ライフサイエンスコーパス: FITC-dextran

1 to a significant increase in permeability to FITC dextran.

2 further assessed in terms of permeability to FITC dextran.

3 xtran and to concentration quenching by free FITC-dextran.

4 s were measured on choroidal flatmount using FITC-dextran.

5 ased paracellular intestinal permeability to FITC-dextran.

6 as assessed after 14 days after perfusion of FITC-dextran.

7 paracellular permeability to macromolecular FITC-dextran.

8 ne-phosphatidylethanolamine or by entrapping FITC-dextran.

9 travenously with fluorescein isothiocyanate (FITC)-dextran.

10 el was compared to experimental data for the FITC-dextrans.

11 48/80 (25 microg/ml) increased clearance of FITC-dextran-10 K about 4-fold to 2.26+/-0.25 ml/sx10(-6

12 The clearance of FITC-dextran-10 K during superfusion with compound 48/80

13 erfusion with vehicle (saline), clearance of FITC-dextran-10 K from pial vessels was modest and remai

14 ted disruption of the blood-brain barrier to FITC-dextran-10 K in response to compound 48/80.

15 led dextran; molecular weight 10000 daltons; FITC-dextran-10 K) was determined while suffusing with v

16 ked disruption of the blood-brain barrier to FITC-dextran-10 K.

17 microM) produced an increase in clearance of FITC-dextran-10K and diameter of pial arterioles.

18 ng/ml) produced an increase in clearance of FITC-dextran-10K and dilated pial arterioles.

19 ion with vehicle, clearance of FITC-albumin, FITC-dextran-10K and NaFl from pial vessels and diameter

20 During suffusion with vehicle, clearance of FITC-dextran-10K from pial vessels and diameter of pial

21 erfusion with vehicle (saline), clearance of FITC-dextran-10K from pial vessels was minimal and diame

22 uring superfusion with vehicle, clearance of FITC-dextran-10K from pial vessels was minimal, and diam

23 NAP or SIN-1 markedly increased clearance of FITC-dextran-10K from the cerebral microcirculation and

24 of the blood-brain barrier to FITC-albumin, FITC-dextran-10K or NaFl.

25 labeled dextran; molecular weight 10,000 Da; FITC-dextran-10K) and diameter of pial arterioles were m

26 ed dextran; molecular weight 10,000 daltons; FITC-dextran-10K) and diameter of pial arterioles were m

27 fluorescent-labeled dextran (M(w)=10000 Da; FITC-dextran-10K) during suffusion with vehicle, S-nitro

28 orescent-labeled dextran (mol.wt.=10,000 Da; FITC-dextran-10K) or sodium fluorescein (mol.wt.=376; Na

29 lyzed on cerebral microvessels perfused with FITC-dextran 14 days after ischemia using LSCM and a 3-D

30 was found to be higher than that of 250 kDa FITC dextran (3.7 (+/- 0.6) x 10(-5) and 1.8 (+/- 0.3) x

31 .2 microns, 21 capillaries in 8 animals) and FITC-dextran (4.3 +/- 0.2 microns, 21 capillaries in 8 a

32 The FITC-dextrans (4 and 20 kDa) were able to migrate in the

33 hemichambers, and transscleral diffusion of FITC-dextrans (4.4-77 kDa) was measured with a spectroph

34 ml DMPS in the transport milieu, the flux of FITC-Dextran-4k was enhanced by 80-fold and reached 175

35 mically injected fluorescein isothiocyanate (FITC)-dextran 70.

36 NO production, and elevating permeability to FITC-dextran 70 in monolayers of cells expressing wild-t

37 PAF failed to increase permeability to FITC-dextran 70 in monolayers of cells transfected with

38 acting molecule [fluorescein isothiocyanate (FITC)-dextran, 70 kDa] was slowed 4.5 +/- 0.5-fold compa

39 an inert macromolecular fluorescent marker (FITC-dextran, 70 kDa) in the ECS by fluorescence recover

40 Using a nonpenetrating fluorescent probe (FITC-dextran, 70,000-73,000 molecular weight [MW]), RT w

41 The permeability of 10 kDa FITC dextran across the descending colonic crypt wall wa

42 Hubs had no effect on uptake of FITC-dextran, adaptor distribution, organelle integrity

43 was also determined from the initial rate of FITC dextran advance along the crypt lumen.

44 ccessible to a fluorescent endocytic tracer (FITC-dextran) after a 24-h incubation, at which time all

45 nsitivity of the fluorescein isothiocyanate (FITC)-dextran and tetramethylrhodamine isothiocyanate-AG

46 trate macropinocytosis through the uptake of FITC-dextran and amiloride inhibition of Francisella LVS

47 Two fluorescent tracers (FITC-dextran and Evans blue) were then sequentially admi

48 7 +/- 0.01 (fibroblasts), and independent of FITC-dextran and Ficoll size (gyration radii [RG] 40-300

49 The independence of D/Do on FITC-dextran and Ficoll size does not support the concep

50 as Fu(live), the animals were perfused with FITC-dextran and Fu determined.

51 e to the displacement of the majority of the FITC-dextran and to concentration quenching by free FITC

52 the translational diffusion of microinjected FITC-dextrans and Ficolls in the cytoplasm and nucleus o

53 n films of fluorescein and size-fractionated FITC-dextrans and Ficolls, and multi-component alpha(D)

54 cs include fluid phase macromolecule uptake (FITC-dextran) and activation of resting T cells.

55 porating fluorescein isothiocyanate dextran (FITC-dextran) and tetramethylrhodamine isothiocyanate co

56 ssessed microscopically after perfusion with FITC-dextran, and preretinal nuclei were quantified by P

57 circulating plasma was labeled with a 70-kDa FITC-dextran, and the capillaries were examined before a

58 e absence of glucose, TRITC-Con A binds with FITC-dextran, and the FITC fluorescence is quenched thro

59 on is highly reproducible and that levels of FITC-dextran are not significantly influenced by vascula

60 f raffinose, and fluorescein isothiocyanate (FITC)-dextran as the luminal volume marker.

61 the pressure gradient, although for 150-kDa FITC-dextran at 60 mm Hg a 10-fold decrease was observed

62 DMEC and lung microvascular EC monolayers to FITC-dextran beads, and, in vivo, it enhanced accumulati

63 ous injection of fluorescein isothiocyanate (FITC)-dextran before their recovery, followed by spectro

64 Bcl-2-HUVEC-lined vessels retain 70-kDa FITC-dextran, but not 3-kDa dextran; local histamine rap

65 vere, allowing the entry of 3 kDa and 40 kDa FITC-dextrans, but the membrane was not completely broke

66 decorin) each increased diffusion of 10 kDa FITC-dextran by approximately 2-fold.

67 sm to determine the binding of ConA to 4 kDa FITC-dextran by measuring the change in the rotational c

68 and mannose receptor-mediated endocytosis of FITC-dextran by murine bone marrow-derived DCs by flow c

69 Endocytosis of FITC-dextran by the growth cone is enhanced during Sema3

70 pillaries in 4 animals) and the width of the FITC-dextran column from 4.1 +/- 0.2 to 4.6 +/- 0.3 micr

71 of this ligand, the ranges of ConA and 4 kDa FITC-dextran concentrations capable of being explored we

72 Using FITC dextran conjugates, we demonstrate that sea urchin

73 /ANTU group, there was concentration of BALF FITC-dextran, consistent with permeability edema and inc

74 a 24-h incubation, at which time all of the FITC-dextran-containing vesicles contain ankyrin-3 and v

75 Permeability to 150-kDa FITC-dextran decreased by a little more than one half wh

76 In aqueous media (viscosity 1 cP), D for the FITC-dextrans decreased from 75 to 8.4 x 10(-7) cm2/s wi

77 FITC-dextran diffusion varied greatly in different regio

78 model of vasogenic (leaky capillary) edema, FITC-dextran diffusion was reduced more than fourfold in

79 sity of the ML and PCL from the diffusion of FITC-dextran dissolved in the ASL of unperturbed, well-d

80 subtilis TUA-containing cells labelled with FITC-dextran exhibited little fluorescence.

81 Using FITC-dextran (FD) as a fluid phase marker, we determined

82 Mice were anaesthetized, gavaged with FITC-dextran for measures of gastrointestinal permeabili

83 jury assessed by fluorescein isothiocyanate (FITC)-dextran, GFAP immunoreactivity, and microtubule as

84 these models, as shown by the reductions of FITC-dextran gut translocation, serum interleukin-6 (IL-

85 sessed using both albumin-Alexa568 and 69-kD FITC-dextran; however, diabetic animals demonstrated sig

86 FRAP of either 10 or 250 kDa FITC dextran in crypt lumens was almost complete within

87 permeability, assayed by the accumulation of FITC-dextran in plasma.

88 Measurement of the diffusion of 70 kDa FITC-dextran in spinal cord in living mice indicated tha

89 Partition of sized FITC-dextrans in polyacrylamide gel showed a relationshi

90 nate (FITC)-labelled 10 and 250 kDa dextran (FITC dextran) in isolated rat descending colonic crypts

91 o detect fluorescein-isothiocyanate-dextran (FITC-dextran) in acidic vesicles.

92 robes of FITC-annexin V, JC-1, YO-PRO-1, and FITC-dextran indicated that RGD-tachyplesin could induce

93 Simulation of the flow of Na+, water and FITC dextran into the crypt lumen and across the crypt w

94 Furthermore, fluorescein isothiocyanate (FITC)-dextran intravenous injection demonstrated leaky v

95 tight junction protein expression, increased FITC dextran leakage, decreased transcellular electrical

96 ne (NAC) reduced ROS formation and decreased FITC-dextran leakage in Hcy treated HRECs.

97 Increased FITC-dextran leakage was observed from pre-existing vess

98 yers, 3h OGD and 24h reoxygenation increased FITC-dextran leakage, indicating disruption of intercell

99 I.v. administered 40 kDa FITC-dextran leaked slowly from the vasculature of VEGF1

100 nd 800 mg/dL was obtained with a TRITC-Con A/FITC-dextran mass ratio of 500:5 micrograms/mL PEG.

101 t of either membrane dye mixing or contents (FITC-dextran) mixing with target cells.

102 ling the assay concentration using different FITC-dextran molecular weight and total capsule concentr

103 Instead, quantifying diffusivity of FITC-dextran (molecular mass 10, 40, 70, and 150 kDa) th

104 site formation and increase in clearance of FITC-dextran (molecular mass, 70 kDa) from the hamster c

105 Fluorescein isothiocyanate-labelled dextran (FITC dextran; molecular mass 10000 Da) accumulated withi

106 Fluorescein isocyanate-labelled dextran (FITC dextran; molecular mass 10000 Da) was accumulated i

107 ng five sizes of fluorescein isothiocyanate (FITC)-dextran molecules (4.4-, 10-, 38.2-, 70-, and 150-

108 The fraction of mobile FITC-dextran molecules (fmob), determined by the extent

109 the ability to exclude 500 kDa and 2000 kDa FITC-dextran molecules and the maintenance of the cell b

110 FITC-dextran molecules were chosen as models of migrant

111 monolayers to [14C]sucrose (Mw 342), but not FITC-dextran (Mw 4000) was significantly increased by tr

112 DNA fragments were nearly immobile, whereas FITC dextrans of molecular size up to 580 kDa were fully

113 FITC-dextrans of various molecular weights (MWT) were di

114 RBE4 cell monolayer permeability measured by FITC-dextran or [14C]sucrose.

115 cal histamine rapidly induces leak of 70-kDa FITC-dextran or India ink.

116 tinopathy was also qualitatively assessed in FITC-dextran perfused retinas by fluorescence microscopy

117 a intravital microscopic analysis of 150 kDa FITC-dextran-perfused blood vessels within discrete woun

118 FITC-dextran-perfused retinas exhibited prominent neovas

119 Retinopathy was qualitatively assessed in FITC-dextran-perfused retinas, and preretinal NV was qua

120 icantly (P<0.05) increased the percentage of FITC-dextran-perfused vessels compared with saline and f

121 n angiography, histology, double-staining of FITC-dextran perfusion and elastin immunohistochemistry,

122 FITC-dextran perfusion was compared with our technique.

123 CNV volumes calculated on the basis of FITC-dextran perfusion were significantly lower than vol

124 arlier stage and more reproducibly than with FITC-dextran perfusion, providing a more accurate precli

125 O mice compared with WT mice (P < 0.001) and FITC-dextran permeability assay suggested a higher exten

126 d to a loss of EBF with TPN (60% increase in FITC-dextran permeability, 40% decline in transepithelia

127 fluorescein (376Da) and weakly anionic 70kDa FITC-dextran), probe concentration (50 to 200 ppm), and

128 njugated bovine serum albumin, FITC-IgG, and FITC dextrans ranging in molecular weight from 4 to 150

129 cose were conducted for multiple TRITC-Con A/FITC-dextran ratios.

130 lity and soluble dye retention within cells (FITC-dextran) remained at the same high levels for 3 h w

131 by measuring apical-basolateral movements of FITC-dextran, respectively.

132 ive glucose binding to TRITC-Con A liberates FITC-dextran, resulting in increased FITC fluorescence p

133 rements of cerebral microvessels perfused by FITC-dextran revealed that combination treatment with 7E

134 weeks later, areas of CNV were determined by FITC-dextran staining of choroidal flatmounts.

135 throughout the cell, whereas, in the case of FITC-dextran, the fluorescence was sometimes in the nucl

136 rated, utilizing fluorescein isothiocyanate (FITC)-dextran to probe the wall pH, that a low pH exists

137 permeability as indicated by the ability of FITC-dextran to enter the cytoplasm.

138 (42-kDa fluorescein isothiocyanate dextran (FITC-dextran)), to monitor heterogeneous cell fusion.

139 The FITC-dextran tracer did not penetrate into corneal tissu

140 Permeability was examined using FITC-dextran tracer during the reperfusion phase.

141 l permeability, as revealed by intratracheal FITC-dextran tracking, serum Club Cell protein 16 measur

142 demonstrated by fluorescein isothiocyanate (FITC)-dextran translocation to the circulation.

143 t lumen, as estimated from the rate of total FITC dextran uptake into the crypt lumen and its adjacen

144 1 mM), or in the absence of Na+, the rate of FITC dextran uptake into the crypt lumens was reduced by

145 As expected, both are ts for FITC-dextran uptake by macropinocytosis, for internalisi

146 of microinjected fluorescein isothiocyanate (FITC) dextrans was faster than that of comparably sized

147 FITC-albumin (70 kDa) and 70-kDa and 150-kDa FITC-dextran was determined at transscleral pressures fr

148 FITC-dextran was increased in the PBS/ANTU group as comp

149 ercent change in fluorescence intensity when FITC-dextran was liberated by increasing glucose concent

150 BBB permeability to 70kDa FITC-Dextran was measured 24h following injury and quant

151 particles degrade in a pH-dependent manner: FITC-dextran was released with a half-life at 37 degrees

152 In both tissues, permeability to FITC-dextran was significantly greater 24 h after irradi

153 ving mice, translational diffusion of 10 kDa FITC-dextran was slowed 2- to 3-fold (compared with its

154 IVVM with FITC-dextran was used to determine the percentage of cap

155 covery after photobleaching of microinjected FITC-dextran, was 4.9 +/- 0.2- vs. 2.2 +/- 0.2-fold grea

156 ger macromolecules, FITC-albumin and 500 kDa FITC-dextran, was slowed by up to 40-fold at 0.5 mm and

157 d viscosity, determined by photobleaching of FITC-dextran, was threefold increased in pilocarpine-sti

158 ficant differences in permeability to 70-kDa FITC-dextran were observed at pressures from 0 to 60 mm

159 site formation and increase in clearance of FITC-dextran were significantly attenuated by NPC 17647

160 determine the sites of barrier to diffusion, FITC-dextrans with a MWT greater than the calculated REL

161 graded molecular sizes (propidium iodide and FITC-dextrans with molecular sizes of 3, 40, 500, and 20

162 fluorescein isothiocyanate-labeled dextrans (FITC-dextrans) with molecular weight between 10 and 70 k