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 effects across a wide range of doses (25-300 mug/g

9 BrdU ELISA and flow cytometry were used to assess prolif

10 BrdU incorporation assays indicated that in the absence

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-gammaH2AX colabeling is neither an age-related phen

21 BrdU-labeled DNA from each fraction is immunoprecipitate

22 BrdU-labeling experiments show that clusters form by mig

23 BrdU-tracking experiments showed that homing of NPCs spe

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

25 BrdU/EdU labeling and immunohistochemistry assays demons

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

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

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

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

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

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

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

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

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

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

36 ncluding effects on ERK pathway activity and BrdU incorporation.

37 was measured using a colorimetric assay and BrdU incorporation.

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

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

40 This resulted in attenuation of cFos and BrdU-labeled cell changes and prevented associated learn

41 Cell counts and BrdU analysis revealed a significantly higher proliferat

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

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

44 such as the density of mitotic figures, and BrdU and proliferating cell nuclear antigen (PCNA)-react

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

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

47 We similarly observed increased Ki67 and BrdU staining in cultured fresh neonatal rat ventricular

48 of genetic H2B-GFP pulse-chase labeling and BrdU incorporation in mice, we show significant postnata

49 DNA damage suppressed BrdU labeling and BrdU-gammaH2AX colabeling.

50 siding granule cells, proliferating NSCs and BrdU+ neurons in the dDG, whereas newborn neurons of the

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

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

53 Nucleoside analogs such as BrdU, which are incorporated into DNA during S-phase, ha

54 when combined with other techniques such as BrdU.

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

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

57 , with a significant reduction in early-born BrdU(+) cells but no change at later time points.

58 , pro-proliferative conditions promoted both BrdU and gammaH2AX labeling, which could indicate DNA da

59 ports of beta-cell nuclei labeling with both BrdU and gamma-phosphorylated H2A histone family member

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 this method, we detect 5-bromodeoxyuridine (BrdU) incorporated by Saccharomyces cerevisiae to reveal

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

66 5-Bromodeoxyuridine (BrdU) labeling, proliferating cell nuclear antigen (PCNA

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

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

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

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

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

75 lation and hepatocellular bromodeoxyuridine (BrdU) incorporation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 Cell proliferation was evaluated by BrdU incorporation test.

92 ithelial cell proliferation was evaluated by BrdU incorporation test.

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

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

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

96 Proliferation was measured by BrdU incorporation.

97 stimulate cell proliferation as measured by BrdU incorporation.

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

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

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

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

102 llowing capsaicin administration as shown by BrdU incorporation.

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

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

105 The number of SVZ stem cells (BrdU+GFAP+) was decreased in SNCA-A30P mice, whereas pro

106 different thymidine analogs including CldU, BrdU, IdU as well as EdU alone or coupled to Biotin and

107 After 8 weeks of continuous BrdU administration, fewer than 10% of homeostatic ZCs i

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

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

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

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

112 5-Bromo-2'-deoxyuridine (BrdU) has been investigated as a radiosensitizing agent

113 hen given pulses of 5-bromo-2'-deoxyuridine (BrdU) in their drinking water, followed by chase periods

114 SisterC employs 5-bromo-2'-deoxyuridine (BrdU) incorporation during S-phase to label newly replic

115 e administration of 5-bromo-2'-deoxyuridine (BrdU) interferes with cell proliferation and leads to th

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

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

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

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

120 n was quantified by 5-bromo-2'-deoxyuridine (BrdU) uptake (10 mum).

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

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

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

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

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

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

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

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

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

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

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

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

133 5-Bromo-2-deoxyuridine (BrdU, 50 mg/kg) was intraperitoneally delivered every ot

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

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

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

137 ell proliferation (5'-bromo-2'-deoxyuridine [BrdU]), (b) neural precursor (nestin), (c) neuronal phen

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

139 5-Bromo-2'-dioxyuridine (BrdU) assay was performed to evaluate proliferation of R

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

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

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

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

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

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

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

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

148 Furthermore, BrdU incorporation assays and Ki67 staining demonstrated

149 Furthermore, BrdU-labeled CD163(+)CD206(+) DP and CD163(+)CD206(-) SP

150 When mice were given BrdU at the same time as tamoxifen, more than 90% of cel

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

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

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

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

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

156 ration, D-NAscent detects the differences in BrdU incorporation frequency across individual molecules

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

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

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

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

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

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

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

164 re immunopositive for Ki 67 and incorporated BrdU.

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

166 wer than 10% of homeostatic ZCs incorporated BrdU, whereas 88% of neck cells were labeled.

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

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

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

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

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

172 Indeed, BrdU incorporation assays revealed that recombinant huma

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

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

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

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

177 Under conditions of limiting BrdU concentration, D-NAscent detects the differences in

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

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

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

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

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

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

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

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

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

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

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

189 the stratum corneum abnormalities and normal BrdU uptake.

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

191 saline injected rats, the administration of BrdU impairs the proliferative behavior of neuroepitheli

192 4-Bromo- and 5-bromopyridone analogues of BrdU were synthesized and incorporated into oligonucleot

193 ntial loss of C-strand DNA while analysis of BrdU uptake during leading and lagging-strand telomere r

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

195 rformed experiments to clarify the causes of BrdU-gammaH2AX double labeling in mouse and human beta-c

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

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

198 nt findings also revealed that high doses of BrdU lead to the activation of apoptotic cellular events

199 have raised questions about the fidelity of BrdU to label S-phase, especially during conditions when

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

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

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

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

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

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

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

207 enhanced SC proliferation and the number of BrdU(+)-S100B(+)-SCs over time.

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

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

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

211 ell fate analysis showed a greater number of BrdU-labeled cells which co-expressed Prox-1 in the DG o

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

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

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

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

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

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

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

219 ver time, we observed that the proportion of BrdU-positive ZCs remained greater than 60% up to 11 mon

220 alpha2 blocked the T(3) + IGF-1 reduction of BrdU uptake and dramatically reduced ERK and Akt signall

221 NH3 blocked the T(3) + IGF-1 reduction of BrdU uptake without altering the phosphorylation of ERK

222 Co-staining of BrdU+ cells with NeuN or S100B permitted the parallel st

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

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

225 re effects were found with 300 mug/g b.w. of BrdU.

226 ound in rats injected with 100 mug/g b.w. of BrdU.

227 uced in rats injected with 100 mug/g b.w. of BrdU.

228 d in animals injected with 300 mug/g b.w. of BrdU.

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

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

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

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

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

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

235 precursor (nestin), (c) neuronal phenotype (BrdU/beta3-tubulin), and (d) neuronal maturity (NeuN) in

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

237 were evaluated at 2, 5, 14, and 30 days post BrdU administration, with the use of selected markers (g

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

239 y (no tamoxifen), ZCs became the predominant BrdU-labeled population, whereas other cells, including

240 In mice whose ZCs were the principal BrdU-positive population, acute injury by tamoxifen or c

241 esulted in SPEM cells becoming the principal BrdU-positive population.

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

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

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

245 ctionated irradiation reduced proliferation (BrdU, p = 0.0064), increased DNA damage (yH2AX, p = 0.00

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

247 in 135 dGA cardiomyocytes, NH3 alone reduced BrdU uptake (-28%, P < 0.05), as well as T(3) -induced p

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

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

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

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

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

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

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

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

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

257 In the present study, BrdU-dated cells of the structurally and functionally di

258 DNA damage suppressed BrdU labeling and BrdU-gammaH2AX colabeling.

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

260 After withdrawal of tamoxifen, BrdU-positive ZCs reappeared.

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

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

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

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

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

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

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

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

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

270 can be revealed through a combination of the BrdU/EdU pulse-chase, based on the circadian pattern of

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

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

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

274 Experiments using TUNEL, BrdU, progenitor labeling, and stem cell elimination dur

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

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

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

278 We assessed BSM proliferation using BrdU incorporation.

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

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

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

282 highly proliferative as assessed by in vivo BrdU incorporation.

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

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

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

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

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

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

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

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

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

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

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

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

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

296 The pregnant rats were injected with BrdU at embryonic day 13, and their fetuses were sacrifi

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

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

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

300 ing water, followed by chase periods without BrdU, or combined with intraperitoneal injections of 5-e