr
139     Using intravital microscopy of the mouse cremaster muscle, we found that TNF-alpha and IL-17 also
140 al confocal microscopy of anesthetized mouse cremaster muscle, we separately examined the crawling an
141  confocal intravital microscopy to the mouse cremaster muscle, we show that neutrophils responding to
142 here to the endothelium in TNF-alpha-treated cremaster muscle, whereas PI3Kdelta was not required.
143 assessing experimental angiogenesis, the rat cremaster muscle, which permits live videomicroscopy and
144 mals in the peritonitis model but not in the cremaster muscle.
145  by using intravital microscopy of the mouse cremaster muscle.
146 died the permeability of microvessels in the cremaster muscle.
147 zed with a microcirculation model of exposed cremaster muscle.
148  50 V) in 2nd or 3rd order arterioles of the cremaster muscle.
149 ravital microscopic observations in the mice cremaster muscle.
150 ctions in postcapillary venules of the mouse cremaster muscle.
151 ibroblast growth factor implanted on the rat cremaster muscle.
152 n in lung, skin and postcapillary venules of cremaster muscle.
153 of neutrophil arrest in venules of the mouse cremaster muscle.
154 tion to mCRP in inflamed but not noninflamed cremaster muscle.
155 heir firm adhesion to the endothelium in rat cremaster muscle.
156 d histamine-induced leukocyte rolling in the cremaster muscle.
157 easured in mice after arterial injury in the cremaster muscle.
158 as consistent with that reported for the rat cremaster muscle.
159 oth muscle cells (SMCs) compared to those of cremaster muscle.
160 ned using microparticle image velocimetry in cremaster-muscle arterioles of wild-type mice.
161 n venules of untreated and TNF-alpha-treated cremaster muscles and in Peyer's patch high endothelial
162 sinophil extravasation into CCL11-stimulated cremaster muscles and into the inflamed peritoneal cavit
163 cruitment in untreated and TNF-alpha-treated cremaster muscles comparing ppGalNAcT-1-deficient mice (
164   Intravital microscopy of TNFalpha-inflamed cremaster muscles in Myo1e-deficient mice revealed that
165 recruited more effectively in mouse inflamed cremaster muscles in vivo.
166 rosis factor-alpha (TNF-alpha)-treated mouse cremaster muscles in wild-type mice and gene-targeted mi
167 applied directly to resistance arterioles in cremaster muscles of anaesthetized (pentobarbital sodium
168  fibres underlying a group of capillaries in cremaster muscles of anaesthetized hamsters were electri
169 tor-alpha (TNFalpha)-pretreated autoperfused cremaster muscles of C2GlcNAcT-I-deficient (core 2(-/-))
170                                          The cremaster muscles of these mice were treated with TNF-al
171                                          The cremaster muscles of these mice were treated with tumor
172 ere assessed by intravital microscopy of the cremaster muscles of wild-type mice following perivenula
173 rosis factor-alpha (TNF-alpha)-treated mouse cremaster muscles to quantitatively investigate the pote
174 ital confocal microscopy applied to inflamed cremaster muscles.
175 ex, and a striated muscle microvascular bed (cremaster) of the rat.
176 umour necrosis factor-alpha-challenged mouse cremaster post-capillary venules, we demonstrate that fl
177 ative whole blood were investigated in mouse cremaster postcapillary venules and in flow chambers coa
178 hil slow rolling and adhesion whereas in the cremaster RPA, induced by both vascular and tissue solub
179 K 14,304 + prazosin) tone was induced in rat cremaster skeletal muscle arterioles and venules (contro
180 o consistent with decreased STOC activity in cremaster SMCs was an absence of detectable Ca2+ sparks
181  membrane potentials in cerebral compared to cremaster SMCs.
182 asation of both monocytes and neutrophils in cremaster tissue and the peritoneal cavity.
183                               Homogenates of cremaster tissue produced 20-oxygen HETE when incubated
184 sLe(x) interacted with surgically stimulated cremaster venules in a P-selectin-dependent manner.
185 and transmigration of neutrophils on ear and cremaster venules in tumor necrosis factor-alpha-induced
186 ct in LPS-induced neutrophil emigration from cremaster venules into the tissues of P2X1(-/-) mice.
187 esion, we performed intravital microscopy in cremaster venules of mice reconstituted with bone marrow
188 es using intravital microscopy of live mouse cremaster venules showed that these vesicles can selecti
189  severe deficiencies of leukocyte rolling in cremaster venules with or without addition of TNF-alpha,
190 was required to open half of the channels in cremaster versus 16 mum [Ca(2+)]i in cerebral VSMCs.
191 cells isolated from mouse lungs, or in mouse cremaster vessels, was dependent on TSAd expression, and
192                            At 5 microM Ca2+, cremaster VSM showed a significantly (P < 0.05) lower cu
193 es were more left-shifted in cerebral versus cremaster VSMCs as cytoplasmic Ca(2+) was raised from 0.
194 mes were evident in BKCa channel events from cremaster VSMCs at either -30 or 30 mV at any given [Ca(
195  compared with 101 +/- 10 to -63 +/- 7 mV in cremaster VSMCs.
196 t of BKCa channels in cerebral compared with cremaster VSMCs.

 
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