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1 142 to 2530 mOsm, with and without 0.5 mg/mL trypan blue.
2 C-labeled OS before and after quenching with trypan blue.
3 briefly with physiological buffer containing Trypan blue.
4  of SLCLs was determined by cell counts with trypan blue.
5 emarkably toxic to RPE cells with or without trypan blue.
6  the number of rod-shaped myocytes excluding trypan blue.
7  +/- 3% (n = 5) of the 28-day cells excluded trypan blue.
8 ure, as many as 90% of the cells accumulated trypan blue.
9 ells at 48 hours as assessed by exclusion of trypan blue.
10 y in vivo staining of the choroidal layer by trypan blue.
11  paracellular tracer flux was evaluated with trypan blue.
12  sensitive than human RPE (ARPE-19) cells to trypan blue.
13 staining of the inner limiting membrane with trypan blue.
14 ane integrity, blocking propidium iodide and Trypan blue.
15 scence was quenched by a cell viability dye, trypan blue.
16 reated with four different concentrations of trypan blue (0.1%, 0.05%, 0.025%, and 0.0125%), in combi
17 Y5Y cells as examined by oxygen consumption, trypan blue, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-t
18 , compared with images obtained prior to MGd/trypan blue administration (11.6 +/- 4.2 [standard devia
19 udies, nonviable cell nuclei were labeled by trypan blue after cold preservation and brief warm reper
20  the penetration and distribution of the MGd/trypan blue agent into CBD walls.
21               Morphologically, staining with trypan blue and alizarin red S showed an apparently inta
22                                              Trypan Blue and Indocyanine Green appear to be most effe
23                                              Trypan blue and phenol red are used as examples of synth
24 s assessed by permeability to the vital dyes trypan blue and propidium iodide.
25  factors for posterior capsule staining with trypan blue and techniques to avoid this complication.
26 eath within 24 h as assayed by the uptake of trypan blue and the release of lactate dehydrogenase.
27 l of serum-starved C2C12, HSM, and NCM (MTT, trypan blue) and prevented taxol-induced apoptosis (casp
28 ransepithelial resistance, impermeability to trypan blue, and confocal microscopy confirmed functiona
29               Tissue was also incubated with trypan blue, and cross-species immunoreactivity was dete
30 ssessment of endothelial cell injury in H&E, trypan blue, and immunostained (TIE2/Tek) biopsy specime
31   Cell survival and apoptosis were tested by Trypan blue, annexin V, and cleaved caspase-3 assays.
32                                          The trypan blue assay and a microscope-based propidium iodid
33              Cell survival was determined by trypan blue assay and ATP levels were measured with ATP
34 xyuridine triphosphate nick-end labeling and trypan blue assays to quantitate apoptosis and necrosis.
35 alysed in methylthiazoltetrazolium (MTT) and trypan blue assays.
36 e majority of apoptotic eosinophils excluded trypan blue at 48 hours post CD69 ligation.
37 ed by incubating ARPE-19 for 10 minutes with trypan blue, brilliant blue, bromophenol blue, fast gree
38 ion of colony formation or for cell death by trypan blue by up to 2 logs for paclitaxel and up to 1 l
39  Inadvertent posterior capsule staining with trypan blue can occur in eyes that appear structurally n
40 e and the small intestine as demonstrated by Trypan blue cholangiography, and a liver histological pi
41                                              Trypan blue colocalized to the cut edge of retinal flatm
42                                              Trypan blue distribution time, an indicator of the hepat
43                                              Trypan blue distribution time, which is used to index th
44  in the rinse effluent, serum transaminases, trypan blue distribution to index microcirculation, and
45                   EC injury was evaluated by trypan blue, DNA fragmentation, membrane phosphatidylser
46       Secondary measures included the use of trypan blue during CCC and correlating errant CCC and su
47         Cell viability was determined with a trypan blue dye assay.
48 ty or cellular DNA synthesis as evaluated by trypan blue dye exclusion and [3H]-thymidine incorporati
49                  Cell death was evaluated by trypan blue dye exclusion and a more efficient specific
50             Cell viability was measured by a trypan blue dye exclusion assay.
51        Cell survival was determined with the trypan blue dye exclusion test.
52                                              Trypan blue dye exclusion was used to assess cell viabil
53                Cell viability was assayed by trypan blue dye exclusion, and cleaved caspase-3 immunor
54 ion of the tetrazolium compound to formazan, trypan blue dye exclusion, and clonogenic assays.
55 ated from the rat retina were assessed using trypan blue dye exclusion, perforated-patch recordings,
56 ntaining retinal microvessels was assayed by trypan blue dye exclusion.
57 lution (gadopentetate dimeglumine mixed with trypan blue dye) in and around the prostate, thereby con
58                   Toxicity was determined by trypan blue dye-exclusion and WST-1 mitochondrial dehydr
59 function, and DNA synthesis were measured by trypan blue dye-exclusion assay, mitochondrial dehydroge
60      Cell viability (CV) was determined by a trypan blue dye-exclusion assay.
61           Cell viability was determined by a trypan blue dye-exclusion assay.
62  assessed by viable cell recovery (VCR) with trypan blue, ethidium bromide/acridine orange staining,
63                                              Trypan blue exclusion analysis suggested that the loss o
64 ious human tumor cell lines were assayed for trypan blue exclusion and ability to form colonies after
65                    Viability was assessed by trypan blue exclusion and apoptosis by morphologic asses
66 enza virus-induced cell death as measured by trypan blue exclusion and caspase activity.
67  attenuation of cytotoxicity, as measured by trypan blue exclusion and colony formation after treatme
68                Cell survival was assessed by trypan blue exclusion and demonstrated a dose-dependent
69 lular toxicity or apoptosis as determined by trypan blue exclusion and FACS analyses.
70 e number of viable thymocytes as assessed by trypan blue exclusion and fluorescence-activated cell so
71 o reduce MTT which was followed by decreased Trypan blue exclusion and increased Lactate dehydrogenas
72                   Necrosis was determined by trypan blue exclusion and lactate dehydrogenase release
73 ted to 90 min of SI and 2 h RO for necrosis (trypan blue exclusion and lactate dehydrogenase release)
74  and DNA laddering, or necrosis, assessed by trypan blue exclusion and lactate dehydrogenase release.
75                Necrosis was determined using trypan blue exclusion and LDH release assay and apoptosi
76 s exhibited no cytotoxicity, as evaluated by trypan blue exclusion and mitochondrial function assays.
77                                              Trypan blue exclusion and MTT assays evaluated TSA cytot
78                                        Using trypan blue exclusion and MTT assays, there was no evide
79 s following toxin treatment, as evidenced by trypan blue exclusion and neutral red uptake.
80 th than non-ischemic controls as assessed by Trypan Blue exclusion and propidium iodide (PI) uptake o
81                                          The trypan blue exclusion and TUNEL assays were used to stud
82 lant were evaluated histologically utilizing trypan blue exclusion as an indicator of cell viability.
83  disruption was measured quantitatively by a trypan blue exclusion assay and by release of (3)H from
84 ination induced up to 40-50% cell death by a trypan blue exclusion assay in a dose-dependent manner u
85                  Cell death was evaluated by trypan blue exclusion assay in corneal fibroblasts treat
86 d PDLF and GF by DNA fragmentation assay and trypan blue exclusion assay, either in the presence or a
87 sensitive fluorescent dye, Fluo-3, AM, and a trypan blue exclusion assay, we evaluated the ability of
88 344 lymphoid cells in a complement-dependent trypan blue exclusion assay.
89 ble cell number was also evaluated using the Trypan blue exclusion assay.
90              Cell viability was evaluated by trypan blue exclusion assay.
91 s and cell proliferation on the basis of the trypan blue exclusion assay/methylthiazolyldiphenyl-tetr
92 and apoptosis of hFOB cells were assessed by trypan blue exclusion assays and 4',6-diamidino-2-phenyl
93   Cytotoxicity was examined qualitatively by trypan blue exclusion assays and quantitatively by chrom
94           Cytotoxic activity was assessed by trypan blue exclusion assays with two cytotoxic strains
95 e-mediated dUTP-biotin nick end labeling and trypan blue exclusion assays, as well as lactate dehydro
96 n survival assays, and cytotoxic activity by Trypan blue exclusion assays.
97 48.8% +/- 10.3% of the cells being viable by trypan blue exclusion at 600 and 300 microg/ml, respecti
98 ehydrogenase into the medium and decrease in trypan blue exclusion by cells in the monolayer.
99              Cell viability was assessed via Trypan Blue exclusion cell counts, and neuronal damage w
100               No change in RPE morphology or trypan blue exclusion compared with controls was observe
101                    Viability measurements by trypan blue exclusion confirmed that the injury was larg
102                                              Trypan blue exclusion deemed that these doses were not c
103                        Viability measured by trypan blue exclusion indicated that cells were intact u
104 l morphology were also assessed by using the trypan blue exclusion method and scanning electron micro
105                                          The trypan blue exclusion method was used to test RPE cell v
106    Human RECs exposed to TA were assayed for trypan blue exclusion or activated caspase-3.
107            Our data from microscopy studies, trypan blue exclusion staining, and apoptotic DNA ladder
108                              Morphologic and trypan blue exclusion techniques were used for toxicity
109                           Cytotoxic effects (trypan blue exclusion) are first noted at 50 microM EB i
110 so-PGF2alpha had no effect on the viability (Trypan Blue exclusion) of U937 monocytes or HMEC.
111 ell number (by cell counting), viability (by trypan blue exclusion), and cellular metabolic activity
112 , Bcl-2 inhibited loss of cell viability (by trypan blue exclusion), the appearance of morphologicall
113 iated EC apoptosis (DNA content analysis and trypan blue exclusion).
114                                              Trypan blue exclusion, [(3)H]thymidine incorporation, an
115 ieved and assessed, were < or = 2% intact by trypan blue exclusion, and none of the intact cells were
116                  Cell growth was measured by trypan blue exclusion, and the MTT assay and apoptosis w
117  XTT conversion, (3)H-leucine incorporation, trypan blue exclusion, and the presence of DNA laddering
118 poptosis, and proliferation were measured by trypan blue exclusion, annexin-V/7-Aminoactinomycin D st
119  10 of 11 cell lines evaluated as well as in trypan blue exclusion, cellular ATP or caspase 3/7, 8 an
120 HA-BAD-expressing clones was demonstrated by trypan blue exclusion, clonogenic cell assay, and flow c
121                   Apoptosis was monitored by trypan blue exclusion, colorimetric cell assay, CPP32 ac
122                  Apoptosis was quantified by trypan blue exclusion, DNA fragmentation, and caspase 3
123                 Apoptosis was examined using trypan blue exclusion, laddering of DNA, CPP32 assay, an
124 lity as measured by total ATP concentration, trypan blue exclusion, or 3-(4,5-dimethylthiazol-2-yl)-2
125 vival by bromodeoxyuridine incorporation and trypan blue exclusion, respectively, upon stimulation of
126 orphology, release of lactate dehydrogenase, trypan blue exclusion, the 3-(4,5-dimethylthiazol-2-yl)-
127                                     Based on trypan blue exclusion, the cells obtained from clinical
128  MPO release was noncytotoxic as assessed by trypan blue exclusion.
129 fected in parallel were intact, as judged by trypan blue exclusion.
130 cell growth and survival as determined using trypan blue exclusion.
131 age against the conventional assays, such as Trypan blue exclusion.
132 stances from the impact site was assessed by trypan blue exclusion.
133             Cell viability was analyzed with trypan blue exclusion.
134 briefly with physiological buffer containing trypan blue for determination of sinusoidal endothelial
135                                   The use of trypan blue increased from 55.3% in the baseline cohort
136 ise ratios of CBD walls before and after MGd/trypan blue infusions were compared in the two groups by
137 s of a transcholecytic access to deliver MGd/trypan blue into CBD walls of six living pigs.
138 eriments demonstrated the penetration of MGd/trypan blue into the CBD walls.
139                                              Trypan blue is US Food and Drug Administration-approved
140               Cell viability was assessed by Trypan Blue, lactate dehydrogenase (LDH) release and MTT
141 teries of seven living pigs, and the MGd and trypan blue mixture was infused into arterial walls with
142                          In addition, an MGd/trypan blue mixture was locally infused into CBD walls o
143 ere also associated with marked increases in trypan blue nuclear staining of A549 monolayers.
144 d by lactate dehydrogenase (LDH) release and trypan blue nuclear staining.
145                 Addition of contrast agents (trypan blue or brilliant blue R) improve the signal-to-n
146  preserved cellular integrity as measured by trypan blue or propidium iodide exclusion and [ATP].
147 gene-vector media by mixing Magnevist with a trypan-blue or a lentiviral vector carrying a green fluo
148  cells (14.8% at 24 h and 34.4% at 48 h) and trypan blue-positive apoptotic cells (8.4% at 24 h and 2
149 the level of DNA fragmentation and decreased trypan blue-positive cells in PDLF compared to GF during
150 reduced necrosis as indicated by decrease in trypan blue-positive myocytes and leakage of lactate deh
151 nusoidal endothelial cell injury by counting trypan blue-positive nuclei in histological sections.
152 time, position, and mode of fusion, aided by trypan blue quenching of Qdot fluorescence, revealed tha
153  vivo experiment confirmed the uptake of MGd/trypan blue, showing an increased contrast-to-noise rati
154 o observed reduced cell death, visualized by trypan blue stain and reduced electrolyte leakage, in th
155 ce under basal conditions and an increase in trypan blue stained cells.
156 ecrease in cell viability and an increase in trypan blue-stained cells, cell apoptosis, and cleaved c
157                   None of the samples showed trypan blue-stained cells.
158 ificantly greater number of hepatocytes were trypan blue-stained in fatty livers (32 vs. 0.6%), accom
159 ified by specular microscopy and counting of trypan-blue-stained cells.
160 ttenuated neuronal cell death as assessed by trypan blue staining 5-6 h after the exposures.
161 idative stress; cell death was determined by trypan blue staining and deoxyribonucleic acid (DNA) lad
162  Cytotoxicity was assessed by observation of trypan blue staining and measurement of lactate dehydrog
163                                              Trypan blue staining confirmed cell death and demonstrat
164                                              Trypan blue staining demonstrated the viability of endot
165 l with the population-averaged viability and trypan blue staining experiments.
166                                              Trypan blue staining indicated that 72 to 100% of cells
167 ng after storage/reperfusion, as assessed by Trypan blue staining of nonparenchymal cells.
168                                              Trypan blue staining revealed that PMNs cocultured with
169 ametazime-labeled leukocytes examined by the trypan blue staining technique at 6-hr postradiolabeling
170 sion (gentamicin survival) and cytotoxicity (trypan blue staining) of PA103 mutants deficient in spec
171 xyuridine incorporation), cell viability (by trypan blue staining), and apoptosis (by annexin V stain
172  of MLO-Y4 osteocyte-like cells, assessed by trypan blue staining, caspase-3 cleavage, and TUNEL assa
173               Cell viability was assessed by trypan blue staining, cell counting, and phase-contrast
174 hmmeter), and cytotoxicity was determined by trypan blue staining.
175 l)-2,5-diphenyltetrazolium bromide assay and Trypan blue staining.
176           Cell viability was determined with trypan blue staining.
177 on of p44/42 MAP kinase and reduced both the trypan-blue staining (n = 13) and the release of lactate
178             Cell viability was determined by Trypan Blue (TB) exclusion; cell injury was determined b
179  a greater percentage of cells staining with trypan blue than when cells were transfected with either
180 rvest, proteolytic activity and the time for trypan blue to distribute homogeneously were elevated th
181 e membrane-impermeable fluorescence quencher trypan blue to selectively image internalized alpha-syn
182 e staining by allowing the posterior flow of trypan blue under the iris and through the zonules to th
183 nces of caspase-3 activity, cell detachment, trypan blue uptake and aberrant nuclei were all delayed
184                                The increased trypan blue uptake and thiobarbituric acid reactive subs
185                                              Trypan blue uptake by the HL-60, but not the K562 cells,
186                                The increased trypan blue uptake in 355 nm-irradiated cells in the pre
187    A 24-h exposure to 250-300 nM resulted in trypan blue uptake in 50% of A549 cells at 72 h and a 50
188                                      The SLC trypan blue uptake was increased but similar in both gro
189     Plasma membrane permeability assessed by trypan blue uptake was used to measure cell damage in mu
190                           Hepatocyte and SLC trypan blue uptake were minimal and similar in both grou
191 hibiting less lactate dehydrogenase release, trypan blue uptake, and apoptotic cell death (terminal d
192 by inhibition of colony formation, increased trypan blue uptake, and development of apoptotic morphol
193 y included leakage of lactate dehydrogenase, trypan blue uptake, morphology, and formazan production.
194 rter proteins, GFP and luciferase, or induce trypan blue uptake, which indicated that expression of D
195 n, caspase activation, PARP degradation, and trypan blue uptake.
196 s assessed morphologically and quantified by trypan blue uptake.
197 ed after irradiation did not cause increased trypan blue uptake.
198 a significant decrease in hepatocyte and SLC trypan blue uptake.
199                                              Trypan blue was infused at completion of reperfusion to
200 x vivo evaluation, a 2-mL mixture of MGd and trypan blue was locally infused into coronary artery wal
201 ifference in the rate of errant CCCs whether trypan blue was used or not.
202 a prelude to necrotic cell death and the dye trypan blue was used to confirm that swelling can result
203 leting model of ischemia, cells permeable to trypan blue were counted as killed by 60 and 120 min of
204 ive cases of posterior capsule staining with trypan blue were identified from cataract surgeries perf
205                    R28 cells exposed to 0.1% trypan blue with and without light showed a significant
206             ARPE-19 and R28 cells exposed to trypan blue with or without illumination did not show an
207                     ARPE-19 cells exposed to trypan blue, with or without light, did not show any sig
208 essful intracoronary infiltration of MGd and trypan blue within coronary artery walls.

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