ライフサイエンスコーパス: OVX

1 OVX caused a 17% decrease in plasma glucose, which was c

2 OVX caused a reduction in osteocyte density in alveolar

3 OVX female mice had increased lung SPP1 expression in re

4 OVX increased choice of the large, risky reward (increas

5 OVX mice had increased adiposity that was prevented with

6 OVX NTG, CRPtg, and CRPtg lacking Fc gamma RI, Fc gamma

7 OVX produced the expected changes in trabecular and cort

8 OVX showed the lowest and ZOL the highest Ca and Pi cont

9 OVX was associated with a significant decline in perform

10 OVX+E mice exhibit negative feedback in the A.M. and pos

11 OVX-associated spine loss in somatosensory cortex was al

12 OVX-Diet rats showed enhanced osteoblastogenesis and ost

13 OVX-induced bone loss was associated with increased oste

14 27%), and increases in relaxation time (10% OVX) with preserved ejection fraction.

15 ) decreases vs. ageing in stroke volume (13% OVX and 15% for OVF), stroke work (34% and 52%) and card

16 (SHAM) were treated as follows: OVX (n = 5): OVX plus saline solution; zoledronic acid-treated group

17 zoledronic acid-treated group (ZOL) (n = 6): OVX plus ZOL; SHAM (n = 4): SHAM plus saline solution.

18 modifications in BV/TV (intact, 28.7+/-1.6; OVX, 16.3+/-0.9; OVX+E2, 25.7+/-1.4%).

19 llowed the same pattern (intact, 33.1+/-1.6; OVX, 34.4+/-3.7; OVX+E2, 42.4+/-2.1%).

20 attern (intact, 33.1+/-1.6; OVX, 34.4+/-3.7; OVX+E2, 42.4+/-2.1%).

21 en replacement (intact, 55+/-8; OVX, 59+/-7; OVX+E2, 92+/-4%).

22 d with estrogen replacement (intact, 82+/-7; OVX, 61+/-9; OVX+E2, 90+/-4%), which corresponded with s

23 d with estrogen replacement (intact, 55+/-8; OVX, 59+/-7; OVX+E2, 92+/-4%).

24 BV/TV (intact, 28.7+/-1.6; OVX, 16.3+/-0.9; OVX+E2, 25.7+/-1.4%).

25 en replacement (intact, 82+/-7; OVX, 61+/-9; OVX+E2, 90+/-4%), which corresponded with similar modifi

26 he depolarizing sag and was increased across OVX --> diestrous --> proestrous mice.

27 changes in synaptic functions, we used adult OVX rats to evaluate the consequences of short-term (7-1

28 the liver estrogen receptor alpha, E2 after OVX limited adiposity but failed to improve insulin sens

29 omotor activity and energy expenditure after OVX can explain these metabolic changes.

30 to 14 months (M14) after laparotomy or after OVX-Diet, with intermediate time points at M3 and M12.

31 d in mice 1-3 weeks (but not 10 weeks) after OVX by the selective ERbeta agonist, LY3201, given as co

32 ltiple beneficial cognitive effects in aged, OVX rhesus macaque females.

33 lation in obese animals prior to OVX plus an OVX-induced positive energy imbalance might cooperate to

34 el into GnRH neurons from OVX, OVX+E AM, and OVX+E PM mice.

35 were recorded in GnRH neurons from OVX+E and OVX mice in coronal and sagittal slices.

36 owever, both VCD-induced ovarian failure and OVX led to a dramatic reduction in the extent of excitot

37 male rats, ovariectomized (OVX) females and OVX females treated with 17beta-estradiol (E2).

38 administration, intact males and females and OVX+E but not OVX+Veh females were less sensitive to the

39 Untreated ovarian-intact and OVX animals were compared with OVX animals receiving est

40 s increased to a larger extent in intact and OVX females as compared to males.

41 es using expression profiles from intact and OVX mice from a panel of inbred strains.

42 fects of OFQ were dose dependent in male and OVX animals and were reversibly antagonized by UFP-101 (

43 In both male and OVX female control mice, subcutaneous E(2) implant impro

44 Male and OVX female rats were significantly more sensitive than i

45 rger extent in intact female versus male and OVX females.

46 aspect of energy storage was manipulated and OVX itself had no overall effect on post-breeding surviv

47 d GnRH neuron response in cells from OVX and OVX+E mice in the morning but not afternoon.

48 ute in vitro treatment of cells from OVX and OVX+E mice with estradiol rapidly increased HVA currents

49 n brain slices from ovariectomized (OVX) and OVX+estradiol (OVX+E) female mice during estradiol negat

50 tes a statistical difference in the sham and OVX D-spacing distributions (P<0.01).

51 Implants remained in place in SHAM and OVX ewes but were lost in all ZOL ewes.

52 In sham and OVX mice, HFD feeding induced fatty liver, and insulin r

53 , and showed no differences between SHAM and OVX.

54 r neuron was equivalent in young OVX+Veh and OVX+E groups.

55 acological inhibition of ERRalpha attenuated OVX-induced bone loss in mice.

56 , indicators of CKD-MBD were similar between OVX and Sham (similar kidney weight, plasma blood urea n

57 mediate between the high levels of bilateral OVX (no reproductive investment) and the low levels of S

58 he expression of four modules was altered by OVX, including module 23 whose expression was decreased

59 module 23 whose expression was decreased by OVX across all strains.

60 n young rats, vasodilation was diminished by OVX and restored with estrogen replacement (intact, 82+/

61 old animals, vasodilation was unaffected by OVX but enhanced with estrogen replacement (intact, 55+/

62 tion of caffeine/ovariectomy; or 4) caffeine/OVX = ingestion of caffeine/ovariectomy.

63 The OVX and caffeine/OVX groups presented a greater number of TRAP(+) cells a

64 hate; OMSC, orofacial mesenchymal stem cell; OVX, ovariectomized.

65 experienced either short-term (10 d, control OVX) or long-term (5 months, OVX(LT)) ovarian hormone de

66 In the control OVX neurons, E(2) acutely increased IE and reduced the s

67 r duration of severe seizures among control, OVX and VCD-treated mice, OVX+E mice exhibited seizures

68 variectomized and received a deficient diet (OVX-Diet).

69 e expression is significantly reduced in DIO OVX rats.

70 from ovariectomized (OVX) and OVX+estradiol (OVX+E) female mice during estradiol negative feedback re

71 In addition, following OVX, there was an increase in plasma ghrelin that was te

72 lary, and mandibular alveolar bone following OVX, yet was increased in lingual mandibular alveolar bo

73 ge in the efficacy for E2 5 months following OVX.

74 E2) therapy when initiated shortly following OVX but not after substantial delay.

75 lacement therapy initiated shortly following OVX but not after substantial delay.

76 sham surgery (SHAM) were treated as follows: OVX (n = 5): OVX plus saline solution; zoledronic acid-t

77 increased GnRH neuron response in cells from OVX and OVX+E mice in the morning but not afternoon.

78 Acute in vitro treatment of cells from OVX and OVX+E mice with estradiol rapidly increased HVA

79 urnal changes in PSC frequency in cells from OVX mice in either slice orientation.

80 X+E mice were lower than those in cells from OVX mice in the A.M. but were higher in the P.M.

81 ice; this response was blunted in cells from OVX mice.

82 he transient potassium current in cells from OVX or OVX+E mice were combined in silico with passive p

83 with time of day; HVA currents in cells from OVX+E mice were lower than those in cells from OVX mice

84 itiated more action potentials in cells from OVX+E PM mice than negative feedback or OVX (open feedba

85 tentials (PSPs) were smaller in neurons from OVX than OVX+E mice; blocking transient potassium curren

86 ts (PSCs) were recorded in GnRH neurons from OVX+E and OVX mice in coronal and sagittal slices.

87 e membrane potential of arcuate neurons from OVX+E mice; this response was blunted in cells from OVX

88 the daily surge model into GnRH neurons from OVX, OVX+E AM, and OVX+E PM mice.

89 In both kisspeptin neuron populations from OVX mice, the frequency of GABAergic spontaneous postsyn

90 identified GnRH neurons in brain slices from OVX+E or OVX female mice were recorded during the mornin

91 Furthermore, OVX increased food intake and body weight in wild-type m

92 Contrary to our hypothesis, OVX did not produce evidence of development of the CKD-M

93 mplant (OVX), 17-beta estradiol (E) implant (OVX+E) or E implant plus cyclic oral progesterone (OVX+E

94 ent with either a subcutaneous sham implant (OVX), 17-beta estradiol (E) implant (OVX+E) or E implant

95 bearing constant-release estradiol implants (OVX+E), GnRH neuron firing is suppressed in the morning

96 subset was treated with estradiol implants (OVX+E).

97 In OVX rats, 5-min intracerebroventricular infusion of a PA

98 In OVX+E cells in both orientations, PSC frequency was low

99 ne resorption, and promoting angiogenesis in OVX mice.

100 tation induces activated T-cell apoptosis in OVX mice via Fas ligand (FasL)-mediated Fas pathway acti

101 anges in any aspect of HVA-mediated I(Ca) in OVX mice.

102 In contrast, in OVX+E mice, HVA-mediated currents varied with time of da

103 sponse to vascular injury provoked by CRP in OVX CRPtg depends on Fc gamma RI and probably requires i

104 iol, and produced a dose-dependent effect in OVX females treated with 1 ng to 100 microg of estradiol

105 Experiments in OVX mice given estradiol replacement identified an estra

106 ssel number and stimulates bone formation in OVX mice.

107 atment showed TTX decreased PSC frequency in OVX+E cells in sagittal slices, but not coronal slices.

108 tenuated the orexigenic action of ghrelin in OVX female and male rats.

109 ut not the CA3, region of the hippocampus in OVX compared to intact rats.

110 ve stress, a process known to be involved in OVX-induced bone loss.

111 r were similar in SHAM and ZOL, and lower in OVX (P < 0.05).

112 A1), piriform cortex, and BNST were lower in OVX+E2 females compared to females without E2.

113 e mass marker) were down-regulated at M12 in OVX-Diet rats.

114 ggest that cognitive impairments observed in OVX rats may be associated with morphological changes in

115 k; no time-of-day-dependent changes occur in OVX mice.

116 ion of F4/80+CRP+ cells was revealed only in OVX CRPtg.

117 ast development in vitro and osteoporosis in OVX rat models.

118 and ameliorates the osteopenia phenotype in OVX mice.

119 ation would be sufficient to restore pLTF in OVX rats.

120 for restoring thermoregulatory processes in OVX rats.

121 ient in Snca and observed a 40% reduction in OVX-induced bone loss.

122 oss associated with oestrogen replacement in OVX rats, we food restricted a separate group of OVX rat

123 ng enhanced bone formation and resorption in OVX-Diet rats.

124 was also higher than ShA control subjects in OVX+E but not OVX+Veh females after ExA self-administrat

125 ood restricted rats were similar to those in OVX rats treated with the oil vehicle.

126 ficantly suppressed by estrogen treatment in OVX ERalpha-/AA mice.

127 y relevant regimen of estradiol treatment in OVX rats increases Pet-1 and 5-HTT mRNA levels in the mi

128 and protects mice from ovariectomy-induced (OVX-induced) osteoporosis.

129 The loaded OVX group showed a significant increase in the number of

130 res among control, OVX and VCD-treated mice, OVX+E mice exhibited seizures of a significantly longer

131 (10 d, control OVX) or long-term (5 months, OVX(LT)) ovarian hormone deficiency.

132 Nevertheless, OVX females treated with vehicle exhibited a substantial

133 r than ShA control subjects in OVX+E but not OVX+Veh females after ExA self-administration, confirmin

134 , intact males and females and OVX+E but not OVX+Veh females were less sensitive to the effects of D1

135 insulin sensitivity and body composition of OVX rats bred for low-running capacity.

136 In contrast, the average T(CORE) of OVX, KNDy-ablated rats was lower than OVX control rats a

137 eated female rats, as well as the effects of OVX on plasma ghrelin and hypothalamic orexigneic neurop

138 eing, which was higher in the endocardium of OVX and OVF groups.

139 and biomechanics confirmed bone fragility of OVX-Diet rats, and quantitative RT-PCR revealed a higher

140 rats, we food restricted a separate group of OVX rats and evaluated Isop-induced changes in MAP, HR a

141 ds to increased tumor burden in the lungs of OVX + E(2) mice.

142 ar bone loss and improved bone metabolism of OVX-periodontitis rats as compared with the vehicle-trea

143 ys and with performance levels below that of OVX+E animals.

144 re also found to be reduced in the tibias of OVX mice.

145 ty that was prevented with E2 at the time of OVX.

146 ntact, 3) young ovariectomized (OVX), 4) old OVX, 5) young OVX plus estrogen replacement (OVX+E2), an

147 us estrogen replacement (OVX+E2), and 6) old OVX+E2.

148 ow endogenous estrogen (i.e., intact and old OVX), vasodilation was correlated with BV/TV (R(2) = 0.6

149 ed on neurons from approximately 7-month-old OVX rats that experienced either short-term (10 d, contr

150 stent and protective effects of SPI diets on OVX-induced bone loss were associated with down-regulati

151 male C57BL/6J mice underwent sham operation, OVX, or OVX with estradiol (E2) treatment and were fed a

152 Increased energy intake in both HFD and/or OVX groups, and decreased locomotor activity and energy

153 n mesenteric adipose tissue after HFD and/or OVX, independent of previous postnatal programming, yet

154 d GnRH neurons in brain slices from OVX+E or OVX female mice were recorded during the morning or afte

155 from OVX+E PM mice than negative feedback or OVX (open feedback loop) trains in all three animal mode

156 sient potassium current in cells from OVX or OVX+E mice were combined in silico with passive properti

157 BL/6J mice underwent sham operation, OVX, or OVX with estradiol (E2) treatment and were fed an HFD.

158 ologic treatment of intact aged male rats or OVX female rats with Scl-Ab had no effect on morphologic

159 had higher bone density as compared to other OVX mice groups.

160 Ovariectomized (OVX) female rats with and without estradiol replacement

161 Ovariectomized (OVX) females were also included to assess the role of ov

162 Ovariectomized (OVX) mice treated or not with estradiol (E) were studied

163 Ovariectomized (OVX) rats (n=5-6/group) were treated with 0, 2, or 10 mi

164 Ovariectomized (OVX) rats 24 h (but not 6 or 72 h) after estradiol benzo

165 f caffeine/sham surgery); 3) ovariectomized (OVX) = non-ingestion of caffeine/ovariectomy; or 4) caff

166 cose homeostasis in male and ovariectomized (OVX) female control and liver-specific Foxo1 knockout (L

167 cl-Ab) in aged male rats and ovariectomized (OVX) female rats were used to study the effects of scler

168 , intact male and intact and ovariectomized (OVX) female rats with and without estradiol replacement

169 female (freely cycling), and ovariectomized (OVX) females treated with either estrogen benzoate (EB;

170 Intact males, females, and ovariectomized (OVX) females with and without estradiol (vulnerable, OVX

171 Eleven ovariectomized (OVX) ewes and four ewes subjected to sham surgery (SHAM)

172 neurons in brain slices from ovariectomized (OVX) and OVX+estradiol (OVX+E) female mice during estrad

173 ertaken in brain slices from ovariectomized (OVX), diestrous, and proestrous kisspeptin-GFP mice.

174 ects of exogenous ghrelin in ovariectomized (OVX) and estradiol (E2)-treated female rats, as well as

175 activity was not enhanced in ovariectomized (OVX) female mice as a result of cardiac stress, but admi

176 prefrontal cortex (dlPFC) in ovariectomized (OVX) female rhesus monkeys, and that E induces a corresp

177 y subsequent E2 treatment in ovariectomized (OVX) female Thy1M-EGFP mice.

178 lar injury is exaggerated in ovariectomized (OVX) human C-reactive protein transgenic mice (CRPtg) co

179 nisms mediating bone loss in ovariectomized (OVX) mice, a model of human menopause, using co-expressi

180 (2) pLTF would be absent in ovariectomized (OVX) rats and in physiological conditions in which serum

181 and the cecal microbiota in ovariectomized (OVX) rats bred for low-running capacity (LCR), a model t

182 inding, in male rats, and in ovariectomized (OVX) rats given estradiol benzoate (EB) or oil vehicle (

183 culating levels of AngII, in ovariectomized (OVX) rats treated with oestradiol benzoate (EB).

184 odontitis was established in ovariectomized (OVX) rats, and the OVX-periodontitis rats were treated w

185 However, in ovariectomized (OVX) WT and in ERbeta(-/-) mice, there was a marked redu

186 solitary tract (NTS) of lean ovariectomized (OVX) rodents.

187 exosomes of the bone-losing ovariectomized (OVX) mice, while it was significantly decreased by knee

188 rol Spp1+/+ (C57BL/6J) mice, ovariectomized (OVX) female mice, and estrogen-treated male mice were tr

189 ore temperature (T(CORE)) of ovariectomized (OVX) control rats was significantly elevated, and this v

190 of Hdac4 in the amygdala of ovariectomized (OVX) female mice.

191 Treatment of ovariectomized (OVX) rats with estradiol benzoate (EB) caused rapid and

192 istered to intact male rats, ovariectomized (OVX) females and OVX females treated with 17beta-estradi

193 the sex and estrogen status [ovariectomized (OVX) female and E2-treated male].

194 he administration of CpdX to ovariectomized (OVX) mice does not induce a fatty liver nor type 2 diabe

195 loading to the spine, using ovariectomized (OVX) mice as a model of osteoporosis.

196 Two-month-old rats were ovariectomized (OVX) or had maxillary molars removed from one side to in

197 Mice were ovariectomized (OVX), and a subset was treated with estradiol implants (

198 sk acquisition, animals were ovariectomized (OVX).

199 act, 2) old intact, 3) young ovariectomized (OVX), 4) old OVX, 5) young OVX plus estrogen replacement

200 signaling in rats 1 week after ovariectomy (OVX).

201 ice exhibited elevated LH after ovariectomy (OVX).

202 ided into an aged group, aged + ovariectomy (OVX) and aged + ovariectomy + 10% fructose (OVF) in drin

203 D via the tail vein ameliorates ovariectomy (OVX)-induced osteopenia by reducing T-helper 1 (Th1) and

204 using unilateral and bilateral ovariectomy (OVX) along with intact (SHAM) control.

205 d hormone deprivation caused by ovariectomy (OVX) in young adult rats prevents the ability of estroge

206 cision-making task, followed by ovariectomy (OVX), orchiectomy (ORX), or sham surgery.

207 fter weaning, followed later by ovariectomy (OVX; as a model of menopause).

208 Rats then underwent either ovariectomy (OVX) or sham surgery and thereafter either continued to

209 s of ovarian hormones following ovariectomy (OVX) elevates the risks of cognitive impairment and deme

210 ovarian hormone loss following ovariectomy (OVX) is associated with cognitive impairment.

211 ffeine is influenced by gender, ovariectomy (OVX), and then exogenous estrogen in the mouse 1-methyl-

212 r surgically-induced menopause [ovariectomy (OVX)], on tests of memory and attention.

213 (HFD) when given at the time of ovariectomy (OVX) in mice.

214 imed to determine the effect of ovariectomy (OVX) on the biochemical and skeletal manifestations of C

215 In the ovariectomy (OVX)-induced osteoporotic mouse model, serum and bone ma

216 y, the GNPs-ALD were applied to ovariectomy (OVX)-induced osteoporotic mice and the experiments were

217 nce, female mice also underwent ovariectomy (OVX) surgery and a hormone replacement protocol prior to

218 uced periodontitis in rats with ovariectomy (OVX) that are or are not treated with estrogen replaceme

219 s of ovarian function (surgical ovariectomy; OVX).

220 aily surge model into GnRH neurons from OVX, OVX+E AM, and OVX+E PM mice.

221 atment and from oophorectomized guinea pigs (OVX-GPs) treated with vehicle, estradiol (E2), medroxypr

222 were spayed and either treated with placebo (OVX), estrogen alone (E), progesterone alone (P) or E+P.

223 ared to intact rats beginning at 1 week post OVX for OR and 4 weeks post OVX for OP.

224 g at 1 week post OVX for OR and 4 weeks post OVX for OP.

225 Golgi impregnation at 7 weeks post OVX showed significantly lower spine densities (17-53%)

226 same chronological age as the 19-month post-OVX group, estrogen replacement significantly increased

227 However, by 19 months post-OVX, the same estrogen replacement was unable to induce

228 ity at CA3-CA1 synapses up to 15 months post-OVX.

229 Furthermore, the post-OVX rise in serum LH was significantly suppressed by est

230 ly in early life protected against 1 wk post-OVX-associated bone loss.

231 cortical bone mineral density loss 3 wk post-OVX.

232 ly to reappear at or nearby the sites of pre-OVX spines than those in control mice treated with vehic

233 ramming effects on bone formation to prevent OVX-induced bone loss in adult female rats.

234 ramming effects on bone formation to prevent OVX-induced bone loss in adult female rats.-Chen, J.-R.,

235 or E implant plus cyclic oral progesterone (OVX+EP).

236 lper 17 (Th17) cell numbers in the recipient OVX mice.

237 OVX, 5) young OVX plus estrogen replacement (OVX+E2), and 6) old OVX+E2.

238 This SHED-mediated immunomodulation rescues OVX-induced impairment of bone marrow mesenchymal stem c

239 out estradiol (vulnerable, OVX+E; resistant, OVX+Veh) were given either short access (ShA) (three fix

240 SNCA-OVX mice display age-dependent loss of nigrostriatal dop

241 Aged SNCA-OVX mice exhibit reduced firing of SNc dopamine neurons

242 is longitudinal phenotyping strategy in SNCA-OVX mice thus provides insights into the region-specific

243 artificial chromosome transgenic mice (SNCA-OVX) that express wild-type alpha-synuclein from the com

244 RE) of OVX, KNDy-ablated rats was lower than OVX control rats at 33 degrees C, and not altered by E(2

245 (PSPs) were smaller in neurons from OVX than OVX+E mice; blocking transient potassium currents elimin

246 We also found that OVX-associated reduction of spine density in somatosenso

247 We hypothesized that OVX would accelerate development of the biochemical and

248 lapse in vivo two-photon imaging showed that OVX-associated reduction in spine density is achieved by

249 These results suggest that OVX-induced bone loss, in part, is a result of increased

250 These results suggest that OVX-induced bone loss, in part, is a result of increased

251 , but not in Ghsr(-/-) mice, suggesting that OVX increases food intake by releasing ghrelin from a to

252 The OVX and caffeine/OVX groups presented a greater number o

253 The OVX animals were then assigned to treatment with either

254 The OVX+E animals also performed significantly better in the

255 The OVX+E animals performed significantly better on the dela

256 The OVX+EP animals also showed improved performance in the d

257 eine group presented the greatest BL and the OVX group the highest number of TRAP-positive (TRAP(+))

258 lished in ovariectomized (OVX) rats, and the OVX-periodontitis rats were treated with berberine for 7

259 ts in vitro profile, 21 was evaluated in the OVX and ORX rat models and exhibited an osteoanabolic, t

260 Furthermore, in the OVX mouse model, the mice treated GNPs-ALD had higher bo

261 rized AVPV kisspeptin neurons, except in the OVX PM group in which GABA did not alter membrane potent

262 e regulation of IE by E(2) was absent in the OVX(LT) neurons.

263 neocortical slices with E2 also rescued the OVX-associated reduction in mEPSC frequency, which could

264 ART-immunopositive area in comparison to the OVX control group with Student's t-test, but not with AN

265 Furthermore, compared to the OVX group, exosomes, derived from the loading group, pro

266 In contrast, within the OVX groups, responding was enhanced from control levels

267 Estradiol administration to OVX mice also exerted a significant neuroprotective effe

268 tabolic regulation in obese animals prior to OVX plus an OVX-induced positive energy imbalance might

269 odents differ in their metabolic response to OVX-induced weight gain, and whether this difference aff

270 ed E2-induced 4T1BR5 BM to levels similar to OVX mice.

271 red to normal males and females subjected to OVX.

272 Berberine-treated OVX-periodontitis rats consistently showed improved inte

273 In parallel, berberine-treated OVX-periodontitis rats harbored a higher abundance of bu

274 sponses were attenuated in berberine-treated OVX-periodontitis rats with a lower serum level of proin

275 the area postrema was greater in EB-treated OVX rats compared to those in OIL-treated OVX and male r

276 ured at 22 h after MCAO in estradiol-treated OVX animals in the presence and absence of STAT3 inhibit

277 Similarly, the endometria of MPA treated OVX-GPs displayed decreased alphaSMA staining and fewer

278 ed OVX rats compared to those in OIL-treated OVX and male rats.

279 is rats as compared with the vehicle-treated OVX-periodontitis rats.

280 veolar bone as compared with vehicle-treated OVX-periodontitis rats.

281 basis in ovariectomized, estradiol-treated (OVX+E) mice; GnRH neurons are suppressed in the morning

282 tablished ovariectomized, estradiol-treated (OVX+E) mouse model exhibiting daily surges to investigat

283 Female Cy/+ rats underwent OVX (n = 8) or Sham (n = 8) surgery at 15 weeks of age.

284 As predicted, unilateral OVX (intermediate reproductive investment) induced level

285 without affecting infarct size in untreated OVX rats.

286 ales with and without estradiol (vulnerable, OVX+E; resistant, OVX+Veh) were given either short acces

287 pLTF was abolished with OVX, but was re-established by acute E2 replacement (3 h

288 in females, that weight gain associated with OVX is ghrelin mediated, and that this endocrine interac

289 an-intact and OVX animals were compared with OVX animals receiving estradiol (E) alone or E with prog

290 fter tone-shock presentations, compared with OVX-homecage control females.

291 the treatment of periodontitis in rats with OVX that are or are not given estrogen replacement thera

292 mal rats; 2) rats with OVX; and 3) rats with OVX with estrogen replacement.

293 o three groups: 1) normal rats; 2) rats with OVX; and 3) rats with OVX with estrogen replacement.

294 treatment increased insulin sensitivity with OVX and HFD.

295 female FVB/NJ mice were ovariectomized with (OVX+E, n=6) or without (OVX, n=8) estrogen replacement.

296 ovariectomized with (OVX+E, n=6) or without (OVX, n=8) estrogen replacement.

297 g ovariectomized (OVX), 4) old OVX, 5) young OVX plus estrogen replacement (OVX+E2), and 6) old OVX+E

298 d by cyclic E administration, although young OVX+Veh monkeys still had a higher complement of small s

299 ative to vehicle control values (group young OVX+Veh) but nonetheless led to a robust increase in spi

300 of spines per neuron was equivalent in young OVX+Veh and OVX+E groups.