ライフサイエンスコーパス: BrdU

1 BrdU (100mg/kg, ip) was given 36 h after the last inject

2 BrdU analysis confirmed that the extra hair cells arose

3 BrdU analysis demonstrated significantly increased proli

4 BrdU and Ki-67 detection at neonatal and adult ages show

5 BrdU and ki67 staining confirmed extensive hepatocyte pr

6 BrdU and TUNEL assays were used to evaluate cell prolife

7 BrdU assay demonstrated proliferation in approximately h

8 BrdU ELISA and flow cytometry were used to assess prolif

9 BrdU incorporation assays indicated that in the absence

10 BrdU incorporation studies indicate that Tregs undergo p

11 BrdU label-retaining cells, a key characteristic of epit

12 BrdU labeling and adoptive transfer experiments confirm

13 BrdU labeling and GFP electroporation into postnatal SVZ

14 BrdU pulse-chase experiments demonstrated the longevity

15 BrdU pulse-labeling experiments revealed that virtually

16 BrdU staining showed an inhibited proliferation of CGPs

17 BrdU was infused for 7 days before euthanasia at days 10

18 BrdU(+) /GABA(+) (gamma-aminobutyric acid) cells were al

19 BrdU(+) MenC-PS-specific plasma cells were also reduced

20 BrdU-labeled DNA from each fraction is immunoprecipitate

21 BrdU-labeling experiments show that clusters form by mig

22 BrdU-tracking experiments showed that homing of NPCs spe

23 BrdU/beta-tubulin/HNA/DAPI, BrdU/GFAP/HNA/DAPI, Ngn1/DAP

24 BrdU/EdU labeling and immunohistochemistry assays demons

25 for DCX, cell proliferation markers (Ki-67, BrdU), pallial/subpallial developmental origin (Tbr1, Sp

26 cated less (P < 0.05) than controls during a BrdU pulse after 3 days in media containing 10% control

27 subset of type B cells that label with acute BrdU administration.

28 ects were perfused 24 hours or 28 days after BrdU to assess cellular proliferation or neurogenesis an

29 At 24 and 48 hours after BrdU inoculation, 30% of MAC387(+) monocytes/macrophages

30 ogenitor cells were in S phase 2 hours after BrdU labeling in vivo, suggesting that these cells were

31 h in the DG and at 3 months in the MOB after BrdU injections.

32 away from the ependyma even at 5 weeks after BrdU injection.

33 survived 2 days, 2 weeks, and 6 weeks after BrdU injections.

34 sue was collected 48 h, 2 wk, and 6 wk after BrdU injection to examine the initial stages of neurogen

35 We demonstrated that 78.1% of all BrdU(+) cells in DRGs were also MAC387(+).

36 d a single injection of the thymidine analog BrdU (75 mg/kg), which is incorporated into replicating

37 random incorporation of the thymidine analog BrdU into the genes of dividing cells makes the fate of

38 ncluding effects on ERK pathway activity and BrdU incorporation.

39 was measured using a colorimetric assay and BrdU incorporation.

40 ration blocker, markedly reduced BrdU(+) and BrdU/NeuN(+) cells and abolished the effect of social in

41 n increased the numbers of BrdU(+) cells and BrdU(+)NeuN(+) neurons.

42 Cell counts and BrdU analysis revealed a significantly higher proliferat

43 ytes was characterized by flow cytometry and BrdU (5-bromo-2-deoxyuridine) staining following synchro

44 ed neuronal differentiation (BrdU/DCX(+) and BrdU/NeuN(+) cells) and increased apoptosis and neurodeg

45 Furthermore, EdU and BrdU co-localized to the same cells within the DG.

46 gnificantly increased the number of EdU- and BrdU-positive cells in the DG.

47 anciclovir (GCV) depleted Dcx-expressing and BrdU-labeled cells from the rostral subventricular zone

48 yHC isoform expression, Pax7 expression, and BrdU incorporation.

49 ing, fluorescence in situ hybridization, and BrdU incorporation analysis, we demonstrate that DDR pro

50 Simultaneous analysis of Ki67 and BrdU kinetics revealed a complex in vivo turnover profil

51 ncisor microdontia, small cervical loops and BrdU labeling reveals a defect in epithelial cell prolif

52 n the number of mitotic neuroblasts (NB) and BrdU incorporation in the brain, consistent with the not

53 A significant number of BrdU/NeuN- and BrdU/calbindin-colabeled cells were observed in topograp

54 ydroxylase immunoreactive neuron numbers and BrdU-positive cells in the SNpc.

55 quitin levels decreased JMJD2A occupancy and BrdU incorporation at target sites.

56 Vein dilation, arterial tortuosity, and BrdU incorporation gradually increased over time.

57 when combined with other techniques such as BrdU.

58 ic membrane (CAM) was examined by MTT assay, BrdU labeling, cell proliferation assay, cell death dete

59 erved increase was specific to PDGs, because BrdU incorporation in cells of the pancreatic duct was n

60 Bromodeoxyuridine (BrdU) labeling indicated the same number of retinal cell

61 Bromodeoxyuridine (BrdU) labeling of proliferating cells showed that ASCs p

62 Bromodeoxyuridine (BrdU) was added to all the microcosms to label newly syn

63 Bromodeoxyuridine (BrdU) was given systemically to label dividing cells thr

64 GFP label retention and 5-bromodeoxyuridine (BrdU) incorporation.

65 5-Bromodeoxyuridine (BrdU) labeling, proliferating cell nuclear antigen (PCNA

66 uclear incorporation of 5-bromodeoxyuridine (BrdU; 7-day minipump infusion).

67 turnover measured using a bromodeoxyuridine (BrdU)-based transit assay.

68 he later developed analog bromodeoxyuridine (BrdU) have revolutionized our ability to identify dividi

69 of the thymidine analog, bromodeoxyuridine (BrdU) to mark new cells.

70 A thymidine analogue, bromodeoxyuridine (BrdU), was added to the microcosms and incorporated into

71 in situ hybridization and bromodeoxyuridine (BrdU) incorporation analysis showed that these DDR prote

72 incisor organ culture and bromodeoxyuridine (BrdU) pulse-chase experiments to identify and evaluate s

73 ry cells were detected by bromodeoxyuridine (BrdU) incorporation and anti-CD45 staining, respectively

74 iferation was assessed by bromodeoxyuridine (BrdU) incorporation, and cell viability and metabolic ac

75 marker of cell division, bromodeoxyuridine (BrdU), in combination with several markers, the maturati

76 lation and hepatocellular bromodeoxyuridine (BrdU) incorporation.

77 ibitor valproic acid into bromodeoxyuridine (BrdU)-infused rats inhibited the increased EC uptake of

78 the proliferation marker bromodeoxyuridine (BrdU) after a lesion.

79 bits the incorporation of bromodeoxyuridine (BrdU) into DNA, an effect proposed to reflect a G1 arres

80 raperitoneal injection of bromodeoxyuridine (BrdU), similar numbers of BrdU-positive keratinocytes we

81 c and cytostatic based on bromodeoxyuridine (BrdU) assay, propidium iodide (PI) staining and growth c

82 ion, the rabbits received bromodeoxyuridine (BrdU) injections.

83 -native chemical species, bromodeoxyuridine (BrdU), was imaged within single HeLa cells using time-of

84 or saline; subsequently, bromodeoxyuridine (BrdU) was injected daily intraperitoneally.

85 ll mice were subjected to bromodeoxyuridine (BrdU) injection and sacrificed at different time points

86 that I3 colocalizes with bromodeoxyuridine (BrdU)-labeled nascent viral genomes and that these genom

87 titutively proliferating (bromodeoxyuridine [BrdU]+) cell populations, including a radial glial-like

88 erated cells (marked with bromodeoxyuridine [BrdU]) and those expressing brain-derived neurotrophic f

89 Parabiosis, bromodoxyuridine (BrdU) pulse-chase analysis, and intranasal instillation

90 multipotent differentiation were analyzed by BrdU labeling, flow cytometry, reverse transcriptase-pol

91 eration was measured by cell counting and by BrdU assay.

92 Proliferation was assayed by BrdU uptake and cell counts of calcein AM/ethidium bromi

93 eration and differentiation were assessed by BrdU incorporation and immunohistochemistry with specifi

94 Liver regeneration was assessed by BrdU incorporation and Ki-67 immunostaining.

95 immune activation by turnover of T cells by BrdU decay and Ki67 expression.

96 ate in culture during 72 h, as determined by BrdU-uptake detection.

97 Cell proliferation was evaluated by BrdU incorporation test.

98 ithelial cell proliferation was evaluated by BrdU incorporation test.

99 n retinal cell proliferation as indicated by BrdU assay and exhibited no acute toxicity in retinal ti

100 cling marker, indicate that cells labeled by BrdU during the second half of embryonic life are slow-c

101 stimulate cell proliferation as measured by BrdU incorporation.

102 s undergoing DNA replication, as measured by BrdU incorporation.

103 Proliferation was measured by BrdU incorporation.

104 ased epithelial proliferation as measured by BrdU labeling, longer colonic crypts and an expansion of

105 or the interpretation of results obtained by BrdU as an index of the number of neurons produced, and

106 by flow cytometry and cell proliferation by BrdU incorporation.

107 rative crypt epithelial cells as revealed by BrdU or Ki67 staining at days 3 and 5 after start of tam

108 emonstrate ongoing cell turnover as shown by BrdU incorporation and activated caspase-3 and TUNEL sta

109 llowing capsaicin administration as shown by BrdU incorporation.

110 dU(+) cells were MAC387(+); however, CD163(+)BrdU(+) macrophages were present in the meninges and cho

111 and increased the number of new glial cells (BrdU/GFAP-positive).

112 maging (fMRI), and neuronal precursor cells (BrdU+/Nestin+) were detected by immunofluorescence.

113 hemistry (PCNA-staining) and flow cytometry (BrdU incorporation) revealed that a discrete proportion

114 BrdU/beta-tubulin/HNA/DAPI, BrdU/GFAP/HNA/DAPI, Ngn1/DAPI, and BMP4/DAPI were measur

115 G(0)/G(1) phase of the cell cycle, decreased BrdU (5-bromo-2'-deoxyuridine) incorporation, and led to

116 matical modeling of 5-bromo-2' deoxyuridine (BrdU) labeling dynamics demonstrated a significantly inc

117 response to analogs 5-bromo-2'-deoxyuridine (BrdU) and 5-ethynyl-2'-deoxyuridine (EdU).

118 We used 5'-bromo-2'-deoxyuridine (BrdU) and retroviral methodologies to birth date cells b

119 5-Bromo-2'-deoxyuridine (BrdU) has been investigated as a radiosensitizing agent

120 te progenitors were 5-bromo-2'-deoxyuridine (BrdU) labeled in bone marrow, and CNS macrophages were l

121 cycle change using 5-bromo-2'-deoxyuridine (BrdU) pulse-labeling and DAPI (4',6-diamidino-2-phenylin

122 We used 5-bromo-2'-deoxyuridine (BrdU) to identify and localize proliferation zones in th

123 toneal injection of 5-bromo-2'-deoxyuridine (BrdU) to label progenitors in the hippocampal subgranula

124 ase mitotic marker 5'-bromo-2'-deoxyuridine (BrdU) was administered at the conclusion of each stage f

125 By using 5-bromo-2'-deoxyuridine (BrdU), a label-retaining cell population was characteriz

126 ically labeled with 5-bromo-2'-deoxyuridine (BrdU), deuterium, or the fluorescent dye carboxy-fluores

127 d the BMP-2-induced 5-bromo-2'-deoxyuridine (BrdU)-positive cell numbers at the injected site on day

128 of DNA replication 5-bromo-2'-deoxyuridine (BrdU).

129 he exogenous marker 5-bromo-2'-deoxyuridine (BrdU, 200mg/kg, ip) was administered 2h into the 4-h smo

130 nal marker NeuN and 5-bromo-2'-deoxyuridine (BrdU; a marker for proliferating cells) in vivo, consequ

131 he nucleotide analog 5-bromo-2-deoxyuridine (BrdU) and sorted into S-phase fractions on the basis of

132 ting quail eggs with 5-bromo-2-deoxyuridine (BrdU) at various stages between embryonic day (E)3 and E

133 IP) with 50 mg/kg of 5-bromo-2-deoxyuridine (BrdU) immediately after anesthesia.

134 of new nuclei using 5-bromo-2-deoxyuridine (BrdU) labelling by isolating individual myofibres.

135 ow to the DRGs using 5-bromo-2-deoxyuridine (BrdU) pulse, and serially measured IENFD.

136 received intravenous 5-bromo-2-deoxyuridine (BrdU).

137 5-Bromo-2-deoxyuridine (BrdU, 50 mg/kg) was intraperitoneally delivered every ot

138 ing ImageJ software, and bromo-deoxyuridine (BrdU) labeling was used to visualize proliferation of re

139 injected with 5-bromo-2&prime-deoxyuridine (BrdU) at 0-3 weeks posttransection.

140 roliferation (Ki67, 5-bromo-2'-deoxyuridine [BrdU]) and cell death (caspase-3, terminal deoxynucleoti

141 signaling impaired neuronal differentiation (BrdU/DCX(+) and BrdU/NeuN(+) cells) and increased apopto

142 5-Bromo-2'-dioxyuridine (BrdU) assay was performed to evaluate proliferation of R

143 jection enhances the number of doublecortin, BrdU/NeuN, and c-fos-positive cells in the dentate gyrus

144 Decreased IENFD was associated with elevated BrdU(+) cells in the DRG.

145 tes and chronic pancreatitis jointly enhance BrdU incorporation and production of pancreatic cancer-s

146 han 10% of the BDNF-positive cells expressed BrdU, but this percentage was greater in juveniles than

147 sis, including reduced NG2 expression, fewer BrdU-positive OLs, altered BMP4 signaling and inhibitor

148 period of sexual differentiation (following BrdU injections on days 6-10) and in adulthood (followin

149 Cells colabeled for BrdU and five different neuronal markers were observed w

150 poration and survival determined by FACS for BrdU+ cells.

151 Double-label immunofluorescence for BrdU and the protein Fos revealed that a subset of puber

152 Triple-label immunofluorescence for BrdU, the mature neuron marker neuronal nuclear antigen,

153 hippocampal sections were immunostained for BrdU (proliferating cell marker), NeuN (neurons), GFAP (

154 veloped qBrdU-seq, a quantitative method for BrdU incorporation analysis of replication dynamics, and

155 Furthermore, BrdU incorporation assays and Ki67 staining demonstrated

156 replicated 20% less (P < 0.05) during a 2 h BrdU pulse.

157 differentiated carcinomas (pdSCCs) with high BrdU-labelling and elevated cyclin D1/E2 expression leve

158 nic 19(+)45R(lo) cells exhibited homeostatic BrdU uptake in vivo and actively transcribed cell cycle

159 mulation of neutral lipid droplets; however, BrdU incorporation into keratinocytes was normal.

160 ins like cyclin E, cyclin D1 and decrease in BrdU incorporation.

161 that previously reported sex-differences in BrdU-labeling along the adult VZ (males>females) result

162 of J in Leishmania tarentolae via growth in BrdU resulted in cell death and indicated a role of J in

163 incorporation) but a significant increase in BrdU+ myocytes.

164 and ventricle, but there was no increase in BrdU+ myocytes.

165 ation Discrimination ability, an increase in BrdU-labelled cells in the subgranular zone of the denta

166 cells, as reflected by a marked increase in BrdU-negative lin(-) c-kit(+) Sca-1(+) cells in the bone

167 nanolone was administered had an increase in BrdU-positive cells in the SNpc.

168 re driven into proliferation and incorporate BrdU in response to high ex vivo concentrations of IL-2,

169 ng cells: new hair cells did not incorporate BrdU, supporting cells upregulated the pro-hair cell gen

170 , B19V-infected 4 N cells still incorporated BrdU, indicating active DNA synthesis.

171 e increased cell proliferation and increased BrdU incorporation in insulin-treated cells as well as i

172 ortion of slow MyHC myofibers, and increased BrdU-positive satellite cells.

173 co-localization) was paralleled by increased BrdU cells that did not co-localize with any of the phen

174 oting effect of WISP2 was shown by increased BrdU incorporation in vivo and Tg serum increased mesenc

175 ks post exposure to IR resulted in increased BrdU incorporation and cancer incidence.

176 ges in the growth plate, including increased BrdU incorporation and matrix production.

177 Indeed, BrdU incorporation assays revealed that recombinant huma

178 weeks (12 weeks postexercise) after initial BrdU injections.

179 ly portray the distribution of intracellular BrdU as well as other intracellular structures.

180 On PD80, animals were injected with 200mg/kg BrdU.

181 mical markers for tumor proliferation (Ki67, BrdU) as well as hENT1, TK1, or TS expression was detect

182 At 4 wk after the last BrdU injection, animals were allowed to interact with a

183 ta demonstrate that newly recruited MAC387(+)BrdU(+) macrophages may play a significant role in DRG p

184 Proliferation makers (BrdU, cyclin D1, p53) and cancer stem cell markers (CD13

185 Colabeling of the cell proliferation marker BrdU with the neuronal marker NeuN and peptides revealed

186 hological and electrophysiological measures; BrdU (5-bromo-2-deoxyuridine) injections were used to qu

187 to 5-bromo-2'-deoxyuridine-5'-monophosphate (BrdU) in vitro.

188 Cerulein administration led to more BrdU(+) cells in PDGs of obese mice compared with lean m

189 Moreover, BrdU incorporation in MK-stimulated OBs was blocked by t

190 Moreover, BrdU(+) cells with plasma cell morphology can be detecte

191 The lesion site had the most BrdU labeling at all times, correlating with an increase

192 al and microglial activation), neurogenesis (BrdU-labeled newborn cells), and amyloidosis [soluble am

193 Significantly enhanced neurogenesis (BrdU/NeuN-positive cells) was seen in the dentate gyrus

194 to measure vascularity (vWF), neurogenesis (BrdU TUJ1, DCX and NeuN), synaptogenesis (synaptophysin)

195 minished numbers of newly generated neurons (BrdU/NeuN co-localization) was paralleled by increased B

196 ecreased the number of new immature neurons (BrdU/DCX-positive) and transition neurons (BrdU/DCX/NeuN

197 (BrdU/DCX-positive) and transition neurons (BrdU/DCX/NeuN-positive) and increased the number of new

198 No BrdU(+) /DCx(+) cells were found but about 7.5% of new c

199 the stratum corneum abnormalities and normal BrdU uptake.

200 cycle in S phase, nor did it induce de novo BrdU incorporation.

201 sacrificed 2-4h after the administration of BrdU.

202 4-Bromo- and 5-bromopyridone analogues of BrdU were synthesized and incorporated into oligonucleot

203 rmined by unbiased stereological analysis of BrdU incorporation and survival determined by FACS for B

204 Using assays of BrdU incorporation, flow cytometry, and ELISA, we measur

205 Flow cytometry of BrdU incorporation or Ki67 expression in conjunction wit

206 investigate cell survival, the same dose of BrdU was administered 24h before the start of the 14-day

207 ce senescence, as evaluated by inhibition of BrdU incorporation and quantification of senescence-acti

208 of LPS causes even more severe inhibition of BrdU incorporation in the Tyro3(-/-)Axl(-/-)Mertk(-/-) t

209 rcise study received 10 weekly injections of BrdU (75 mg/kg), and brain tissue was collected at 16 an

210 y 5.5-7 years) received single injections of BrdU and survived 2 days, 2 weeks, and 6 weeks after Brd

211 s and cells with both high and low levels of BrdU incorporation in the PUT and SPD microcosms, but no

212 The number of BrdU label-retaining cells (LRCs) was dramatically reduc

213 uses a significant increase in the number of BrdU label-retaining NSCs in the SVZ, whereas NSC/astroc

214 The number of BrdU(+) monocytes correlated with severe DRG histopathol

215 Concomitantly, the number of BrdU(+)/NeuN(+) cells in the hippocampal dentate gyrus w

216 m cells in vitro and decreased the number of BrdU+ (5-bromo-2'-deoxyuridine+) myocytes detected at th

217 There was no difference in the number of BrdU+ cells in AE, SI and SC groups on PD80.

218 ation, as evident by the decreased number of BrdU- and beta-III tubulin-positive cells.

219 abeled cells was comparable to the number of BrdU-labeled cells in both the control and running mice.

220 wed a significant reduction in the number of BrdU-positive myonuclei in satellite cell-depleted muscl

221 A significant number of BrdU/NeuN- and BrdU/calbindin-colabeled cells were obser

222 iviral transduction increased the numbers of BrdU(+) cells and BrdU(+)NeuN(+) neurons.

223 erent than control, but increased numbers of BrdU+ myocytes were found when BrdU was infused during i

224 bin ablation had little effect on numbers of BrdU-labeled and TUNEL-labeled SCs, suggesting mechanism

225 olated dominant males had similar numbers of BrdU-labeled cells compared with dominant males that wer

226 d cell proliferation, we compared numbers of BrdU-labeled cells in multiple brain nuclei among fish o

227 In the POM, large numbers of BrdU-positive cells were observed in subjects injected f

228 bromodeoxyuridine (BrdU), similar numbers of BrdU-positive keratinocytes were observed in the skin of

229 the adjacent spinal cord, the percentage of BrdU labeling was higher in the ependymal than in nonepe

230 The survival of BrdU cells labeled before defeat stress was also not alt

231 ed rats inhibited the increased EC uptake of BrdU at poststenotic sites.

232 Moreover, uptake of BrdU was dose-dependently reduced in cells treated with

233 ified intestinal epithelial renewal based on BrdU incorporation, villus height and crypt depth, and c

234 In juveniles only, BrdU-positive cells appeared in contact with vimentin-la

235 acaque monkeys exposed to either [(3)H]dT or BrdU as embryos.

236 There are more PCNA, BrdU, PHH3 and Ki67 positive cells in Nfib(-)/(-) lungs

237 By performing BrdU labeling and parabiosis experiments in adult mice,

238 By performing BrdU pulse-labeling studies, we found that MBC formation

239 ating monocytes (bromodeoxyuridine positive [BrdU(+)] CD163(+)), suggesting that the increased blood

240 s of NG2(+) phenotypes were affected by post-BrdU survival periods, monkey age, and possibly a postex

241 After MenC-PS booster, proliferating (BrdU(+)) MenC-PS-specific naive B cells (CD138(-)/B220(+

242 bit increased basal astrocyte proliferation (BrdU incorporation) indistinguishable from neo(CKO) astr

243 ificant reduction in cellular proliferation (BrdU incorporation) but a significant increase in BrdU+

244 increased endogenous cellular proliferation (BrdU-positive cells) in the injury boundary zone and hip

245 Additionally, animals received BrdU injections during training to assess the role of ne

246 anular zone of the dentate gyrus and reduced BrdU incorporation, suggesting that CBP/p300 activation

247 Compared to saline, MenC-PS booster reduced BrdU(+) IgG(+) MenC-PS-specific B cells in spleen (P = .

248 cell proliferation blocker, markedly reduced BrdU(+) and BrdU/NeuN(+) cells and abolished the effect

249 BrdU label, uhrf1 mutant hepatocytes retain BrdU throughout outgrowth, reflecting cell cycle arrest.

250 ased number of Drd1-positive cells retaining BrdU in postnatal day (P) 0 Rarb(-/-) striatum.

251 -administration enhanced the survival of SGZ BrdU cells, and methamphetamine seeking during protracte

252 T-maze and had a fewer number of 2-h-old SGZ BrdU cells than nondrug and I-ShA rats, suggesting that

253 maze and had a greater number of 2-h-old SGZ BrdU cells than nondrug controls.

254 Some BrdU-labeled cells were also double labeled by antibodie

255 f ANP (0.003 nm) inhibited Ang II-stimulated BrdU uptake by 68%.

256 TAg induction stimulated BrdU uptake by Muller glia in mixed retinal cultures fro

257 Two-hour-old and 28-day-old surviving BrdU-immunoreactive cells were quantified.

258 clear addition to enlarged fibers, long-term BrdU labeling showed a significant reduction in the numb

259 Recent reports that BrdU yields DNA interstrand cross-links (ICLs) in non-ba

260 e reductase inhibitor, Spd1, suggesting that BrdU causes dNTP pool imbalance in fission yeast, as in

261 The BrdU was localized to the nucleus of cells, whereas stru

262 in serum-free conditions, as assessed by the BrdU incorporation assay.

263 during hepatic outgrowth and thus dilute the BrdU label, uhrf1 mutant hepatocytes retain BrdU through

264 ficient in PACAP exhibited a decrease in the BrdU labeling index (LI) in E9.5 cortex, suggesting that

265 Notably, the BrdU incorporation was caused neither by viral DNA repli

266 Most of the BrdU(+) cells were MAC387(+); however, CD163(+)BrdU(+) m

267 s of the arcopallium (RA), about half of the BrdU-positive cells expressed BDNF across sexes and ages

268 In addition, we confirm through BrdU-labeling experiments that the posterior (Dp) zone i

269 We then confirmed through BrdU and other experiments that OPC proliferation double

270 Finally, we demonstrate that the response to BrdU is influenced by the ribonucleotide reductase inhib

271 rebellar circumference there are fewer total BrdU-labeled granule cells in the mutants, and these fai

272 orescein staining, 5-bromo-2'-deoxy-uridine (BrdU) labeling.

273 Here, we used BrdU incorporation to track DNA synthesis during BIR and

274 Fate mapping using BrdU pulse-chase experiments revealed that such deficits

275 n addition, proliferation was measured using BrdU incorporation and both TrkA and matrix metalloprote

276 We assessed BSM proliferation using BrdU incorporation.

277 We assessed cell proliferation using BrdU, flow cytometry, and cell count; signaling intermed

278 A subset of mice received i.v. BrdU injection 20 h after challenge.

279 n be detected for 10 years after vaccination/BrdU administration, indicating that plasma cells may pe

280 highly proliferative as assessed by in vivo BrdU incorporation.

281 In vivo BrdU injection was performed to evaluate the kinetics an

282 We used in vivo BrdU labeling and markers specific to stages of macropha

283 Using in vivo BrdU labeling techniques, we demonstrated alpha- and del

284 used in vivo bioluminescent imaging, in vivo BrdU labeling, and three different experimental GVHD sys

285 cKit+ cardiac progenitor cells were BrdU labeled during injury.

286 30% of MAC387(+) monocytes/macrophages were BrdU(+), consistent with their being recently infiltrate

287 ed numbers of BrdU+ myocytes were found when BrdU was infused during injury.

288 n more detail in a companion paper, in which BrdU/IdU cell-labelling experiments were performed under

289 In winter, BrdU labeling was seen primarily in the subventricular a

290 cytes/macrophages were increased, along with BrdU(+) cells, in the DRGs of SIV-infected macaques.

291 Pulse-chase assays with BrdU confirmed intracellular replication of pneumococci

292 s and avoid indirect effects associated with BrdU toxicity and genetic deletions, we inhibited J synt

293 Of the cells colabeled with BrdU and a neuronal marker, at least half had an inhibit

294 genome integrity and labeled comparably with BrdU to parasites within iNOS(-) cells, suggesting that

295 used four-color-interphase-FISH coupled with BrdU incorporation and analyses of senescence features t

296 Pulse-chase-pulse experiments with BrdU and EdU, and DNA content analysis indicate that uhr

297 from adult and newborn sheep (injected with BrdU and analyzed at different survival times) were proc

298 parate AE, SI, and SC rats not injected with BrdU were tested for the context preexposure facilitatio

299 of surviving new cells (-20%), labeled with BrdU in the dentate gyrus.

300 We labeled newborn HVC neurons with BrdU, and RA-projecting HVC neurons (HVCRA) with retrogr