ライフサイエンスコーパス: TUNEL-positive

1 ivated HSCs or telomerase positive HSCs were TUNEL positive.

2 greater number of SEC and hepatocytes became TUNEL positive.

3 ile two-thirds were ZVAD-fmk insensitive but TUNEL-positive.

4 2393 +/- 124 total), of which very few were TUNEL-positive.

5 depleted and 87% of the remaining TAFs were TUNEL-positive.

6 sfected with pseudophosphorylated Tau became TUNEL-positive.

7 transferase-mediated dUTP nick-end labeling (TUNEL)-positive.

8 t neuron specific nuclear protein and became TUNEL-positive 3 days after ischemia.

9 however, resulted in significant apoptosis (TUNEL positive: 48 hr cold: 2+/-0.6%, 48 hr cold and 24

10 tric mucosa contain cytokeratin-positive and TUNEL-positive AEC material, indicating that gastric pha

11 They are TUNEL-positive and have increased levels of caspase 3 ac

12 d areas of renal cells with chromatin nicks (TUNEL positive) and single-stranded DNA, (3) absence of

13 ation within the synapse-without evidence of TUNEL-positive apoptosis in the photoreceptor cell body-

14 TUNEL-positive apoptotic and Ki-67-positive proliferatin

15 is associated with enhanced O2- production, TUNEL-positive apoptotic cells and decreased levels of N

16 TUNEL-positive apoptotic cells were dramatically decreas

17 However, irrespective of immune status, TUNEL-positive apoptotic cells were present mainly in ar

18 The TUNEL-positive apoptotic cells, and several apoptotic pr

19 of AECs and higher levels of nonphagocytosed TUNEL-positive apoptotic material, consistent with a def

20 layer (IPL) compared with the percentage of TUNEL-positive apoptotic neurons in the GCL.

21 cl2, increased Bax expression, and increased TUNEL-positive apoptotic nuclei characterized the restor

22 easured by auditory brainstem recordings and TUNEL-positive-apoptotic cochlear cells.

23 48 h whereas some Hsp70 stained neurons were TUNEL positive at 72 h after reperfusion.

24 In addition, Bergmann glia were TUNEL positive at P21, and they expressed activated casp

25 hosphate (dUTP)-rhodamine nick end labeling (TUNEL) -positive at 1 week after injury (39.3 +/- 5.6%),

26 In wild-type lenses, nuclei were TUNEL positive before denucleation, indicating that 3'-O

27 cated that cells undergoing apoptosis became TUNEL positive before loss of mitochondrial function.

28 Approximately 40-50% of neurons were TUNEL positive by 6 and at 24 h >70% of the neurons show

29 retinas were quantitated, and the number of TUNEL-positive capillary cells and degenerated capillari

30 actosemic rats showed increased frequency of TUNEL-positive capillary cells at 6 to 8 months and vasc

31 The number of TUNEL-positive capillary cells in the retinal microvesse

32 TUNEL-positive cardiomyocyte nuclei (n/1000 nuclei) were

33 positive microvessels, whereas it normalized TUNEL-positive cardiomyocytes and caspase-9 and -3 activ

34 The rate of TUNEL-positive cardiomyocytes was high in the pre-VAD gr

35 respectively), leading to a 21% increase in TUNEL-positive CECs in FECD (P=0.015) but no change in n

36 TUNEL-positive cell count was 3.8-fold (P<0.05) higher i

37 al cells, with an almost complete absence of TUNEL-positive cell death at P7.

38 osporine-stimulated caspase-3 activation and TUNEL-positive cell death by lowering p53 promoter trans

39 ced neuronal death and significantly reduced TUNEL-positive cell numbers induced by exposure of cultu

40 ased beta-cell mass, decreased the number of TUNEL positive cells and improved glucose tolerance afte

41 e-3 protein as well as cleaved caspase-3 and TUNEL positive cells at 24h and percent loss of ipsilate

42 rall number, distribution, and morphology of TUNEL positive cells in long-term sleep deprived rats di

43 The type I TUNEL positive cells in the ischemic cortex underwent ne

44 The type II TUNEL positive cells in the thalamus and the cortex penu

45 ttenuated, while caspase 3 and the number of TUNEL positive cells was enhanced in CD-pretreated cells

46 n tissue was subjected to TUNEL staining and TUNEL positive cells were quantified.

47 e, reduction of infarction size, decrease of TUNEL positive cells, and increase of Bcl-2 (anti-apopto

48 mice have increased bile infarcts, increased TUNEL positive cells, increased neutrophil infiltration,

49 ifferences, designated as type I and type II TUNEL positive cells.

50 deoxyuridine triphosphate nick end-labeling (TUNEL)-positive cells and mortality compared with vehicl

51 he NE-induced increase in nick end-labeling (TUNEL)-positive cells compared with control (NE, 33+/-3%

52 rase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells in several regions of the brain.

53 transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells were approximately 3-fold more fre

54 rase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells were detected in situ.

55 mediated biotinylated UTP nick end labeling (TUNEL)-positive cells were detected in the INL and GCL,

56 transferase-mediated dUTP nick end labeling (TUNEL)-positive cells) at 6 hours, followed by transmigr

57 transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, and iv) DEVDase activity.

58 No terminal UTP nicked-end labeling (TUNEL)-positive cells, as a detection of cell death, wer

59 transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells, NASH, and fibrosis.

60 mediated biotinylated UTP nick end labeling (TUNEL)-positive cells.

61 -9 versus 45+/-8%, P<0.05) and the number of TUNEL-positive cells (7.9+/-1.0 versus 1.3+/-0.9%, P<0.0

62 - animals exhibited fourfold lower levels of TUNEL-positive cells (a marker for programmed cell death

63 implants significantly reduced the number of TUNEL-positive cells (P < 0.05).

64 , whereas in the CNV lesions there were more TUNEL-positive cells 6 hours after PDT.

65 or sections revealed significantly increased TUNEL-positive cells after combination treatment compare

66 The numbers of blue light-induced TUNEL-positive cells also increased in advance of the in

67 ent increase in numbers of sunburn cells and TUNEL-positive cells although their proliferation was su

68 We also observed an increase of TUNEL-positive cells and activities of caspase-3 and cas

69 -out of TAT-D in S. cerevisiae increases the TUNEL-positive cells and cell survival in response to hy

70 A injection, there were increased numbers of TUNEL-positive cells and cells with elevated HSP72 immun

71 s a significant positive correlation between TUNEL-positive cells and expression of caspase-3 (r = 0.

72 that the differences between groups for both TUNEL-positive cells and expression of caspase-3 were st

73 TUNEL-positive cells and mitochondrial release of cytoch

74 TUNEL-positive cells and serum alanine aminotransferase

75 PANT- and TUNEL-positive cells appeared in similar numbers 16 h fo

76 A significant number of TUNEL-positive cells appeared only in the CA1 pyramidal

77 The sopB mutant induced the same amount of TUNEL-positive cells as the wild type, but it was attenu

78 ce exhibited increased amount of PL, AC, and TUNEL-positive cells compared with control mice.

79 ber of GCL neurons and a 10-fold increase in TUNEL-positive cells compared with the fellow sham contr

80 The number of TUNEL-positive cells decreased with age.

81 ins Bak and Bax and the higher percentage of TUNEL-positive cells in both diseased groups suggests th

82 The number of TUNEL-positive cells in CNV increased at 3 hours after P

83 y activated Akt and suppressed the number of TUNEL-positive cells in CNV, and the effects of IGF-1 we

84 rbation of LV dysfunction, and the number of TUNEL-positive cells in DM+MI was significantly inhibite

85 ta-cell mass, and reduction in the number of TUNEL-positive cells in islets.

86 entricular lumen and the increased number of TUNEL-positive cells in periventricular areas led to the

87 The overall percentage of TUNEL-positive cells in the ankle was <1% except on days

88 of the cerebellum and a 10-fold increase in TUNEL-positive cells in the dentate gyrus of the hippoca

89 strated a significantly higher percentage of TUNEL-positive cells in the diseased groups compared wit

90 ad up to a 30-fold increase in the number of TUNEL-positive cells in the external granule cell layer

91 injured rat common carotid artery show that TUNEL-positive cells in the first 2 days after injury la

92 mpletely reversed the HS-induced increase in TUNEL-positive cells in the HS/IL-6 group (p=.002).

93 otal DNA, mtDNA deletions, and the number of TUNEL-positive cells in the kidneys increased progressiv

94 ce exhibited marked evidence of necrotic and TUNEL-positive cells in the liver, particularly at 24 ho

95 The number of TUNEL-positive cells in the mice with induced dry eye wa

96 stant light for 1 day dramatically increased TUNEL-positive cells in the outer nuclear layer.

97 cted in the INL and GCL, with low numbers of TUNEL-positive cells in the outer nuclear layer.

98 ression, decreases caspase-3 activation, and TUNEL-positive cells in the peri-infarct region, and sup

99 sone-treated animals had significantly fewer TUNEL-positive cells in the photoreceptor layer than did

100 uced the ROS level, along with a decrease in TUNEL-positive cells in the photoreceptor layer.

101 In rats, there were significantly more TUNEL-positive cells in the photoreceptors 24 hours afte

102 NAME-treated animals had significantly fewer TUNEL-positive cells in the photoreceptors than saline-t

103 iven a subretinal injection of AdNull.11 had TUNEL-positive cells in the retina, but none within area

104 optic nerve damage, decreased the number of TUNEL-positive cells in the RGC layer, and increased HSP

105 0 immunoreactivity and reduced the number of TUNEL-positive cells in the RGCL at 18 h.

106 TUNEL-positive cells in three active, nine chronic activ

107 hibition of Ki-67 expression and increase in TUNEL-positive cells in xenografted tissues.

108 yclic light for 4 days significantly reduced TUNEL-positive cells induced by exposure to constant lig

109 icantly decreased at P14, when the number of TUNEL-positive cells is highest.

110 man atherosclerotic plaques, the majority of TUNEL-positive cells lack detectable c-FLIP.

111 In epidermal sheets, TUNEL-positive cells lined the upper portion of the hair

112 ein (bcl-2 colocalized with TUNEL in 0-2% of TUNEL-positive cells observed).

113 ia, which is mirrored in vivo with apoptotic TUNEL-positive cells of infiltrating macrophage origin.

114 Total TUNEL-positive cells under both peaks exceeded the numbe

115 The number of TUNEL-positive cells was also increased in retinas from

116 An increase in TUNEL-positive cells was also noted with an increasing d

117 morphologically identified sunburn cells and TUNEL-positive cells was detected as early as 1 week aft

118 A decrease in TUNEL-positive cells was found in the NBL at P8.

119 An increase in the number of TUNEL-positive cells was observed at day 28, particularl

120 An increase in TUNEL-positive cells was observed in the ONL at the infe

121 ragmentation was abolished and the number of TUNEL-positive cells was reduced compared to the other g

122 Furthermore, at day 42 when TUNEL-positive cells were absent, Bcl-2 expression was d

123 Unexpectedly, TUNEL-positive cells were also greater in NASH vs. alcoh

124 Subsequently, pyknotic, TUNEL-positive cells were also localized to these region

125 High frequencies of TUNEL-positive cells were also observed at 1 and 2 hours

126 In addition, we found that the majority of TUNEL-positive cells were also positive for c-Jun-like i

127 TUNEL-positive cells were also seen remotely in the hipp

128 Apoptotic TUNEL-positive cells were defined using stringent morpho

129 In contrast, caspase-3 activation and TUNEL-positive cells were depressed in COX-2(-/-) livers

130 TUNEL-positive cells were detected in the ONL of tubby m

131 TUNEL-positive cells were first evident at 3 days and we

132 TUNEL-positive cells were first observed at 12 hr, incre

133 optotic cells in the cortex of rn roots when TUNEL-positive cells were first observed.

134 TUNEL-positive cells were found within the outer nuclear

135 On day one after injection, 57% of the TUNEL-positive cells were identified as alpha-SMA-positi

136 TUNEL-positive cells were most abundant closest to the s

137 Most TUNEL-positive cells were not associated with blood vess

138 Increased numbers of TUNEL-positive cells were noted in both the lotrafilcon

139 Few TUNEL-positive cells were observed between days 0 and 21

140 ymphoid tissues and in kidneys, yet numerous TUNEL-positive cells were observed in glomeruli of Bcl2l

141 More TUNEL-positive cells were observed in MGCM-treated cultu

142 Significant increases in TUNEL-positive cells were observed in the neuroblast lay

143 TUNEL-positive cells were present in retinas from diabet

144 in the presence of synthesized PR39 peptide, TUNEL-positive cells were reduced to 29.6+/-1.9% (P<0.05

145 No TUNEL-positive cells were seen in control hearts or hear

146 TUNEL-positive cells were significantly increased in liv

147 eas caspase-3 activity and the percentage of TUNEL-positive cells were significantly increased in RA-

148 TUNEL-positive cells were sometimes detected adjacent to

149 There were scattered TUNEL-positive cells within the inner retina, peaking at

150 imately 60% (from 30.1+/-5.8% to 12.2+/-2.0% TUNEL-positive cells), which was abolished by pretreatme

151 optotic markers (p53, cleaved caspase-7, and TUNEL-positive cells).

152 -24 hr, immunoreactive p20 was visualized in TUNEL-positive cells, a finding also observed in apoptot

153 a cellular survival factor, Bcl-2, decreased TUNEL-positive cells, and after CAI treatment the normal

154 owed a significant increase in MMP-2 and -9, TUNEL-positive cells, and caspase-3 activity in the lotr

155 l death with 12.81 +/- 0.58-fold increase of TUNEL-positive cells, and overexpression of MIF blocked

156 duction of antiinflammatory cytokines, fewer TUNEL-positive cells, and reduced levels of active caspa

157 ored beta-cell mass, decreased the number of TUNEL-positive cells, and restored normal glucose tolera

158 from T-cell- depleted mice, there were more TUNEL-positive cells, and the areas of apoptosis were mo

159 ease, macrophage infiltration, the number of TUNEL-positive cells, and the expression of proinflammat

160 hylcellulose) using flow cytometry to detect TUNEL-positive cells, and the percentage of positive cel

161 mice with VX-166 decreased active caspase-3, TUNEL-positive cells, and triglyceride content (P < 0.05

162 t reduction in diabetes-induced increases in TUNEL-positive cells, caspase-3 activation, and cytochro

163 In TUNEL-positive cells, Hoechst 33342 staining revealed nu

164 TUNEL-positive cells, identified by immunohistochemistry

165 embrane-damaged cells and by the presence of TUNEL-positive cells, the numbers of nonviable cells inc

166 Hypoxia induced 66.2+/-2.7% TUNEL-positive cells, whereas in the presence of synthes

167 aspase 3 cleavage, cytochrome c release, and TUNEL-positive cells, which were inhibited in the presen

168 rtate aminotransferase levels and numbers of TUNEL-positive cells.

169 f caspase 3 and an increase in the number of TUNEL-positive cells.

170 azl-/- gonads contained increased numbers of TUNEL-positive cells.

171 tial cytotrophoblasts clearly less amount of TUNEL-positive cells.

172 evated the levels of activated caspase-3 and TUNEL-positive cells.

173 interstitial cytotrophoblasts have numerous TUNEL-positive cells.

174 lear layers, and decreased the percentage of TUNEL-positive cells.

175 ed caspase-3 activity, and the percentage of TUNEL-positive cells.

176 Photoreceptors lost are fewer than TUNEL-positive cells.

177 manifested by reduced serum ALT and hepatic TUNEL-positive cells.

178 of caspase-9 and caspase-3, and formation of TUNEL-positive cells.

179 Caspase activation was detected in TUNEL-positive cells.

180 (3 mo) rats (25.4 +/- 5.3 versus 3.5 +/- 2.5 TUNEL-positive cells/0.25 mm2 in old versus young rats,

181 cting the explants, the number of apoptotic (TUNEL-positive) cells in the neopallium was increased.

182 The median (range) percentage of TUNEL-positive chondrocytes in knee OA cartilage (n = 10

183 min of ischemia, 22+/-4% of the SEC stained TUNEL positive compared with 2+/-1% of the hepatocytes (

184 in, were severely depleted and, although not TUNEL-positive, displayed strong immunoreactivity for p5

185 The observations that TUNEL-positive dying cells were present in MS lesions an

186 ed to UW solution and the reperfusion media, TUNEL positive endothelial cells were reduced 63+/-11% (

187 TUNEL-positive epidermal cells and increased oligonucleo

188 Time course study reveals that TUNEL-positive epidermal cells appear before intraepider

189 red with increased numbers of caspase-3- and TUNEL-positive fibroblasts, decreased fibroblast prolife

190 aris on P1 resulted in a gradual increase in TUNEL-positive figures within the ipsilateral olfactory

191 wo lower NMDA concentrations, which produced TUNEL-positive fragmented nuclei and faint ladder patter

192 TUNEL-positive glia were present at all stages studied b

193 However 7 d after injury, a second wave of TUNEL-positive glial cells was noted in the white matter

194 transferase-mediated dUTP nick end labeling (TUNEL) positive hepatocytes were rare and did not increa

195 In 3-day bile duct ligated (BDL) animals, TUNEL-positive hepatocytes and serum ALT values were red

196 tocyte death; (iii) increased percentages of TUNEL-positive hepatocytes; (iv) greater elevations in c

197 ns in INL and ganglion cell layer (GCL) were TUNEL positive in Bax-deficient mice than in their wild-

198 dominantly by apoptosis; viable cells became TUNEL positive, indicating degradation of DNA.

199 nd Ki-67 antigens and that by flow cytometry TUNEL-positive keratinocytes obtained from psoriatic pla

200 of psoriatic plaques revealed that numerous TUNEL-positive keratinocytes were also positive for prol

201 Compared with the control group where TUNEL-positive keratocytes were found only in the superf

202 idyl transferase-mediated nick end labeling (TUNEL)-positive labeling.

203 cated by characteristic morphologic changes; TUNEL-positive labeling; phosphatidylserine (PS) exposur

204 erase (TdT)-mediated dUTP nick-end labeling (TUNEL)-positive lens epithelial cells previously reporte

205 The number of TUNEL-positive liver cells in the HS/P group was increas

206 ynucleotidyltransferase dUTP nick end label (TUNEL)-positive macrophages in the lymph nodes (LNs) and

207 nd labeling (TUNEL), and Purkinje cells were TUNEL-positive most abundantly at P21.

208 leotidyl transferase dUTP nick-end labeling (TUNEL)-positive myocytes in the remote myocardium was in

209 transferase-mediated dUTP nick end-labeling (TUNEL)-positive myocytes was similar in KO and WT mice a

210 rase-mediated dUTP-biotin nick end labeling (TUNEL)-positive myocytes were increased significantly in

211 The number of TUNEL-positive myocytes (0.17 versus 0.28%, P<0.05) and

212 d control mice; however, a low prevalence of TUNEL-positive myocytes and DNA laddering were detected

213 After AdvFGF-5, TUNEL-positive myocytes decreased 6-fold and Ki-67 posit

214 ad larger infarct size and greater number of TUNEL-positive myocytes than control hearts.

215 proximately 3-fold increase in the number of TUNEL-positive myocytes.

216 Myonuclear apoptosis, quantified by TUNEL positive myonuclei and cleaved caspase-3 positive

217 TUNEL positive neurons were found in these two regions,

218 idine triphosphate-biotin nick end labeling (TUNEL)-positive neurons were noted primarily restricted

219 mmunocytochemistry was performed to identify TUNEL-positive neurons (anti-neurofilament monoclonal an

220 However, TUNEL-positive neurons and astrocytes were frequently de

221 We observed TUNEL-positive neurons as early as stage 24, with a larg

222 For controls, non-TUNEL-positive neurons from the cortex of sham-injured a

223 sion profiles or "molecular fingerprints" of TUNEL-positive neurons in the cerebral cortex.

224 TUNEL-positive neurons in the SC and SN showed apoptotic

225 ty and traumatic brain injury, which produce TUNEL-positive neurons without evidence of DNA synthesis

226 rees C, both TUNEL-positive viable cells and TUNEL-positive nonviable cells were observed, indicating

227 erm sleep deprived rats only a few scattered TUNEL positive nuclei (1-3) were found in any given brai

228 TUNEL staining showed that the percent TUNEL positive nuclei in rat hearts increased 10-fold af

229 phate (d-UTP)-digoxigenin nick end labeling (TUNEL)-positive nuclei were found in the ipsilateral str

230 phate (d-UTP)-digoxigenin nick end labeling (TUNEL)-positive nuclei were increased.

231 transferase-mediated dUTP nick end labeling (TUNEL)-positive nuclei, only 6 and 10 Gy significantly i

232 ficantly suppressed the number of cells with TUNEL-positive nuclei and the increase in caspase-3 acti

233 y, the presence of neurite outgrowth and for TUNEL-positive nuclei as a marker of apoptosis.

234 duced internucleosomal DNA fragmentation and TUNEL-positive nuclei as well as nuclear condensation we

235 Ethanol feeding also increased the number of TUNEL-positive nuclei in adipose tissue of wild-type mic

236 The number of TUNEL-positive nuclei in flatmounted retinas increased a

237 n of four Respiratory Burst Oxidase Homologs TUNEL-positive nuclei in meristematic cells indicated th

238 The numbers of TUNEL-positive nuclei in the c-Jun(AA) mice was reduced

239 retinal DNA and a time-related appearance of TUNEL-positive nuclei in the inner retinas after intravi

240 e and showed a reduction in ROS staining and TUNEL-positive nuclei in the meristematic cells.

241 itor of AKT signaling, significantly induced TUNEL-positive nuclei in this high-grade BSG model, but

242 The number of TUNEL-positive nuclei increased from 29+/-4 in controls

243 There were significantly fewer TUNEL-positive nuclei per high-powered field (P<0.01), l

244 id not significantly increase the percent of TUNEL-positive nuclei relative to 10 Gy alone at 6, 24,

245 An increase in the number of TUNEL-positive nuclei was detected 24 hr after stimulati

246 The number of TUNEL-positive nuclei was significantly lower in Tg-CAPK

247 TUNEL-positive nuclei were abundant at day 3.

248 se 3 increased after LVAD support, Bcl-2 and TUNEL-positive nuclei were not significantly different b

249 ng with improved cerebral energy metabolism, TUNEL-positive nuclei were reduced in the hypothermia pl

250 ion of phosphatidylserine and the display of TUNEL-positive nuclei.

251 ced a 5- to 8-fold increase in the number of TUNEL-positive nuclei.

252 TUNEL-positive outer nuclear layer nuclei were most freq

253 Number of TUNEL-positive pericytes was increased in HG condition a

254 e exhibited significantly reduced numbers of TUNEL-positive photoreceptor cells and increased ONL thi

255 TUNEL-positive photoreceptor nuclei were counted in thes

256 treatment in a light-damage model results in TUNEL-positive photoreceptor nuclei within this region.

257 Additionally, INS37217 reduced the number of TUNEL-positive photoreceptors and the enhanced rate of r

258 -/-)Nrl(-/-) mice had an increased number of TUNEL-positive photoreceptors during programmed cell dea

259 We did not detect TUNEL-positive podocytes.

260 nsient photoreceptor protection in rd-1, but TUNEL-positive rod death proceeded, despite the absence

261 uantitatively by counting both surviving and TUNEL-positive rods and cones.

262 bserved in all transplants compared with few TUNEL-positive RPE cells.

263 Neutralizing anti-TNFR1 decreased TUNEL-positive score, while anti-TNFR2 did not affect p2

264 In contrast, TUNEL positive SEC increased 6-fold after reperfusion of

265 ast migration into the decidua and increased TUNEL-positive signal.

266 leotidyl transferase dUTP nick end labeling (TUNEL)-positive soma and the eventual loss of 5HT neuron

267 e the original study reported an increase in TUNEL positive staining with iRGD coadministration.

268 esulted in significantly increased levels of TUNEL-positive staining 3 days after retinal-RPE separat

269 TUNEL-positive staining for apoptosis was detected only

270 blocked NMDA-induced necrosis and attenuated TUNEL-positive staining in slice parenchyma.

271 dizocilpine immediately after decapitation, TUNEL-positive staining no longer occurred in the injury

272 A significant increase in TUNEL-positive staining occurred in corneal stromal cell

273 characteristic nucleosome-sized DNA ladders, TUNEL-positive staining of cells, activation of the cyst

274 This corresponded to a decreased level of TUNEL-positive staining of photoreceptors after retinal-

275 TUNEL-positive staining of photoreceptors was centered a

276 However, no TUNEL-positive staining was found in epithelial cells.

277 TUNEL-positive staining with a different morphology was

278 le, as indicated by lower DNA fragmentation, TUNEL-positive staining, and caspase-3 cleavage, when co

279 rites together with significant increases in TUNEL-positive staining.

280 TUNEL-positive (T+) cells and pyknotic nuclei were first

281 to temperatures of 60 to 66 degrees C, both TUNEL-positive viable cells and TUNEL-positive nonviable

282 cytochemistry showed that dying APR(6)s were TUNEL-positive, which is diagnostic of fragmented DNA.