ライフサイエンスコーパス: castrate

1 ) in obese male Zucker rats, both intact and castrated.

2 testosterone-induced restoration paradigm in castrates.

3 rons was 2.6 times higher in intacts than in castrates.

4 that was blocked by androgen replacement in castrates.

5 d song stability were similar in intacts and castrates.

6 aP tumors with or without NE allografts were castrated 2 weeks after NE tumor inoculation, and change

7 ales, and saporin-treated males who had been castrated 6 weeks previously and given testosterone repl

8 Castrated adult male hamsters were subjected to right sp

9 Androgen target tissue uptake was evident in castrated adult male rats; however, in DES-treated, AR-p

10 To address this issue, we castrated adult male white-crowned sparrows and rapidly

11 We studied this question by castrating adult male canaries in late summer and quanti

12 n(-/-) mice and rescued effector function in castrated and immunized wild-type mice.

13 season in adult male green anoles that were castrated and implanted with either testosterone (T) or

14 Sixty-day-old Sprague Dawley males were castrated and implanted with SILASTIC capsules containin

15 of apoE4 on cognitive function in males, we castrated and sham-castrated apoE4, apoE3, and Apoe-/- m

16 e mice that were gonad-intact, castrated, or castrated and treated with estradiol implants.

17 When castrates and intacts that sang comparable amounts were

18 d males were both demasculinized (chemically castrated) and completely feminized as adults.

19 PCa, but patients invariably relapse despite castrate androgen levels (castration-resistant PCa, CRPC

20 Consistent with castrate androgen levels, androgen-regulated genes were

21 opment, following androgen administration to castrate animals, and during tumor development.

22 When castrated animals are maintained, the emergence of andro

23 Thus, in castrated animals bearing MDA-PCa-2b cancers, the admini

24 e tmeff2 transcription, androgen delivery to castrated animals carrying CWR22 xenografts increases TM

25 ell as the corticosterone response to LPS in castrated animals that had had their testes intact over

26 In the gastrocnemius muscle of castrated animals, HB treatment significantly increased

27 d promote prostate xenograft tumor growth in castrated animals.

28 ndrogen-dependent tumor to one that grows in castrated animals.

29 Castrated ApoE(-/-):Ins2(+/Akita) mice showed a reductio

30 ive function in males, we castrated and sham-castrated apoE4, apoE3, and Apoe-/- male mice and behavi

31 On the contrary, castrated, but not sham-castrated, apoE4 mice showed improved acquisition over t

32 Accordingly, these cells grew in castrated as well as intact male mice.

33 grin is required for tumor growth in vivo of castrated as well as of noncastrated mice.

34 weeks of age; in the second group, mice were castrated at 10 weeks of age, allowed to recover for 10

35 Performance in adult males that had been castrated at birth was still enhanced by exposure to an

36 In the first experiment, males were castrated at birth whereas females were injected with te

37 ondrial DNA-deficient cells formed tumors in castrated athymic mice, whereas LNCaP did not.

38 r the administration of 17-beta-estradiol to castrated B6 male mice as compared with nonoperated male

39 unized BALB/c, BALB/cBy, IL-6-deficient, and castrated BALB/c mice with trifluoroacetyl chloride-hapt

40 elease over the 24 h period in adult animals castrated before puberty in contrast to animals castrate

41 On the contrary, castrated, but not sham-castrated, apoE4 mice showed imp

42 ment partially reduced OS in VP epithelia of castrates, but the level remained higher than in intact

43 growth was partially supported in EB-treated castrates, but this growth was blocked by MK-801 treatme

44 of estradiol benzoate (OVX+E), OVX females, castrated (CAST) males, and intact males.

45 Sixty-eight castrate, chemotherapy-naive men with HRPC were enrolled

46 ntratumoral androgen levels when passaged in castrate compared with eugonadal animals.

47 evious second-line hormonal therapies, and a castrate concentration of testosterone.

48 astration-resistant prostate cancer, who had castrate concentrations of testosterone and an Eastern C

49 SVs that provide a survival advantage under castrate conditions, enabling resistance to hormone ther

50 gression to CRPC by sensitising PC cells to 'castrate' conditions-that is, low levels of testicular a

51 on vs. intact control, P < 0.01; and 68% vs. castrated control, P < 0.05).

52 on vs. intact control, P < 0.01; and 75% vs. castrated control, P < 0.05).

53 Intact females and estrogen-treated castrates demonstrated increased bcl-2 mRNA and protein

54 F18-fluorodihydrotestosterone is active in castrate disease and is emerging as a valuable pharmacod

55 ication of time to hormone refractoriness in castrate disease and overall survival.

56 l. show that germ-free mice, when chemically castrated, do not lose bone - a finding that unequivocal

57 epithelial proliferation in both intact and castrated EAF2-/-Pten+/- mice.

58 Animals were castrated either prepubertally (28 days) or in adulthood

59 n sources may sustain tumor growth despite a castrate environment.

60 s conferred by the selective pressure of the castrate environment.

61 We discovered that small arteries from castrated Ephb6 gene KO males showed increased contracti

62 Consistent with this finding, castrated Ephb6 KO mice presented heightened BP compared

63 ither untreated or T + E2-treated hosts were castrated, epithelial apoptosis was observed in the graf

64 econd experiment, male whiptail lizards were castrated for 1 week or for 6 weeks.

65 Male Japanese macaques (Macaca fuscata) were castrated for 5-7 months and then treated for 3 months w

66 differences in sexual behavior in intact and castrated geckos.

67 development and resist androgen ablation in castrated hosts, and they harbor highly tumorigenic cast

68 nsferred quantified precursors into congenic castrated hosts.

69 trated before puberty in contrast to animals castrated in adulthood in which testosterone significant

70 ompared between long and short days, between castrated, intact, and castrated with testosterone repla

71 re effective in restoring sexual activity in castrated KN males than IL males.

72 ty is generally restored in CRPC despite the castrate level of androgens, it is unclear whether AR si

73 that reduce circulating androgen ligands to castrate levels and/or block ligand binding.

74 ors; however, tumors that can proliferate in castrate levels of androgen eventually arise.

75 ndrogen receptor activation persists despite castrate levels of circulating androgens.

76 on complex facilitates reactivation by AR at castrate levels of ligand.

77 1 month prior to 3 of 4 trial days to induce castrate levels of T.

78 or survival and time to progression if lower castrate levels of testosterone (< 0.7 nmol/L) are achie

79 Prostate cancers progressing despite castrate levels of testosterone are considered castratio

80 When castrated long day-housed mice were provided with long d

81 ion of 10b suppressed luteinizing hormone in castrated macaques.

82 eks' gestation, n = 6) were xenografted into castrate male nude mice which were then treated for 35 d

83 Castrate male rats were subjected to behavioral tests af

84 endocardium from control male and female and castrated male (ORCH) and female (OVX) rabbits.

85 sex behaviors toward an estrous female or a castrated male (presented in separate tests), again, whe

86 BM of all the sham shock groups and with the castrated male and both female rat groups subjected to T

87 In castrated male and female GPR-4 rats, the LH pulse frequ

88 Castrated male B6 mice showed higher lipopolysaccharide-

89 MBP-primed T cells isolated from female and castrated male but not from male mice induced the expres

90 However, MBP-primed T cells of female and castrated male but not male mice induced microglial acti

91 MBP-primed T cells isolated from female and castrated male but not male mice were capable of inducin

92 ants in the medial preoptic nucleus (POM) of castrated male canaries (Serinus canaria) increase song

93 Moreover, oral administration of R-13b to castrated male cynomolgus monkeys resulted in a signific

94 ine the response of the SNB in prepubertally castrated male gerbils receiving delayed hormone replace

95 also hormone-resistant when xenografted into castrated male immunodeficient mice.

96 In contrast, female and castrated male MBP-primed T cells expressed both alpha4

97 maze arms and arms that contained intact or castrated male mice and partially prevented loss of this

98 Reversal of nigrostriatal pathologies in castrated male mice by subcutaneous implantation of 5alp

99 Analysis of castrated male mice from other strains (A/J, DBA/2J, AKR

100 ed renal CYP2J5 expression, and treatment of castrated male mice or female mice with 5alpha-dihydrote

101 ation-recurrent CWR22R tumor-bearing athymic castrated male mice produced a 28-fold increase in intra

102 and alpha-synuclein were higher in nigra of castrated male mice than normal male mice.

103 gly, MBP-primed T cells of male, female, and castrated male mice were able to induce microglial activ

104 , treatment of ovariectomized female mice or castrated male mice with 17beta-estradiol causes a furth

105 ed splenic IL-6 and serum estrogen levels in castrated male mice, and IL-6 induction by 17beta-estrad

106 protein (MBP)-primed T cells from female and castrated male mice, but not from male mice, produced pr

107 of 17beta-estradiol on acute wound repair in castrated male mice.

108 in (MBP)-primed T cells of male, female, and castrated male mice.

109 neurons appeared in the SNB of prepubertally castrated male Mongolian gerbils within 2 days of the st

110 rotein and mRNA in the female and neonatally castrated male MPN on PN 4, indicating that the neonatal

111 ated tumor growth in vivo in both intact and castrated male nude mice.

112 Castrated male piglets born to sows fed a vitamin A-depl

113 The population consisted of female and castrated male pigs that were sired by boars represented

114 healthy, anesthetized juvenile (2-3 months) castrated male pigs.

115 uration of action was also determined in the castrated male rat assay to measure the extent (efficacy

116 hibition of luteinizing hormone release in a castrated male rat assay.

117 In a standard castrated male rat model, several compounds showed good

118 ormone release over time was measured in the castrated male rat.

119 y intact male rats, LES was seen reliably in castrated male rats and in female rats, although it fluc

120 uring clonogenic growth of BM progenitors in castrated male rats and in ovariectomized and proestrus

121 NH2] (6) when administered subcutaneously in castrated male rats at a dose of 50 microg in 100 microL

122 80%) release for >72 h after sc injection to castrated male rats at a standard dose of 50 mug/rat in

123 ay), or vehicle were administered acutely to castrated male rats that bore subcutaneous (sc) dihydrot

124 sent in male rats after T/HS is also lost in castrated male rats.

125 is not observed in proestrus female rats and castrated male rats.

126 rmacologic activity of selected compounds in castrated male rats.

127 We housed photostimulated, intact and castrated male starlings with a female or alone.

128 rred to mount an estrous female instead of a castrated male.

129 n stimulation reward in gonadally intact and castrated males and in females at estrous cycle stages a

130 Castrated males and those receiving the competitive andr

131 ay hyperresponsiveness was also decreased in castrated males and was increased in females administere

132 effect was transient in females paired with castrated males but more persistent in those with vasect

133 Castrated males developed more severe hepatitis than did

134 Castrated males had significantly greater numbers of GnR

135 T-replaced castrated males injected centrally with mixed arginine v

136 early- or late-postnatally transected males, castrated males left untreated or treated with estradiol

137 Untreated castrated males served as an additional control group.

138 es treated with estradiol benzoate (EB), and castrated males treated with both EB and MK-801.

139 ly with the NMDA receptor antagonist MK-801, castrated males treated with estradiol benzoate (EB), an

140 ricularly (ICV) or systemically to intact or castrated males with or without concomitant androgen rep

141 Thirty-five castrated males with physiologic T replacement (n=7/grou

142 (approximately 45%) reversed by exogenous T (castrated males with T replacement).

143 obtained from intact males, castrated males, castrated males with T replacement, and intact females.

144 sequently, we found that treating neonatally castrated males with testosterone propionate (TP) in adu

145 showed a higher frequency of mortality than castrated males without hormone replacement or nonoperat

146 s of delayed TP replacement in prepubertally castrated males, and 16 days of treatment did not furthe

147 ffects, RCA were obtained from intact males, castrated males, castrated males with T replacement, and

148 in CBT during the light phase in neonatally castrated males.

149 rostrocaudal extent is not, compared to sham-castrated males.

150 EAE than ovariectomized females or intact or castrated males.

151 zed females and from gonadally intact versus castrated males.

152 les had lower corticosterone than those with castrated males.

153 While vehicle-treated castrated mdx mice exhibited cardiopulmonary impairment

154 sponse and outcomes with enzalutamide in non-castrate men with prostate cancer.

155 rance was increased by approximately 100% in castrated men and was associated with a two-fold reducti

156 A total of 10 noncastrated and 20 castrated men with prostate cancer were studied to achie

157 w circulating levels of androgen reported in castrated men.

158 2-year survival of patients with progressive castrate metastatic disease with reasonable accuracy.

159 and has antitumor activity in patients with castrate metastatic prostate cancer.

160 is upregulated in LAPC-4 AI tumors grown in castrated mice and describe a molecular mechanism by whi

161 androgen-independent CWR22 PCa xenografts in castrated mice and generated a cell line from one of the

162 In contrast, in castrated mice bearing both LNCaP and NE-10 tumors, LNCa

163 dent state to an androgen-independent state, castrated mice carrying 104-S tumors were given the synt

164 5alpha-dihydrotestosterone (DHT) implants in castrated mice increased Kcne4 expression >3-fold (P = 0

165 In addition, 17-beta-estradiol-supplemented castrated mice showed a higher frequency of mortality th

166 natal prostates and re-growth of prostate in castrated mice triggered by hormone replacement.

167 tore neutrophil counts via stabilizing AR in castrated mice, but not in ARKO and testicular feminizat

168 We previously observed that castrated mice, compared to sham-operated mice, perform

169 In DES-treated castrated mice, DHT implants restored SV weights to norm

170 the androgen-dependent LNCaP cell line into castrated mice, has a greatly reduced amount of normal m

171 growth in androgen-depleted agar but not in castrated mice, showing a clear distinction between the

172 ation and prostate xenograft tumor growth in castrated mice.

173 ptor antagonists induce tumour regression in castrated mice.

174 e-growth triggered by hormone replacement in castrated mice.

175 erone replacement slowed barrier recovery in castrated mice.

176 ings related to persistent AR signaling in a castrate milieu can be harnessed to produce significant

177 deficient prostate tumor progression in both castrate-naive and castrate-resistant cancers.

178 support the importance of autophagy for both castrate-naive and castrate-resistant growth in a newly

179 er of tumors as Min/+ mice that were neither castrated nor treated with estrogen replacement (P = 0.8

180 Interestingly, castrated normoglycemic ApoE(-/-) mice developed larger

181 Male castrated nude mice received eight s.c. grafts of juveni

182 different mouse models, including intact or castrated nude mice xenografted with androgen-sensitive

183 cells or androgen-insensitive C81 cells and castrated nude mice xenografted with castration-resistan

184 When orthotopically implanted in castrated nude mice, LNCaP-GRP produced aggressive tumor

185 tation (p53(R273H)) facilitates AI growth in castrated nude mice.

186 rigel into intact or androgen-ablated (i.e., castrated) nude mice.

187 anges in the hormonal milieu such that males castrated on the day of birth have a significant increas

188 Thus, adult male rats neonatally castrated on the first day after birth displayed reducti

189 uction, we paired females with vasectomised, castrated or intact males, or other females.

190 tand these differences, subsets of mice were castrated or ovariectomized at 5 weeks of age.

191 To explore this, we castrated or sham-operated male rats on the day of birth

192 lices from male mice that were gonad-intact, castrated, or castrated and treated with estradiol impla

193 hort day photoperiod and either left intact, castrated, or castrated with testosterone replacement.

194 ubcutaneous (SC) adipose tissue from normal, castrated, or steroid-implanted animals were isolated an

195 ng treatment with single-agent pertuzumab in castrate patients with hormone-refractory prostate cance

196 nically significant single-agent activity in castrate patients with HRPC at either of the tested dose

197 alamic or adrenal stress response in animals castrated prepubertally.

198 High levels of AR predicted shorter time to castrate prostate-specific antigen increase after androg

199 obust PET imaging capacity of PSES-TSTA in a castrated prostate xenograft model.

200 In support of this finding, castrated Pten3CKO mice also exhibited decreased levels

201 we measured the FE related phenotypes of 236 castrated purebred Yorkshire boars, and selected 10 extr

202 ular endocardial AP configuration persist in castrated rabbits, suggesting that extragonadal factors

203 e a dose-dependent suppression of LH in male castrate rats via both i.v. and p.o. dosing.

204 post-MCAO accelerated functional recovery in castrate rats, suggesting a potential therapeutic role f

205 yze the trends observed for LH inhibition in castrated rats and monkeys that served as preliminary in

206 Testosterone replacement in castrated rats partially reduced expression of Noxs but

207 e and terminal branch number relative to the castrated rats receiving empty silastic capsules.

208 ming unit colonies compared with plasma from castrated rats subjected to either sham shock with lapar

209 ypothalamus, the increase in NOS activity in castrated rats was accompanied by an increase in the num

210 The castrated rats were given testosterone replacement.

211 Treatment of castrated rats with physiological levels of testosterone

212 In a 2 week Hershberger model using castrated rats, the compound showed dose-dependent effec

213 FLIP protein expression is downregulated in castrated rats, while in LNCaP cells, androgens regulate

214 l anabolic effect via oral administration in castrated rats.

215 ce expression of fear-potentiated startle in castrated rats.

216 th either E2 or DHT alone, attenuated LES in castrated rats.

217 phology of arcuate neuroendocrine neurons in castrated rats.

218 ates were significantly larger than those of castrates receiving blank capsules (p < 0.0001).

219 Bony metastatic castrate-refractory prostate cancer (CRPC) has a poor pr

220 mechanisms that underlie the pathogenesis of castrate resistance is therefore needed to develop novel

221 respond to ADT, most will eventually develop castrate resistance, defined as disease progression desp

222 during disease progression and contribute to castrate resistance.

223 to AR antagonists in hormone responsive and castrate resistant PC models.

224 h taxanes improves survival in patients with castrate resistant prostate cancer (CRPC).

225 20 (both free and in CSLPHNPs) re-sensitizes castrate resistant prostate cancer cells and tumors to d

226 ying progression of prostate cancer (PCa) to castrate-resistant (CR) and metastatic disease are poorl

227 the field is to identify mechanisms by which castrate-resistant AR activity and pioneer factor functi

228 R-targeted therapy and progression to lethal castrate-resistant cancer, the molecular regulators of A

229 tumor progression in both castrate-naive and castrate-resistant cancers.

230 A with concomitant development of metastatic castrate-resistant disease in a large cohort of prostate

231 growth in models of hormone-sensitive and of castrate-resistant disease was observed.

232 n deprivation, would delay the appearance of castrate-resistant disease.

233 on in tumor growth and delay to the onset of castrate-resistant disease.

234 nce of autophagy for both castrate-naive and castrate-resistant growth in a newly developed GEMM, sug

235 In castrate-resistant metastatic disease, development of no

236 cer that is coincident with the emergence of castrate-resistant metastatic disease.

237 l treatment with curative intent to a lethal castrate-resistant metastatic disease.

238 Eighty-seven men with castrate-resistant metastatic prostate cancer underwent

239 ent prognostic information on OS in men with castrate-resistant metastatic prostate cancer, and this

240 ET/CT with overall survival (OS) in men with castrate-resistant metastatic prostate cancer.

241 agents shown to prolong survival in men with castrate-resistant metastatic prostate cancer.

242 ntain androgen dependence and in a subset of castrate-resistant PCa cells, dependent on Akt activatio

243 stine and estramustine before emergence of a castrate-resistant phenotype.

244 The primary end point was time to castrate-resistant progression as shown by increasing pr

245 secondary hormonal manipulations in men with castrate-resistant prostate cancer (CRPC) creates a comp

246 tially effective, acquired resistance termed castrate-resistant prostate cancer (CRPC) develops.

247 Castrate-resistant prostate cancer (CRPC) is a fatal, me

248 from localized prostate cancer to incurable castrate-resistant prostate cancer (CRPC) is driven by c

249 rsistent androgen signaling is implicated in castrate-resistant prostate cancer (CRPC) progression.

250 s) provide a mechanism of therapy evasion in castrate-resistant prostate cancer (CRPC), yet mechanism

251 (AR) antagonist with activity in metastatic castrate-resistant prostate cancer (CRPC).

252 ease stages, including the advanced stage of castrate-resistant prostate cancer (CRPC).

253 ment shown to prolong survival in metastatic castrate-resistant prostate cancer (CRPC).

254 in human prostate cancer tissues, including castrate-resistant prostate cancer (CRPC).

255 d-line hormonal therapy for the treatment of castrate-resistant prostate cancer (CRPC).

256 Abiraterone treats metastatic castrate-resistant prostate cancer by inhibiting CYP17A,

257 te cancer tumours promote the progression of castrate-resistant prostate cancer by producing lymphoto

258 A9 significantly inhibits proliferation of castrate-resistant prostate cancer cells.

259 The median survival for men with metastatic castrate-resistant prostate cancer is 1-2 years, with im

260 the median survival for men with metastatic castrate-resistant prostate cancer is 1-2 years, with im

261 icate that the increase in ARV expression in castrate-resistant prostate cancer is an acute response

262 both castrate-sensitive and more aggressive castrate-resistant prostate cancer is essential to impro

263 Because castrate-resistant prostate cancer is refractory to most

264 molecularly characterize CTCs isolated from castrate-resistant prostate cancer patients (CRPC) recei

265 g remains an important regulatory pathway in castrate-resistant prostate cancer, and its transcriptio

266 omatic, or minimally symptomatic, metastatic castrate-resistant prostate cancer, designed to stimulat

267 Additionally, in patients with advanced castrate-resistant prostate cancer, metastatic lesions e

268 promising alternatives for the treatment of castrate-resistant prostate cancer.

269 a potential alternative treatment pathway in castrate-resistant prostate cancer.

270 t literature on the biology and treatment of castrate-resistant prostate cancer.

271 ic modality in patients with bone metastatic castrate-resistant prostate cancer.

272 d for prostate cancer progression, including castrate-resistant prostate cancer; mechanistically, by

273 candidate therapeutic and imaging target for castrate-resistant prostate cancers.

274 state stromal TGF-beta signaling potentiated castrate-resistant prostate tumors, in a Wnt-dependent m

275 ancer, this disease invariably relapses to a castrate-resistant state that is generally fatal.

276 er cells evolve via multiple mechanisms to a castrate-resistant state, allowing progression to a leth

277 ely abolished outgrowth of a patient-derived castrate-resistant tumor.

278 pies, often advance to a hormone-refractory 'castrate-resistant' PC (CRPC) stage.

279 rstanding new therapeutic paradigms for both castrate-sensitive and more aggressive castrate-resistan

280 uced restoration of nNOS-immunoreactivity in castrates should accompany the restoration of copulation

281 bserved a transient luciferase expression in castrated SPlucTg male mice after supplement of androgen

282 sional Clinical Opinion For men with CRPC, a castrate state should be maintained indefinitely.

283 ains dependence on AR signaling, even in the castrate state.

284 After castrate testosterone concentrations were reached (1.7 n

285 92%) of 121 receiving oestrogen had achieved castrate testosterone concentrations.

286 tive increasing PSA values while on ADT with castrate testosterone levels.

287 learance in patients with noncastrate versus castrate testosterone levels.

288 man prostate cancer xenografts in nude mice, castrated the mice, and blocked IL-6 activity using a ne

289 ause of the erroneous belief that its larvae castrate their hosts.

290 red nonsteroidal antiandrogen in addition to castrate therapy.

291 after castration, but growth is supported in castrates treated with estradiol.

292 ed or treated with estradiol, and transected castrates treated with estradiol.

293 sting behavior toward an estrous female or a castrated, urine-swabbed male (presented simultaneously)

294 saline-treated rats, SNB somata of T-treated castrates were significantly larger than those of castra

295 d short days, between castrated, intact, and castrated with testosterone replacement animals, and bet

296 period and either left intact, castrated, or castrated with testosterone replacement.

297 In castrates with plasma T levels that were undetectable, t

298 O mice presented heightened BP compared with castrated WT controls.

299 ion of PCGEM1 and promoting apoptosis in the castrated xenograft mouse model.

300 These results are important because castrated young male mice may be used as a simple, toxin