ライフサイエンスコーパス: cremaster

1 increased in the interleukin-1beta inflamed cremaster.

2 Studies in cremaster and cerebral VSMCs show heterogeneity of BKCa

3 impairs neutrophil recruitment into inflamed cremaster and peritoneum.

4 (a major source of RGD sequences) also cause cremaster arteriolar vasodilation through the alpha v be

5 n and platelet accumulation in laser-induced cremaster arteriole injury, and PDI(ss-oo) mice had atte

6 FVa and FXa after laser injury in the mouse cremaster arteriole.

7 amined clot response to laser injury in both cremaster arterioles and venules in FVIII(null) mice eit

8 t and a decrease in the beta1:alpha ratio in cremaster arterioles compared to cerebral vessels.

9 ant delay in time to thrombotic occlusion in cremaster arterioles compared with wild-type littermates

10 DSS colitis enhanced thrombus formation in cremaster arterioles of wild-type mice.

11 Similarly, cremaster arterioles showed a decrease in total BKCa pro

12 effect on basal vascular tone or response of cremaster arterioles to vasoactive compounds.

13 and induced potent dilation of isolated rat cremaster arterioles, both of which were specifically bl

14 ed vasodilation when applied to isolated rat cremaster arterioles.

15 In a mouse cremaster artery laser injury model, a single intravenou

16 Cremaster BKCa channels thus demonstrated an approximate

17 llowing injection, the number of MSCs in the cremaster further decreased to 14% of the initial number

18 Transplanted WT cremaster in p75-/- mice showed a robust leukocyte rolli

19 However, in the cremaster injury model, only pcBF8 was more effective, m

20 er, in both a cuticular bleeding model and a cremaster laser arteriole/venule injury model, there wer

21 nesis, we mated activin transgenic mice with CreMaster mice, which are characterized by Cre recombina

22 gfr2-deficient mice with mast cell-deficient CreMaster mice.

23 od vessels of the isolated retina and in the cremaster microcirculation of anesthetized mice.

24 , intravital microscopy studies of the mouse cremaster microcirculation showed that tumor necrosis fa

25 eposited in the postcapillary venules of the cremaster microcirculation, secondary to increased vascu

26 delayed thrombosis after carotid artery and cremaster microvascular injury without affecting paramet

27 We used an in vivo cremaster model (hamster and mouse) in which circulating

28 y roll slower and adhere more readily in the cremaster model than wild-type neutrophils.

29 s identified by intravital microscopy in the cremaster model.

30 In response to field stimulation of the cremaster muscle (0.5, 1, 3 Hz), venular dilator and hyp

31 o the endothelium in the vessels of lung and cremaster muscle and decreased the numbers of inflammato

32 t not of nonclassical monocytes in the mouse cremaster muscle and in in vitro flow chamber assays.

33 vivo, LPS-induced inflammation in the mouse cremaster muscle and peritoneal cavity led to ICAM-1 exp

34 f experiments, the adhesion of leukocytes to cremaster muscle and the dynamics of thrombus formation

35 for rolling in inflamed microvessels of the cremaster muscle are completely Core2GlcNAcT-I dependent

36 lower rolling, and increased adhesion in the cremaster muscle are dependent on L-selectin.

37 Isolated first-order arterioles from rat cremaster muscle are under dual regulation by insulin, w

38 rat vascular smooth muscle (VSM) cells from cremaster muscle arterioles and cerebral arteries.

39 FNIII-1-containing fibronectin fragments to cremaster muscle arterioles in situ, triggered a rapid,

40 Purkinje cell network in vitro and in ECs of cremaster muscle arterioles in vivo.

41 ion of function-blocking FNIII-1 peptides to cremaster muscle arterioles rapidly and specifically dec

42 myography to study rat isolated first-order cremaster muscle arterioles the AT1 R inhibitor candesar

43 and light/dye-induced thrombus formation in cremaster muscle arterioles were measured in wild-type (

44 in vivo thrombosis models in mesenterium or cremaster muscle arterioles, we demonstrate that Bambi-d

45 teric arterioles and laser-induced injury of cremaster muscle arterioles, we herein show that thrombi

46 vital microscopy and laser-induced injury to cremaster muscle arterioles, we show that thrombi formed

47 We have used the mouse cremaster muscle as a model of trauma- and cytokine-indu

48 or macromolecules, RBCs, and WBCs in hamster cremaster muscle capillaries.

49 ation predominates (>/=90% of events) in the cremaster muscle circulation, but transcellular migratio

50 Intravital microscopy of the mouse cremaster muscle confirmed the defect of CXCL1-induced l

51 hemic or tumor necrosis factor-alpha-treated cremaster muscle demonstrated that MAPCs migrate to peri

52 Immunohistochemical analysis of the cremaster muscle demonstrated that neovascularization in

53 l field stimulation was used to contract the cremaster muscle for 15 s at 30 Hz.

54 Surgical preparation of the mouse cremaster muscle for intravital microscopy induced P-sel

55 PAF increased permeability in wild-type cremaster muscle from a baseline of 2.4 +/- 2.2 to a pea

56 Topical application of fMLP onto the whole cremaster muscle generated the same number of adherent l

57 microscopy was performed on an exteriorized cremaster muscle in 11 wild-type mice to study the micro

58 al confocal microscopy of anesthetized mouse cremaster muscle in combination with immunofluorescence

59 was assessed by intravital microscopy of the cremaster muscle in mice treated for 4 days with sustain

60 firm neutrophil attachment to venules in the cremaster muscle in response to N-formyl- methionyl-leuc

61 sed adhesion of leukocytes to endothelium in cremaster muscle in vivo and with thrombosis in a mouse

62 m bovine heart endothelium) and in the mouse cremaster muscle in vivo.

63 mildly inflamed postcapillary venules of the cremaster muscle in vivo.

64 n E-selectin in TNF-alpha-treated venules of cremaster muscle in which P-selectin function was blocke

65 Functional studies in the rat cremaster muscle indicate that alpha1ARs predominate in

66 borated by intravital microscopy of inflamed cremaster muscle microcirculation in bone marrow chimera

67 We used intravital microscopy of rat cremaster muscle microcirculation to track intraarterial

68 mation following laser-induced injury in the cremaster muscle microcirculation.

69 Microvascular thrombosis was induced in cremaster muscle microvessels of normal and colitic mice

70 les, light/dye-induced thrombus formation in cremaster muscle microvessels, as well as disease activi

71 ed interactions with wild-type (WT) inflamed cremaster muscle microvessels.

72 intravital microscopic approach with a mouse cremaster muscle model.

73 arteries and downstream arterioles from the cremaster muscle of C57BL/6 mice.

74 n second-order arterioles (2A) supplying the cremaster muscle of C57BL6, PECAM-1-/-, and eNOS-/- mice

75 2.7 units, while the corresponding values in cremaster muscle of eNOS-/- mice were 1.0 +/- 0.3 and 15

76 l reconstructions were performed in skin and cremaster muscle of guinea-pigs, mice and rats injected

77 croscopy of postcapillary venules within the cremaster muscle of mice revealed that a significantly g

78 avital microscopy of inflamed vessels of the cremaster muscle of mice.

79 Using the in situ cremaster muscle of obese Zucker rats (OZR; with lean Zu

80 sity and ultrastructure were assessed in the cremaster muscle of rats subjected to a 75% surgical red

81 onse to chemoattractants administered to the cremaster muscle or dorsal skin, but neutrophil-dependen

82 otor control in arterioles of the superfused cremaster muscle preparation of anesthetized C57Bl6 mice

83 Cremaster muscle preparations revealed endothelial dysfu

84 Vasopressin was superfused topically on the cremaster muscle resistance arterioles (15 to 25 microns

85 Complementary experiments in the mouse cremaster muscle revealed a pattern of alphaAR subtype d

86 Intravital microscopy of the cremaster muscle revealed almost no rolling at times up

87 In vivo microscopy on the inflamed mouse cremaster muscle revealed that blockade of serine protea

88 t to a venule of the TNF-alpha-treated mouse cremaster muscle significantly increased the number of a

89 vated murine platelets and in venules of the cremaster muscle subjected to trauma.

90 a mouse model of microcirculation using the cremaster muscle that allows direct microscopic examinat

91 ls and intravital microscopy of the inflamed cremaster muscle that CD95 mediates leukocyte slow rolli

92 ocyte adhesion and extravasation in inflamed cremaster muscle venules in comparison with control anim

93 We performed intravital microscopy of cremaster muscle venules in T-GFP mice, in which naive T

94 der flow conditions in vitro and in inflamed cremaster muscle venules in the situation in vivo.

95 investigated neutrophil adhesion in inflamed cremaster muscle venules in tumor necrosis factor (TNF)-

96 ge velocimetry (micro-PIV) was used in mouse cremaster muscle venules in vivo to measure velocity pro

97 Intravital microscopy of cremaster muscle venules indicated that the leukocyte ro

98 e rolling was almost completely abolished in cremaster muscle venules of core2(-/-) mice, but not lit

99 These beads showed no rolling in cremaster muscle venules of core2(-/-) mice, but signifi

100 In inflamed cremaster muscle venules of St3gal6-null mice, we found

101 is of tumor necrosis factor-alpha-stimulated cremaster muscle venules revealed severely compromised l

102 TNF-alpha- treated CD18 null mouse cremaster muscle venules show increased leukocyte rollin

103 microscopy of untreated or TNF-alpha-treated cremaster muscle venules showed EGFP+ cells in vivo, but

104 ticle image velocimetry (micro-PIV) in mouse cremaster muscle venules to estimate the hydrodynamicall

105 In cremaster muscle venules treated with both TNF-alpha and

106 Leukocyte rolling velocities in cremaster muscle venules were increased significantly in

107 ligand, CCL19, triggered T cell sticking in cremaster muscle venules, but failed to induce extravasa

108 cient leukocytes is demonstrated in inflamed cremaster muscle venules, in a peritonitis model, and in

109 were unable to migrate into inflamed murine cremaster muscle venules, instead persisting between the

110 rotein transport following injuries to mouse cremaster muscle venules.

111 oss endothelium of initial lymphatics in rat cremaster muscle was investigated with micropipette mani

112 Intravital microscopy of mouse cremaster muscle was performed after intravenous injecti

113 copy of the microcirculation of exteriorized cremaster muscle was performed in 12 wild-type mice duri

114 y and simultaneous ultrasound imaging of the cremaster muscle was performed in 6 mice to determine wh

115 Intravital microscopy of the cremaster muscle was performed in six wild-type mice and

116 copy of tissue necrosis factor-alpha-treated cremaster muscle was performed to assess the microvascul

117 Quantitative fluorescence microscopy of cremaster muscle whole mounts using rhodamine-labeled Gr

118 ibrils in the extracellular matrix of intact cremaster muscle, demonstrating active polymerization of

119 Using in vivo microscopy on the mouse cremaster muscle, intravascular adherence and subsequent

120 s mediated by P-selectin in the exteriorized cremaster muscle, is not further increased in response t

121 gs indicate that for arterioles in the mouse cremaster muscle, nitric oxide and endothelial-derived h

122 In the multiple tissues analyzed (eg, cremaster muscle, skin, mesenteric tissue), LERs were di

123 By using intravital microscopy of mouse cremaster muscle, the in vivo effects of several particu

124 ired in fMLP-induced transmigration into the cremaster muscle, thioglycollate-induced peritonitis, an

125 l microscopy in postcapillary venules of the cremaster muscle, was markedly decreased 30 min after tr

126 Using intravital microscopy of the mouse cremaster muscle, we found that TNF-alpha and IL-17 also

127 al confocal microscopy of anesthetized mouse cremaster muscle, we separately examined the crawling an

128 confocal intravital microscopy to the mouse cremaster muscle, we show that neutrophils responding to

129 here to the endothelium in TNF-alpha-treated cremaster muscle, whereas PI3Kdelta was not required.

130 assessing experimental angiogenesis, the rat cremaster muscle, which permits live videomicroscopy and

131 mals in the peritonitis model but not in the cremaster muscle.

132 by using intravital microscopy of the mouse cremaster muscle.

133 died the permeability of microvessels in the cremaster muscle.

134 zed with a microcirculation model of exposed cremaster muscle.

135 50 V) in 2nd or 3rd order arterioles of the cremaster muscle.

136 ravital microscopic observations in the mice cremaster muscle.

137 ctions in postcapillary venules of the mouse cremaster muscle.

138 ibroblast growth factor implanted on the rat cremaster muscle.

139 tion to mCRP in inflamed but not noninflamed cremaster muscle.

140 heir firm adhesion to the endothelium in rat cremaster muscle.

141 d histamine-induced leukocyte rolling in the cremaster muscle.

142 easured in mice after arterial injury in the cremaster muscle.

143 as consistent with that reported for the rat cremaster muscle.

144 oth muscle cells (SMCs) compared to those of cremaster muscle.

145 ned using microparticle image velocimetry in cremaster-muscle arterioles of wild-type mice.

146 n venules of untreated and TNF-alpha-treated cremaster muscles and in Peyer's patch high endothelial

147 cruitment in untreated and TNF-alpha-treated cremaster muscles comparing ppGalNAcT-1-deficient mice (

148 rosis factor-alpha (TNF-alpha)-treated mouse cremaster muscles in wild-type mice and gene-targeted mi

149 applied directly to resistance arterioles in cremaster muscles of anaesthetized (pentobarbital sodium

150 fibres underlying a group of capillaries in cremaster muscles of anaesthetized hamsters were electri

151 tor-alpha (TNFalpha)-pretreated autoperfused cremaster muscles of C2GlcNAcT-I-deficient (core 2(-/-))

152 The cremaster muscles of these mice were treated with TNF-al

153 The cremaster muscles of these mice were treated with tumor

154 ere assessed by intravital microscopy of the cremaster muscles of wild-type mice following perivenula

155 rosis factor-alpha (TNF-alpha)-treated mouse cremaster muscles to quantitatively investigate the pote

156 ital confocal microscopy applied to inflamed cremaster muscles.

157 ex, and a striated muscle microvascular bed (cremaster) of the rat.

158 umour necrosis factor-alpha-challenged mouse cremaster post-capillary venules, we demonstrate that fl

159 ative whole blood were investigated in mouse cremaster postcapillary venules and in flow chambers coa

160 hil slow rolling and adhesion whereas in the cremaster RPA, induced by both vascular and tissue solub

161 K 14,304 + prazosin) tone was induced in rat cremaster skeletal muscle arterioles and venules (contro

162 o consistent with decreased STOC activity in cremaster SMCs was an absence of detectable Ca2+ sparks

163 membrane potentials in cerebral compared to cremaster SMCs.

164 asation of both monocytes and neutrophils in cremaster tissue and the peritoneal cavity.

165 Homogenates of cremaster tissue produced 20-oxygen HETE when incubated

166 sLe(x) interacted with surgically stimulated cremaster venules in a P-selectin-dependent manner.

167 ct in LPS-induced neutrophil emigration from cremaster venules into the tissues of P2X1(-/-) mice.

168 esion, we performed intravital microscopy in cremaster venules of mice reconstituted with bone marrow

169 es using intravital microscopy of live mouse cremaster venules showed that these vesicles can selecti

170 severe deficiencies of leukocyte rolling in cremaster venules with or without addition of TNF-alpha,

171 was required to open half of the channels in cremaster versus 16 mum [Ca(2+)]i in cerebral VSMCs.

172 cells isolated from mouse lungs, or in mouse cremaster vessels, was dependent on TSAd expression, and

173 At 5 microM Ca2+, cremaster VSM showed a significantly (P < 0.05) lower cu

174 es were more left-shifted in cerebral versus cremaster VSMCs as cytoplasmic Ca(2+) was raised from 0.

175 mes were evident in BKCa channel events from cremaster VSMCs at either -30 or 30 mV at any given [Ca(

176 compared with 101 +/- 10 to -63 +/- 7 mV in cremaster VSMCs.

177 t of BKCa channels in cerebral compared with cremaster VSMCs.