ライフサイエンスコーパス: luteal

1 teries>NP arteries (follicular)>NP arteries (luteal).

2 es of the menstrual cycle (midcycle and late luteal).

3 rly follicular, follicular, luteal, and late luteal.

4 lar, mid-cycle (ovulatory) and mid- and late luteal.

5 during both the follicular (22% shorter) and luteal (15% shorter) phases.

6 Luteal 16alphaOHE1 excretion decreased from 1.38 +/- 0.2

7 Mean (+/- SEM) luteal 2OHE1 excretion decreased from 3.92 +/- 0.79 to 2

8 The remaining 160 women (19%) did not have luteal activity and are the subject of this report.

9 een 1997 and 1999, 680 women had evidence of luteal activity.

10 usion transcripts, were identified in corpus luteal and endometrial neovasculature after inductive ov

11 es obtained every 5 min; in each human, both luteal and follicular periods were studied in 192 sample

12 e also taken 4 times after injection: in the luteal and follicular phases of 2 cycles in the placebo

13 red t test) during postovulation (average of luteal and late luteal phases), when it was 0.73 +/- 0.0

14 levels from the follicular phase to the mid luteal and late luteal phases.

15 rent oestrous stages: late follicular, early luteal and late luteal stages.

16 eptible individuals, particularly during the luteal and perimenstrual phases.

17 ring the Menses phase when compared to Early-Luteal and Premenstrual phases.

18 eak circadian levels the entire night in the luteal and pseudo luteal phase.

19 s (granulosa, theca, small luteal, and large luteal), and isolated luteal LDs were assessed for LD co

20 steroidogenic cells (granulosa, theca, small luteal, and large luteal), and isolated luteal LDs were

21 nstrual cycle: early follicular, follicular, luteal, and late luteal.

22 rual cycle phases (Menses, Follicular, Early-Luteal, and Premenstrual) based on self-reported start d

23 The accuracy of ISG expression and luteal blood perfusion to predict the pregnancy outcome

24 n another experiment, PMN were isolated, and luteal blood perfusion was measured on D20 post-timed-AI

25 Luteal cell differentiation is impaired, and a disordere

26 essential for progesterone biosynthesis and luteal cell hypertrophy of the rat corpus luteum during

27 t corrected were the aberrant estrus cycles, luteal cell proliferation, and susceptibility to pituita

28 aling plays a central role in follicular and luteal cell survival.

29 nitor cells (low) in bone marrow; (c) corpus luteal cells (high) versus follicular granulosa cells (l

30 In primary cultures of steroidogenic small luteal cells (SLCs), LH, and forskolin stimulated phosph

31 P1 (cytoplasmic YAP1) was mainly detected in luteal cells (terminally differentiated granulosa cells)

32 hat LDs are a major feature of steroidogenic luteal cells and store cholesteryl esters.

33 ed by knocking out (KO) of EGR 1 in cultured luteal cells by CRISPR/Cas9 mediated gene editing techno

34 ings identify a PKA/HSL signaling pathway in luteal cells in response to LH and demonstrate the dynam

35 Luteal cells in this model exhibit defective autophagy a

36 GR 1 message was found to be up-regulated in luteal cells of buffalo at 72 hours of culture.

37 ranulosa cells of preovulatory follicles and luteal cells of corpora lutea had no effect on ovarian m

38 reased SR-BI in the adrenal gland and corpus luteal cells of the ovary.

39 laris of the adrenal gland and to the corpus luteal cells of the ovary.

40 Using LH-responsive bovine small luteal cells our results reveal that LH, forskolin, and

41 Lipid droplets in steroidogenic luteal cells store cholesterol in the form of cholestero

42 Towards this goal, luteal cells were cultured and treated with VEGF A and F

43 Luteal cells were distinguishable from follicular cells

44 numerous and small; whereas, LDs from small luteal cells were large and less numerous.

45 Furthermore, LDs from large luteal cells were numerous and small; whereas, LDs from

46 in both ovarian follicular and steroidogenic luteal cells, demonstrating an increase in its levels as

47 bolic flux analysis in primary steroidogenic luteal cells, evidence is provided for rapid LHCGR-stimu

48 ctivates protein kinase A (PKA) signaling in luteal cells, increasing delivery of substrate to mitoch

49 NA enhanced progesterone production in small luteal cells, whereas adenovirus-mediated overexpression

50 oliferation and steroidogenesis in wild type luteal cells, whereas the response of the growth factors

51 ion of VEGF A and FGF 2 signaling in buffalo luteal cells.

52 ian neoplasms that were derived from ovarian luteal cells.

53 1 (S6K1) signaling pathway in steroidogenic luteal cells.

54 ich increases the translational machinery in luteal cells.

55 kinase C (PKC) and Raf-MEK-Erk signaling in luteal cells.

56 ulosa cells of preovulatory follicles and to luteal cells.

57 in testis Leydig cells and ovarian theca and luteal cells.

58 a rapid and transient expression of Nur77 in luteal cells.

59 s to terminally differentiated, non-dividing luteal cells.

60 anulosa cells terminally differentiated into luteal cells.

61 ation of DRP1 on Ser616 and Ser637 in bovine luteal cells.

62 nt target downstream of PKA in steroidogenic luteal cells.

63 ne granulosa cells (LGCs), a model for large-luteal cells.

64 at hormone sensitive lipase (HSL) hydrolyzes luteal cholesterol esters.

65 ing the soya diet; a slight decrease in mean luteal cycle length was marginally statistically signifi

66 atus, and (for NHS II) menopausal status and luteal day of menstrual cycle for premenopausal particip

67 licular (day 3), ovulatory (day 14), and mid-luteal (day 21).

68 8 subjects and day 11 in 1 subject) and mid-luteal (days 19-25) phases of their menstrual cycle.

69 ess was fully attributable to the underlying luteal defect.

70 he control of mTOR may have implications for luteal development and regression and offer new strategi

71 a cells from the cell cycle, in concert with luteal differentiation and possibly culture-induced sene

72 Neither the peak nor luteal E1G levels were predictive of density after adjus

73 menstrual cycle phase (29 follicular and 16 luteal) effects.

74 degrees C) and was 0.36 degrees C higher in luteal females relative to follicular females and males

75 vels were used to determine menstrual phase: luteal, follicular, and other.

76 (LH) is the primary stimulus for ovulation, luteal formation, and progesterone synthesis, regardless

77 nally regulated folliculogenesis, ovulation, luteal formation/regression and associated vasculature c

78 potential therapeutic target for modulating luteal function.

79 ular (high estradiol, low progesterone), and luteal (high estradiol, high progesterone) phases, with

80 cesses contribute to the proinflammatory mid-luteal implantation window and their dysregulation has b

81 y cytokine TNF-alpha and correlated with the luteal induction of the prolactin receptor signaling inh

82 contributes to infertility in women in whom luteal insufficiency is implicated.

83 Bovine luteal LDs are distinct from LDs in other bovine tissues

84 mall luteal, and large luteal), and isolated luteal LDs were assessed for LD content, LD-associated p

85 Isolated luteal LDs were composed primarily of TG, with lesser am

86 lop corpora lutea, as evident by the lack of luteal marker gene expression, marked reduction of vascu

87 participants provided a timed follicular and luteal menstrual phase blood sample; other women provide

88 s collected from 18,521 women during the mid-luteal menstrual phase.

89 Treatment of luteal microvascular endothelial cells (MVECs) with TNF

90 age depletion, substantial disruption of the luteal microvascular network occurred and was associated

91 Trials were in early-follicular (EF) and mid-luteal (ML) phases in dry (DRY) and humid (HUM) heat mat

92 les during the early follicular (EF) and mid-luteal (ML) phases of the menstrual cycle.

93 ied during the early follicular (EF) and mid-luteal (ML) phases of the menstrual cycle.

94 Follicular and luteal oestradiol and progesterone serum titres were gro

95 port for these dimensions, which include (1) luteal-onset negative affect caused by a sensitivity to

96 were 82.7%, 82.1%, and 79.2% for follicular, luteal, or other phases, respectively.

97 that the follicular (peak oestrogen) vs. the luteal (peak progesterone) phase of the menstrual cycle

98 any of the following cycle endpoints: short luteal phase (< or = 10 days), long follicular phase (>

99 to an increased risk for anovulation, short luteal phase (< or =10 days), long follicular phase (> o

100 ase (59 [17]) compared with women during the luteal phase (53 [14]) and compared with men (46 [16]; P

101 tal cortex and amygdala more than during the luteal phase (6-10 days after luteinizing hormone surge)

102 e the estradiol during the follicular versus luteal phase (Delta), the higher the Deltadrug cue react

103 trajectory showed that its left shift in the luteal phase (e.g., earlier rise in progesterone) expose

104 in the vaginal lumen and increase during the luteal phase (high progesterone).

105 ated from sputum during exacerbations in the luteal phase (low estradiol).

106 ion of Oocyte Retrieval performed during the Luteal Phase (LuPOR) in poor responders, as defined by t

107 en during the early follicular (EFP) and mid-luteal phase (MLP) of the menstrual cycle.

108 s increased sixfold to eightfold in the late luteal phase (P < 0.001) and those of swelling or bloati

109 and neutrophil gene set signatures with the luteal phase (P < 0.05).

110 re higher in the late follicular than in the luteal phase (P = 0.02 and P = 0.04, respectively).

111 re higher in the late follicular than in the luteal phase (P = 0.03 and P = 0.02, respectively).

112 nsive pregnancies were tested during the mid-luteal phase (PRE) and early pregnancy (EARLY; 6.2 +/- 1

113 sion showed that decreases in follicular and luteal phase 17beta-estradiol levels were positively ass

114 hthalate (MCOP) were associated with shorter luteal phase [2nd tertile vs. 1st tertile: -0.5 days (95

115 BPA was also associated with shorter luteal phase [2nd vs. 1st: -0.8 days (95% CI: -1.2, -0.4

116 103), and BPS participants (n = 23) in their luteal phase across a bladder-filling task.

117 t driven by the follicular compared with the luteal phase and directly related to craving and fluctua

118 ic the decidualizing steroidal milieu of the luteal phase and early pregnancy.

119 transformation of the endometrium during the luteal phase and evaluate markers of endometrial recepti

120 ition of uILCs in the endometrium during the luteal phase and in the decidua during early pregnancy.

121 onth, once during their active pill phase or luteal phase and once during their pill pause or menses.

122 traception could mimic the high-progesterone luteal phase and predispose women to human immunodeficie

123 ins indicates that AR(-/-) females exhibit a luteal phase defect.

124 poradic anovulation, irregular cycle length, luteal phase deficiency, long menses, and heavy blood lo

125 e anxiety and dysphoria associated with late luteal phase dysphoria disorder and major unipolar depre

126 lection of gene expression profiles from mid-luteal phase endometrial biopsies (n = 115) from women e

127 o [OR] 1.11, 95% CI 1.03-1.20; p=0.0063) and luteal phase endometrial thickness lower (0.90, 0.83-0.9

128 IUD transcriptome was indistinguishable from luteal phase endometrium.

129 lar phase was more irregular than during the luteal phase for both FSH and LH (P < 0.01).

130 of the menstrual cycle (n=30) or the pseudo luteal phase for oral contraceptive users (n=32).

131 articular susceptibility observed during the luteal phase in nonhuman primate models and ex vivo huma

132 ereas drug reappraisal was higher during the luteal phase in the anterior PFC/orbitofrontal cortex.

133 arker to distinguish the follicular from the luteal phase in univariate and multivariate analyses and

134 th, 16.0 (standard deviation, 4.4) days; and luteal phase length, 12.9 (standard deviation, 1.7) days

135 w or a window determined by assuming a fixed luteal phase length, would be simpler.

136 and increased follicular phase and decreased luteal phase lengths; Hispanic ethnicity with anovulatio

137 Multiple network aberrations during the luteal phase may explain the development of mood symptom

138 Luteal phase MPS was 1.28 +/- 0.27% d(-1) in the control

139 Sodium cravings increased in the luteal phase of all cycles but were not accompanied by i

140 l magnetic resonance imaging during the late luteal phase of fifty-one women diagnosed with PMDD, com

141 er FC during the midfollicular than the late-luteal phase of PMDD.

142 ons comparable to levels observed during the luteal phase of premenopausal women and were significant

143 myomata than myometrium, but only during the luteal phase of the cycle.

144 a1-induced COL1 protein abundance in the mid-luteal phase of the estrous cycle after 48 h (p < 0.05).

145 ats mimics the progesterone component of the luteal phase of the human menstrual cycle, these finding

146 ature levels in women were tested during the luteal phase of the menstrual cycle (n=30) or the pseudo

147 omen using no long-term contraceptive in the luteal phase of the menstrual cycle also had a 3.25 time

148 discrimination of facial emotions during the luteal phase of the menstrual cycle and altered reactivi

149 h levels comparable to those observed in the luteal phase of the menstrual cycle and modestly increas

150 The results for women in the luteal phase of the menstrual cycle are consistent with

151 egnanolone levels from the follicular to the luteal phase of the menstrual cycle by blocking the conv

152 s were significantly (P=0.0078) lower in the luteal phase of the menstrual cycle compared to the foll

153 Changes in neurosteroid levels during the luteal phase of the menstrual cycle may precipitate affe

154 onadotropin secretion was blocked during the luteal phase of the menstrual cycle with a gonadotropin-

155 istered to female rhesus macaques during the luteal phase of the menstrual cycle, 40 min before admin

156 T cell populations were detected during the luteal phase of the menstrual cycle, and longitudinal an

157 In conclusion, TEF decreased during the luteal phase of the menstrual cycle, possibly as a resul

158 often occur during pregnancy and during the luteal phase of the menstrual cycle, when levels of prog

159 vulation phase and with urine PdG during the luteal phase of the menstrual cycle.

160 rder and 11 healthy female volunteers in the luteal phase of the menstrual cycle.

161 with plasma estradiol and estrone during the luteal phase of the menstrual cycle.

162 did not result from sodium retention in the luteal phase of the menstrual cycle.

163 behavioral, and somatic symptoms in the late luteal phase of the menstrual cycle.

164 al Dysphoric Disorder (PMDD) during the late luteal phase of the menstrual cycle.

165 esistance exercise in the follicular vs. the luteal phase of the menstrual cycle.

166 terized by debilitating mood symptoms in the luteal phase of the menstrual cycle.

167 V infection during the progesterone-dominant luteal phase of the menstrual cycle.

168 During the luteal phase of the sodium restriction cycle, significan

169 Shedding increased during the luteal phase only among women with CD4 counts of <350 ce

170 previously, we showed more inhibition in the luteal phase relative to the midfollicular menstrual pha

171 Compared to luteal phase sheep, both ERalpha and ERbeta levels in UA

172 d during the follicular phase and during the luteal phase similarly.

173 Herein, we review the evidence on luteal phase support and highlight remaining uncertainti

174 Despite the proven superiority of various luteal phase support protocols (LPS) over placebo in vie

175 sterone formulations to inform the design of luteal phase support regimens.

176 s used to optimize pregnancy rates; however, luteal phase support remains largely 'black-box' with in

177 gers used to mature oocytes on the degree of luteal phase support required.

178 Consequently, hormonal supplementation with luteal phase support, principally exogenous progesterone

179 ore energy at rest (4.3%; P = 0.0002) in the luteal phase than in the follicular phase.

180 ocytes during IVF results in a dysfunctional luteal phase that can be insufficient to support implant

181 Conversely, during the luteal phase there were factors overexpressed (including

182 Median luteal phase titres of progesterone were 121% higher (p=

183 re collected, characterized as follicular or luteal phase using days since last menstrual period, and

184 evel, in the default mode network during the luteal phase when passively viewing negative emotional s

185 cular phase, 0.70 +/- 0.10 kJ/min during the luteal phase, and 0.76 +/- 0.07 kJ/min during the late l

186 e onset of melatonin levels for women in the luteal phase, but it had little effect on melatonin leve

187 mones measured either midcycle or during the luteal phase, despite good statistical power to detect m

188 During the late luteal phase, females showed a lower predicted binge dri

189 romedial prefrontal cortex and, in the early luteal phase, reduced central and corticomedial amygdala

190 rinking probability and odds ratios vs. late luteal phase, respectively: 17%, odds ratio=1.340, 95% C

191 antly higher than those measured in the late luteal phase, whereas aging and cigarette smoking reduce

192 mmunocytochemically detectable GAL-R1 in the luteal phase, whereas only a twentieth expressed GAL-R1

193 offer candidate mechanisms through which the luteal phase, wherein progesterone is dominant relative

194 Specifically, we outline the physiological luteal phase, which is regulated by progesterone from th

195 modeling and leukocyte infiltration with the luteal phase, which may represent potential hormone-asso

196 rgery during the follicular phase versus the luteal phase.

197 eft fronto-polar cortex more than during the luteal phase.

198 ating hormone and luteinizing hormone in the luteal phase.

199 d a 0.06-log(PdG) decrease (p = 0.03) in the luteal phase.

200 ficantly associated with length of the prior luteal phase.

201 icular phase and then decreased again in the luteal phase.

202 ls the entire night in the luteal and pseudo luteal phase.

203 se, and 0.76 +/- 0.07 kJ/min during the late luteal phase.

204 ity (P = 0.09) during menses than during the luteal phase.

205 id-follicular phase to the symptomatic, late luteal phase.

206 ncreased from the mid-follicular to the late luteal phase.

207 ic environment during the follicular vs. the luteal phase.

208 cination in the follicular phase but not the luteal phase.

209 the development of mood symptoms during the luteal phase.

210 vels as follicular cells transition into the luteal phase.

211 domised order: late follicular phase and mid-luteal phase.

212 wer endometrial expression of FST during the luteal phase.

213 its precursors) were associated with shorter luteal phase.

214 r for half of the menstrual cycle during the luteal phase.

215 teins (P = 5.62E-4) were elevated during the luteal phase.

216 e of 18 proteins that best distinguished the luteal phase.

217 n </= 5 ng/mL and no LH peak in the mid/late luteal phase.

218 men comprised the study cohort: 230 (28%) in luteal phase; 363 (44%) in follicular phase; and 241 gro

219 inary sodium loss, not retention, during the luteal phase; severity of menstrual symptoms was unchang

220 not meet criteria for either follicular- or luteal-phase categories.

221 tinuous (full-cycle dosing) or intermittent (luteal-phase dosing) sertraline.

222 g was associated with decreased midcycle and luteal-phase estradiol levels.

223 5-1988) of a prospective study, midcycle and luteal-phase estrogens and progestins were measured in 1

224 Luteal-phase females showed diminished subjective drug e

225 sing linear mixed models for follicular- and luteal-phase lengths, discrete-time fecundability models

226 ese chemicals in relation to follicular- and luteal-phase lengths, time to pregnancy, and early pregn

227 ases, and directly with the probability of a luteal-phase rise in progesterone.

228 pooled to create follicular-, midcycle-, and luteal-phase samples, respectively, for analysis.

229 rovided) were measured in the follicular and luteal phases of 2 menstrual cycles before a single inje

230 of the first menstrual cycle and during the luteal phases of both the first and third menstrual cycl

231 valuated in clinic during the follicular and luteal phases of each menstrual cycle.

232 metrial explants from the follicular and mid-luteal phases of the estrous cycle.

233 l females, and females in the follicular and luteal phases of the menstrual cycle (FDR-adjusted p-val

234 in the younger women (in the follicular and luteal phases of the menstrual cycle).

235 days apart to distinguish the follicular and luteal phases of the menstrual cycle, and phases were co

236 e glucuronide (E1G) in the periovulatory and luteal phases of the menstrual cycle, and to assess the

237 women during the the mid-follicular and late luteal phases of the menstrual cycle.

238 wice, at the (1) late follicular and (2) mid luteal phases of the menstrual cycle.

239 ding with the follicular, periovulatory, and luteal phases of their menstrual cycle were studied.

240 ching task during the midfollicular and late-luteal phases of their menstrual cycle.

241 lab during the follicular, ovulatory and mid-luteal phases of their menstrual cycles.

242 fertility (n = 5) during the follicular and luteal phases of their reproductive cycles.

243 bitors, taken throughout the cycle or during luteal phases only, is also well established.

244 t is greater during the early follicular and luteal phases than in the late follicular (periovulatory

245 ng postovulation (average of luteal and late luteal phases), when it was 0.73 +/- 0.07 kJ/min, compar

246 es during the follicular, periovulatory, and luteal phases, respectively (P = .01).

247 nd increases in progesterone associated with luteal phases, resulting in safe and potentially lifetim

248 ed in women with PMDD from follicular to the luteal phases, suggesting the absence of effect of the l

249 E1 were determined during the follicular and luteal phases.

250 follicular phase to the mid luteal and late luteal phases.

251 levels during the follicular, ovulatory, and luteal phases.

252 easured in the early and late follicular and luteal phases.

253 -cycle compared with both the follicular and luteal phases.

254 een the early follicular, ovulatory, and mid-luteal phases.

255 ed twice, during the late-follicular and mid-luteal phases.

256 in females (n = 12) in their follicular and luteal phases.

257 gestational weeks 6-8, corresponding to the luteal-placental shift.

258 om Chicago (n = 29) and found that mean-peak-luteal progesterone in the ovulatory cycles of Bolivian

259 maintain equine pregnancy in the absence of luteal progesterone in the third and fourth weeks postbr

260 ate was significantly associated with higher luteal progesterone levels (P trend 0.05).

261 ginally significant association with greater luteal progesterone levels (P trend 0.08).

262 on average, 16.0% (95% CI, 0.5-33.8%) higher luteal progesterone levels compared to women in the 1(st

263 tical mediator of the acute actions of LH on luteal progesterone production.

264 of protein kinase A (PKA) acutely stimulates luteal progesterone synthesis via a complex process, con

265 ship between PKA, HSL, and lipid droplets in luteal progesterone synthesis.

266 ways required for initiating and maintaining luteal progesterone synthesis.

267 A 10-fold increase in luteal progesterone was associated with a 19.4% increase

268 eceiving neoadjuvant chemotherapy during the luteal (progesterone-high) phase compared with those tre

269 were produced, purified, and incubated with luteal proteins.

270 conducted in quasi-follicular (qF) and quasi-luteal (qL) phases in dry (DRY) and humid (HUM) heat mat

271 e(-/-) mice displayed no obvious evidence of luteal regression 24 h after treatment with PGF and were

272 These results indicate that luteal regression at the termination of nonfertile menst

273 easing hormone antagonist-mediated premature luteal regression but failed to prolong the functional l

274 d the PGF-induced decrease in P4 and delayed luteal regression.

275 nial (C1=perimenstrual, C2=periovulatory, C3=luteal seizure exacerbation), noncatamenial, and seizure

276 pro-fibrotic action of TGF-beta1 in the mid-luteal stage of the estrous cycle.

277 and uterus is most abundant during the late luteal stage of the oestrous cycle.

278 eatures, including 174 features in the early luteal stages, well before the current pregnancy diagnos

279 ages: late follicular, early luteal and late luteal stages.

280 nd intracortical inhibition was least in the luteal studies (p<0.05).

281 rone and a more acute withdrawal in the late luteal subphase.

282 os potentially fail to thrive due to lack of luteal support.

283 severity, with symptoms exceeding a minimum luteal symptom severity threshold of 2.5).

284 Bovine luteal tissue contained abundant lipid droplets, LD-asso

285 nancy depends on progesterone synthesized by luteal tissue in the ovary.

286 Luteal tissue was enriched in triglycerides (TGs) compar

287 of the TGs and cholesteryl esters present in luteal tissue.

288 expression pattern during the follicular to luteal transition and its responsiveness to luteotropic

289 arly-perimenopausal women with evidence of a luteal transition.

290 attern of PLIN2 throughout the follicular to luteal transition.

291 These data suggest that most mid-luteal urinary estrogen metabolite concentrations are no

292 during either the follicular (V-FP(imm)) or luteal (V-LP(imm)) menstrual cycle phase.

293 Conversely, during the luteal versus follicular phase, the Deltaprogesterone/es