ライフサイエンスコーパス: propidium iodide

1 and duplex-binding fluorophores (Hoechst or propidium iodide).

2 ion containing the membrane-impermeant label propidium iodide.

3 ells as measured by their ability to exclude propidium iodide.

4 ional binding of annexin V and the uptake of propidium iodide.

5 s measured using annexin V-phycoerythrin and propidium iodide.

6 l injury was measured fluorometrically using propidium iodide.

7 and </=4% of the monocytes were stained with propidium iodide.

8 ed using the fluorescent stains SYBER-14 and propidium iodide.

9 s suspended in physiologic buffer containing propidium iodide.

10 es by demonstrating their ability to exclude propidium iodide.

11 sulted in uptake of membrane-impermeable dye propidium iodide.

12 toskeletal proteins, and counterstained with propidium iodide.

13 later by staining with the cell-death marker propidium iodide.

14 insensitive to the peripheral site inhibitor propidium iodide.

15 ession were analyzed by flow cytometry using propidium iodide.

16 response to acetylcholine and labelling with propidium iodide.

17 ge/ethidium bromide or annexin-V-fluorescein/propidium iodide.

18 sured by tumor cell binding to Annexin V and propidium iodide.

19 cycle phase were tested by staining DNA with propidium iodide.

20 % (n = 7) of the neutrophils were stained by propidium iodide.

21 yrene surfaces for 6 hours were positive for propidium iodide.

22 nsitivity to the 'peripheral site' inhibitor propidium iodide.

23 l cycle, as indicated by flow cytometry with propidium iodide.

24 rmeability to the vital dyes trypan blue and propidium iodide.

25 cell viability as measured by staining with propidium iodide.

26 dye YO-PRO-1 while remaining impermeable to propidium iodide.

27 ralleled by the uptake of the pannexin probe propidium iodide.

28 s matrix that was positive when stained with propidium iodide.

29 oton microscopy of rhodamine 123 (Rh123) and propidium iodide.

30 6-diamidino-2-phenylindole dihydrochloride), propidium iodide (3,8-diamino-5-[3-(diethylmethylammonio

31 Cardiomyocyte viability was quantified with propidium iodide (5 micromol/L), and production of free

32 When labelled with the fluorescent dye propidium iodide, 68 and 36 cells were identified as smo

33 the protein competes the interaction between propidium iodide, a DNA-binding dye, and apoptotic cells

34 s study we used real-time uptake patterns of propidium iodide, a fluorescent cell impermeable model d

35 agent were measured by flow cytometry using propidium iodide, a nucleic acid-binding fluorochrome la

36 showing positive staining for annexin V and propidium iodide after antisense treatment was 40% at 28

37 to ACh and labeling of disrupted cells with propidium iodide), an air bubble was perfused through a

38 icroscopy for viability, after staining with propidium iodide and acridine orange.

39 ssed either as whole mounts and stained with propidium iodide and an antibody against alpha9 integrin

40 osis in tumor-bearing mice was detected with propidium iodide and annexin V staining.

41 evels of thymic apoptosis were determined by propidium iodide and annexin V staining.

42 flow cytometry analysis after staining with propidium iodide and annexin V, we also evaluated the cy

43 Staining of MCF13 MLV-infected cells with propidium iodide and annexin V-fluorescein isothiocyanat

44 -2 H-tetrazolium assay, cell cycle analysis, propidium iodide and annexin-V staining, and caspase-3-m

45 observed rapid membrane permeabilization to propidium iodide and ATP efflux in response to C4.

46 nd polarization were measured using the dyes propidium iodide and bis-(1,3-dibutylbarbituric acid) tr

47 dation) were measured fluorometrically using propidium iodide and chloromethyl dihydrodichlorofluores

48 Further, acridine orange, ethidium bromide, propidium iodide and DAPI staining demonstrated that cel

49 is abolished by the DNA intercalating agents propidium iodide and ethidium bromide and enhanced by th

50 embrane tracers with graded molecular sizes (propidium iodide and FITC-dextrans with molecular sizes

51 The present study using propidium iodide and FITC-TUNEL staining to identify apo

52 for 24 hr before flow cytometric analysis of propidium iodide and fluorescein isothiocyanate-conjugat

53 optosis, as assessed by flow cytometry using propidium iodide and HO33342.

54 The cells were labeled with Syto 9 and propidium iodide and imaged through a fluorescent micros

55 d results in increased apoptosis as shown by propidium iodide and JC-1 staining.

56 the membrane impermeable fluorescent marker propidium iodide and randomized to one of four ventilati

57 ed number of cells that stained positive for propidium iodide and reduced apoptotic markers.

58 Staining with propidium iodide and Syto 16 revealed a decrease in viab

59 ced apoptosis in DAOY cells as determined by propidium iodide and terminal deoxynucleotidyltransferas

60 s confirmed by viable cell counts, annexin V/propidium iodide and tetramethyl-rhodamine ethylester st

61 In addition, a reduction in the uptake of propidium iodide and the number of apoptotic nuclei and

62 jejunum were stained with Hoechst 33342 and propidium iodide and then sorted using fluorescence-acti

63 ain cytoplasmic membrane integrity, blocking propidium iodide and Trypan blue.

64 anginex caused endothelial cells to take up propidium iodide and undergo depolarization, both parame

65 ctivity colocalized with nuclear staining by propidium iodide and was also seen in isolated nuclei.

66 -mediated dUTP nick-end labeling (TUNEL) and propidium iodide and with anti-von Willebrand factor, an

67 asured outcomes included cell viability (via propidium iodide) and oxidant generation (reactive oxyge

68 Annexin V, propidium iodide, and acridine orange staining were meas

69 s were treated with nocodazole, stained with propidium iodide, and analyzed for DNA content by flow c

70 cal/multiphoton microscopy of rhodamine 123, propidium iodide, and calcein.

71 at 5, 10, 15, 28, and 56 days, stained with propidium iodide, and observed (layer by layer) by confo

72 ARPE19 was determined using monotetrazolium, propidium iodide, and TUNEL assays, and Zn(2+) uptake wa

73 orescence-activated cell sorting analysis of propidium iodide- and annexin V-stained transfected cell

74 nd cellular immunofluorescence staining with propidium iodide, anti-Annexin V and DAPI.

75 es of nonphagocytosed Annexin V+, TUNEL+, or propidium iodide+ apoptotic thymocytes suggests there is

76 assessed by the permeability of dextran and propidium iodide as well as by measuring the transendoth

77 cross-linking, gp350-positive cells excluded propidium iodide as well as gp350-negative cells.

78 esult of a fluorescent microscopic annexin V/propidium iodide assay, performed in microfluidics, conf

79 induces apoptosis, assayed by the supravital propidium iodide assay, through modulation of the apopto

80 Annexin V and propidium iodide assays demonstrated that SingleBond ind

81 in cell death, as measured by alamarBlue and propidium iodide assays, respectively.

82 cated by PARP-1, caspases 3/7, and annexin V/propidium iodide assays.

83 ssays, including Western blotting, annexin-V/propidium iodide binding, comet, and micronuclei assays,

84 tate dehydrogenase or increase the uptake of propidium iodide, both indicators of membrane integrity.

85 ere analyzed for expression of annexin-V and propidium iodide by flow cytometry.

86 ell death was measured by using a calcein-AM/propidium iodide cell-survival assay.

87 ransient permeabilization of 83% of cells to propidium iodide, cells placed at 37 degrees C resealed

88 confocal microscopy in cells recorded with a propidium iodide-containing electrode for longer than 30

89 Staining of infected cells with propidium iodide demonstrated that M. tuberculosis induc

90 ung epithelial cells, as measured by annexin/propidium iodide detection by flow cytometry.

91 sts on new and treated disks were assayed by propidium iodide/DNA stain assay and confocal microscopi

92 cell death (determined by failure to exclude propidium iodide dye).

93 aliva) were examined with Hoechst dye 33342, propidium iodide/eithidium bromide, and FITC-annexin V t

94 Chondrocyte nuclei were stained with propidium iodide, examined by fluorescence microscopy, a

95 ular integrity as measured by trypan blue or propidium iodide exclusion and [ATP].

96 ))-dependent cytotoxicity was observed using propidium iodide exclusion and annexin V staining.

97 d cell death to 25.4% compared with control (propidium iodide exclusion assay, P<0.001).

98 optosis, as confirmed by annexin V staining, propidium iodide exclusion, and identification of cells

99 iazolyl blue tetrazolium bromide methods and propidium iodide exclusion, gene expression by real-time

100 nce assay (Promega, Madison, WI, USA) and by propidium iodide exclusion.

101 striction to phenylephrine and labeling with propidium iodide), FCD was perifused around the vessel a

102 ity was measured using fluorescein diacetate/propidium iodide (FDA/PI) cell viability assay.

103 intact nuclei while gaining permeability to propidium iodide, features characteristic of necrosis ra

104 Annexin-propidium iodide flow cytometry assays, cell morphology

105 eoxyuridine, a thymidine analog) and annexin-propidium iodide flow cytometry was performed to determi

106 lungs labeled during injurious ventilation, propidium iodide fluorescence identifies all cells with

107 in lungs labeled after injurious ventilation propidium iodide fluorescence identifies only cells with

108 luorescence plate scanner equipped to detect propidium iodide fluorescence.

109 14 days, and neuronal damage assessed using propidium iodide fluorescence.

110 Cell viability was determined by way of propidium iodide fluorometry.

111 ium bromide (MTT) assay, flow cytometry with propidium iodide, gene expression profiling, RT-PCR, and

112 Agents that bind to DNA, including propidium iodide, Hoechst dye 33258, and coralyne chlori

113 However, the propidium iodide/Hoechst assay gives morphological infor

114 A combination of the sulforhodamine B and propidium iodide/Hoechst assays would provide the most a

115 The trypan blue assay and a microscope-based propidium iodide/Hoechst staining assay assess only late

116 Cells were fixed and stained with propidium iodide, imaged using a confocal microscope, an

117 tudies of HL-60 cell membrane integrity with propidium iodide impermeability and light scatter using

118 ccompanied by an enhanced cellular uptake of propidium iodide in a Ca(2+)- and ROCK-dependent manner

119 size of conjunctival follicles stained with propidium iodide in rabbits ranging in age from 2 days t

120 e identified as those that were stained with propidium iodide in such populations.

121 ase activation, and membrane permeability to propidium iodide in the absence and presence of sPLA(2).

122 f cells that bound annexin V and accumulated propidium iodide in the absence of a population that bou

123 with use of the non-vital fluorescent marker propidium iodide, in organotypic slice cultures of male

124 mined by labeling with biotinylated dUTP and propidium iodide, increased staining with annexin V, inc

125 by PMNs, and internalized bacteria excluded propidium iodide, indicating intact bacterial membranes.

126 Propidium iodide influx assay demonstrated the lysis of

127 tocellular injury was assessed by histology, propidium iodide injection, and alanine aminotransferase

128 The injection of propidium iodide into either endothelial or smooth muscl

129 d from the spleen and liver at necropsy, and propidium iodide labeled target-specific cytolysis was d

130 Flow cytometric analysis of annexin V- and propidium iodide-labeled cells showed a marked induction

131 nd flow cytometry showed increased annexin V/propidium iodide-labeled cells when grown on AGE-Matrige

132 otic eosinophils was determined by annexin V-propidium iodide labeling, and CD30 expression was exami

133 the gain of pyknotic nuclear morphology and propidium iodide labeling.

134 Apoptosis was measured by annexin V/propidium iodide labeling.

135 r treated with glioma conditioned medium, by propidium iodide labelled flow cytometry demonstrated no

136 -treated cells undergo an annexin V-positive/propidium iodide-negative phase of death consistent with

137 cl-xL, lactate dehydrogenase, annexin V, and propidium iodide) nor VEGF or TGF-beta levels, but siIL-

138 is was quantified by flow cytometry by using propidium iodide nuclear staining.

139 longest applied pulses, immediate uptake of propidium iodide occurred consistent with electroporatio

140 occurred with significantly later uptake of propidium iodide occurring after 60 ns pulses compared t

141 Samples were mounted with propidium iodide or DAPI.

142 or BrdU and/or Ki-67 and counterstained with propidium iodide or Syto 59.

143 islet viability (>90% fluorescein diacetate/propidium iodide) or the insulin secretion profile in dy

144 , a membrane-impermeable nucleic acid stain (propidium iodide), or a fluorescein-labeled antibody and

145 ifferential staining patterns after combined propidium iodide (PI) and 4', 6-diamidino-2-phenylindole

146 he intracellular concentration of Ca(2+) and propidium iodide (PI) and the delivery of 3 kDa dextran

147 ther development, using anthers stained with propidium iodide (PI) and/or 5-ethynyl-2'-deoxyuridine (

148 ial transmembrane potential distribution and propidium iodide (PI) dye diffusion experiments demonstr

149 lic uptake of Hst 5 that invariably preceded propidium iodide (PI) entry, demonstrating that transloc

150 n uptake of the non-vital fluorescent marker propidium iodide (PI) of 150-500% above control levels,

151 eration was determined by direct counting of propidium iodide (PI) or 4',6'-diamino-2-phenylindole (D

152 In fixed lenses, DNA was stained with propidium iodide (PI) or 4',6-diamidino-2-phenylindole,

153 it is generally assumed that probes, such as propidium iodide (PI) or 7-amino-actinomycin D (7-AAD),

154 s, Ro and La were predominantly nuclear, and propidium iodide (PI) stained the nucleus.

155 tic based on bromodeoxyuridine (BrdU) assay, propidium iodide (PI) staining and growth curves, and bl

156 so induced G1 growth arrest, as evidenced by propidium iodide (PI) staining and induction of retinobl

157 WST-1 cytotoxicity assay and annexin V-FITC/propidium iodide (PI) staining as apoptosis-necrosis ass

158 Propidium iodide (PI) staining of the chamber neutrophil

159 Analysis by annexin V/propidium iodide (PI) staining revealed that the concent

160 antly necrotic as indicated by annexin V and propidium iodide (PI) staining, absence of caspase activ

161 ptosis was measured using annexin V-FITC and propidium iodide (PI) staining, and DNA fragmentation.

162 in 8 of 10 CLL samples measured by annexin V/propidium iodide (PI) staining.

163 We have used propidium iodide (PI) to investigate the dynamic propert

164 competence, and mounted in medium containing propidium iodide (PI) to visualize all nuclei.

165 e S-phase), and mounted in medium containing propidium iodide (PI) to visualize all nuclei.

166 showed conspicuous cell death as measured by propidium iodide (PI) uptake and chromatin condensation,

167 rogenase (LDH) release in culture medium and propidium iodide (PI) uptake in slices were used to eval

168 ols as assessed by Trypan Blue exclusion and propidium iodide (PI) uptake on a flow cytometer.

169 solated primary HSCs; data using fluorescent propidium iodide (PI) uptake revealed that leptin, like

170 Propidium iodide (PI) uptake was used to detect membrane

171 ctate dehydrogenase (LDH) release in medium, propidium iodide (PI) uptake, and Nissl staining as mark

172 In addition, phosphatidylcholine (PC) and propidium iodide (PI) were used as the cell membrane and

173 h was associated with increased Annexin-V(+)/propidium iodide (PI)(-) cells, cleaved PARP, cleaved ca

174 cell wall fluorescence in cells stained with propidium iodide (PI), and (3) changes in apical wall fl

175 rescent plasma membrane integrity indicator, propidium iodide (PI), in HL60 human leukemia cells resu

176 culture with fluorescein diacetate (FDA) and propidium iodide (PI), respectively, showed a clear pred

177 LIVE/DEAD staining kit, based on Syto 9 and propidium iodide (PI), was also applied to assess cell e

178 n detection of active caspase 1 (Casp1)- and propidium iodide (PI)-positive cells.

179 eously with the fluorescent stains SYTO9 and propidium iodide (PI).

180 ) single-positive cells that bind AV but not propidium iodide (PI); and (b) double-positive cells tha

181 incubation to label nuclei (Hoechst 33342 & propidium iodide [PI]); cytosol (CellTracker Red CMTPX,

182 cell injury was quantified as the number of propidium iodide-positive cells per alveolus.

183 sporin A significantly reduced the number of propidium iodide-positive ePTFE and Dacron adherent neut

184 the CNS showed significantly fewer annexin V/propidium iodide-positive lymphocytes in the CNS of P2X7

185 enase release from cells, and an increase in propidium iodide-positive nuclei in response to thapsiga

186 he authors used the positively charged dyes, propidium iodide (PrI) and 4'-6-diamidino-2-phenylindole

187 cellular viability (calcein AM and annexin-V/propidium iodide), reactive oxygen species (ROS; mitosox

188 een fluorescent protein, and costaining with propidium iodide revealed a predominantly nucleolar loca

189 Cell cycle analysis with propidium iodide revealed that CD11b expression at 24 h

190 , staining with the cell viability indicator propidium iodide revealed that Zn2+ is responsible for t

191 Propidium iodide/RNAase staining and flow cytometry was

192 d [Ca2+]i was studied by flow cytometry with propidium iodide, seminaphthorhodafluor (SNARF)-1-AM, an

193 Staining with propidium iodide showed no nuclear condensation in cells

194 ce resulting from exposing sampled tissue to propidium iodide solution 16-24 h after sampling.

195 ncer cells has been determined via Annexin V/Propidium iodide stain and flow cytometry.

196 ty (relative fluorescence), and cellularity (propidium iodide stain).

197 Flow cytometry analyses of propidium iodide-stained cells demonstrated cell death o

198 Flow cytometric analysis of propidium iodide-stained cells demonstrated that about 5

199 Flow cytometry of propidium iodide-stained cells revealed that I3C induces

200 Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and Pl

201 uorescence-activated cell sorter analysis of propidium iodide-stained cells, indicated a relative def

202 IH, Bethesda, MD) to count Ki67-positive and propidium iodide-stained cells.

203 Counts of propidium-iodide-stained nuclei for 2.2 MPa open-chest M

204 ble as determined by differential Syto 9 and propidium iodide staining after MazF(Sa) induction.

205 Cell death was measured by Hoechst/propidium iodide staining and activation of caspase-3.

206 l-cycle progression was demonstrated by both propidium iodide staining and bromodeoxyuridine incorpor

207 related with rRNA transcription, as shown by propidium iodide staining and BrUTP incorporation.

208 sorafenib-induced apoptosis as determined by propidium iodide staining and by assessing the mitochond

209 r a 18-h period as assessed by Hoechst 33342/propidium iodide staining and caspase-3 and -9 activatio

210 tosis of freshly isolated IEC as assessed by propidium iodide staining and DNA laddering.

211 Cell death was monitored by propidium iodide staining and FACS analysis.

212 cycle by bromodeoxyuridine incorporation or propidium iodide staining and flow cytometry and measure

213 Anoikis was quantified by YO-PRO-1/propidium iodide staining and flow cytometry.

214 Cell viability was monitored with propidium iodide staining and lactate dehydrogenase rele

215 activated cell sorting (FACS) analysis using propidium iodide staining and the TUNEL assay.

216 -mediated dUTP-biotin nick end labeling, and propidium iodide staining assays, it was shown that rSV5

217 bodies and quantified by a cell death assay (propidium iodide staining in the subdiploid peak) or cel

218 increased DNA strand breaks as determined by propidium iodide staining in unstimulated T cells cocult

219 treated neutrophils was determined using the propidium iodide staining method.

220 s, and monitored cell death by annexin V and propidium iodide staining of lymphocytes, using flow cyt

221 BrdUrd incorporation and propidium iodide staining of prostate LNCaP cells arrest

222 Propidium iodide staining revealed that KB1050 accumulat

223 TUNEL and propidium iodide staining showed DNA fragmentation and p

224 G(2) cell cycle arrest as determined by propidium iodide staining was not a result of mitotic ar

225 n assay, and annexin V binding combined with propidium iodide staining was used for the distinction o

226 assayed for annexin V binding, DNA content (propidium iodide staining), and DNA fragmentation (termi

227 , and increases cell death (as determined by propidium iodide staining).

228 is of a lactate dehydrogenase release assay, propidium iodide staining, and measurement of the total

229 aluated by quantitative flow cytometry after propidium iodide staining, and the decrease in the total

230 ed by internucleosomal DNA fragmentation and propidium iodide staining, and was associated with incre

231 , G(2)/M accumulation, typically assessed by propidium iodide staining, begins to be measurable only

232 early cell cycle entry; this was assessed by propidium iodide staining, CFSE labeling profiles, [(3)H

233 aining of select yeast cells which also show propidium iodide staining, indicating ZCOE is a "dead" s

234 th based on early LDH release, annexin V and propidium iodide staining, morphological changes of infe

235 Conversely, propidium iodide staining, PARP cleavage patterns, and r

236 o anti-Fas-induced apoptosis was analyzed by propidium iodide staining, TUNEL (terminal deoxynucleoti

237 bicin, or H2O2 and was measured by annexin V/propidium iodide staining.

238 le with TUNEL (Roche) and dual annexin V and propidium iodide staining.

239 T cells, as judged by reduction in annexin V/propidium iodide staining.

240 nfirmed with cell cycle analysis and annexin-propidium iodide staining.

241 tic cell death was measured by annexin V and propidium iodide staining.

242 ound cells were identified by differences in propidium iodide staining.

243 cted by [(3)H]thymidine incorporation and by propidium iodide staining.

244 cent-activated cell scanning using annexin V/propidium iodide staining.

245 eoxynucleotidyl transferase end-labeling and propidium iodide staining.

246 ndritic cells was evaluated by annexin-V and propidium iodide staining.

247 using a green fluorescent nucleic acid stain/propidium iodide staining.

248 ad decreased membrane integrity, as shown by propidium iodide staining.

249 primarily necrotic as judged using Annexin V/propidium iodide staining.

250 death in the CA1 region was quantified using propidium iodide staining.

251 pe (TEM), as well as the nuclear labeling by propidium iodide staining; terminal deoxynucleotidyl tra

252 permeant (calcein) and membrane impermeant (propidium iodide) stains.

253 Live/dead (calcein AM and propidium iodide) testing revealed that a certain fracti

254 mic group had significantly more cell death (propidium iodide) than non-ischemic controls at 24 hr an

255 Using propidium iodide to label nuclei and 5-bromo-2'-deoxyuri

256 hesis by immunofluorescence and stained with propidium iodide to measure DNA content by fluorescence-

257 e M-phase), and mounted in medium containing propidium iodide to visualize all nuclei.

258 tericidal effect on H. pylori as revealed by propidium iodide uptake and a morphological shift from s

259 Cell death and apoptosis were quantified by propidium iodide uptake and annexin-V staining, respecti

260 Based on propidium iodide uptake and cell morphology, the majorit

261 Propidium iodide uptake assays revealed that FD11 cells

262 Propidium iodide uptake assays were used to examine acut

263 Propidium iodide uptake highly correlated with cell viab

264 ase in neuronal death assessed 24 h later by propidium iodide uptake in dead cell nuclei.

265 s to CORT and NMDA synergistically increased propidium iodide uptake in each hippocampal region, effe

266 Exposure to NMDA caused significant propidium iodide uptake in each hippocampal region, whil

267 te on neuronal cell death using fluorescence propidium iodide uptake in rat organotypic hippocampal-e

268 nduced cell death was developed by using the propidium iodide uptake method adapted to a fluorescence

269 For nanosecond pulses, more delayed propidium iodide uptake occurred with significantly late

270 Experimental measurements of propidium iodide uptake provided evidence of a real memb

271 luciferase reporter), and cell necrosis (via propidium iodide uptake).

272 NEL positivity, phosphatidylserine exposure, propidium iodide uptake, and caspase-3 cleavage.

273 increases in phosphatidylserine exposure and propidium iodide uptake, was also inhibited by cariporid

274 nduced cell lysis of FD11 cells, assessed by propidium iodide uptake, was partially prevented by leup

275 privation was neuroprotective as measured by propidium iodide uptake, with an EC(50) between 1 and 10

276 xposure alone did not significantly increase propidium iodide uptake.

277 oxicity assessed by fluorescent detection of propidium iodide uptake.

278 failed to reduce the significant increase in propidium iodide uptake.

279 s rapid adenosine triphosphate depletion and propidium iodide uptake.

280 ly 30% of cultured EC to die, as assessed by propidium iodide uptake.

281 later, neuronal death was again assessed by propidium iodide uptake.

282 membrane asymmetry (annexin V staining), and propidium iodide uptake.

283 reactive oxygen species (ROS) production and propidium iodide uptake.

284 ra-AM] abolished cytotoxicity as measured by propidium iodide uptake.

285 ssessed by lactate dehydrogenase leakage and propidium iodide uptake.

286 easured by lactate dehydrogenase leakage and propidium iodide uptake.

287 Syncytia were detected by DNA staining with propidium iodide using flow cytometry to determine cell

288 (approximately 100 nM), while the uptake of propidium iodide was absent.

289 The increase in membrane permeability to propidium iodide was accompanied by a two- to threefold

290 lls, membrane permeability as measured using propidium iodide was greater in the presence of AbiZ.

291 r staining with the membrane impermeable dye propidium iodide was observed immediately following kain

292 nutes at high tidal volume settings, whereas propidium iodide was perfused either during or after inj

293 MDAR-dependent neuronal death as assessed by propidium iodide was similar with both co-agonists.

294 s an indicator of microvascular leakage, and propidium iodide was used to stain for irreversibly inju

295 m (P<0.05) while intercellular dye transfer (propidium iodide) was maintained.

296 No necrotic cells labeled with propidium iodide were detected in moribund animals on da

297 Fluo-3 and propidium iodide were employed to evaluate calcium fluxe

298 Neuronal injury was quantified using propidium iodide, which becomes fluorescent only when it

299 developmental stages, processed either with propidium iodide, which stains pyknotic nuclei intensely

300 orimetric assay, based on the interaction of propidium iodide with DNA, that allows either real-time