ライフサイエンスコーパス: cremaster muscle

1 ctions in postcapillary venules of the mouse cremaster muscle.

2 ibroblast growth factor implanted on the rat cremaster muscle.

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

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

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

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

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

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

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

10 by using intravital microscopy of the mouse cremaster muscle.

11 died the permeability of microvessels in the cremaster muscle.

12 zed with a microcirculation model of exposed cremaster muscle.

13 50 V) in 2nd or 3rd order arterioles of the cremaster muscle.

14 ravital microscopic observations in the mice cremaster muscle.

15 ital confocal microscopy applied to inflamed cremaster muscles.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Immunohistochemical analysis of the cremaster muscle demonstrated that neovascularization in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 intravital microscopic approach with a mouse cremaster muscle model.

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

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

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

69 2.7 units, while the corresponding values in cremaster muscle of eNOS-/- mice were 1.0 +/- 0.3 and 15

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

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

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

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

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

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

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

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

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

79 The cremaster muscles of these mice were treated with tumor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 rotein transport following injuries to mouse cremaster muscle venules.

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

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

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

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

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

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

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

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

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

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

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

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

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