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 gammaH2AX) and the ratio of apoptotic cells (TUNEL-positive) and senescent cells (SA-betagal-positive

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

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

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

17 TUNEL-positive apoptotic cells were dramatically decreas

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

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

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

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

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

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

24 48 h whereas some Hsp70 stained neurons were TUNEL positive at 72 h after reperfusion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 Reduced overall TUNEL positive cells were observed in HT+M (47.1 cells/m

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

49 crease in mortality and in brain cell death (TUNEL positive cells) throughout the whole brain, and in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 -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

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

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

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

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

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

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

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

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

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

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

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

76 TUNEL-positive cells and mitochondrial release of cytoch

77 TUNEL-positive cells and serum alanine aminotransferase

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

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

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

81 treatment reduced (P < 0.001) the number of TUNEL-positive cells compared to vehicle at 24 h and day

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 0 immunoreactivity and reduced the number of TUNEL-positive cells in the RGCL at 18 h.

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

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

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

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

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

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

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

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

118 Liver and kidney function markers and TUNEL-positive cells significantly increased, and struct

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Apoptotic TUNEL-positive cells were defined using stringent morpho

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

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

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

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

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

139 TUNEL-positive cells were found within the outer nuclear

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

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

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

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

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

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

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

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

148 TUNEL-positive cells were present in retinas from diabet

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

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

151 TUNEL-positive cells were significantly increased in liv

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

153 pase-3 expression/activity and the number of TUNEL-positive cells were significantly low.

154 TUNEL-positive cells were sometimes detected adjacent to

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

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

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

158 -24 hr, immunoreactive p20 was visualized in TUNEL-positive cells, a finding also observed in apoptot

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

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

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

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

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

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

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

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

167 distorted liver morphology, accumulation of TUNEL-positive cells, and transcriptional upregulation o

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

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

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

171 TUNEL-positive cells, identified by immunohistochemistry

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

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

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

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

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

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

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

179 interstitial cytotrophoblasts have numerous TUNEL-positive cells.

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

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

182 Photoreceptors lost are fewer than TUNEL-positive cells.

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

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

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

186 Caspase activation was detected in TUNEL-positive cells.

187 (3 mo) rats (25.4 +/- 5.3 versus 3.5 +/- 2.5 TUNEL-positive cells/0.25 mm2 in old versus young rats,

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

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

190 ng CHOP, TNFa, IL-1B, MMP-13, pS6, number of TUNEL-positive chondrocytes, and senescence marker p16 I

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

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

193 eotidyl transferase dUTP nick end labelling (TUNEL)-positive dying cells and reduced infarct growth f

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

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

196 TUNEL-positive epidermal cells and increased oligonucleo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 TUNEL positive neurons were found in these two regions,

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

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

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

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

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

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

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

234 both cleaved caspase-3-positive neurons and TUNEL-positive neurons were significantly less in 0.7 g/

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

236 DNA fragmentation, TUNEL-positive neurons, cleaved caspase-3-positive neuro

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

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

239 tential, mPTP, and ROS levels increased; and TUNEL positive nuclei and apoptosis-related proteins sho

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 TUNEL-positive nuclei were abundant at day 3.

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

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

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

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

264 TUNEL-positive outer nuclear layer nuclei were most freq

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

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

267 TUNEL-positive photoreceptor nuclei were counted in thes

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

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

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

271 We did not detect TUNEL-positive podocytes.

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

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

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

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

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

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

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

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

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

281 TUNEL-positive staining for apoptosis was detected only

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

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

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

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

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

287 TUNEL-positive staining of photoreceptors was centered a

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

289 TUNEL-positive staining with a different morphology was

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

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

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

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

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