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

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

17 Luteal cell differentiation is impaired, and a disordere

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

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

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

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

22 Luteal cells in this model exhibit defective autophagy a

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

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

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

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

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

28 anulosa cells terminally differentiated into luteal cells.

29 1 (S6K1) signaling pathway in steroidogenic luteal cells.

30 ich increases the translational machinery in luteal cells.

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

32 ulosa cells of preovulatory follicles and to luteal cells.

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

34 8 subjects and day 11 in 1 subject) and mid-luteal (days 19-25) phases of their menstrual cycle.

35 ess was fully attributable to the underlying luteal defect.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 Follicular and luteal oestradiol and progesterone serum titres were gro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 wer endometrial expression of FST during the luteal phase.

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

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

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

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

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

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

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

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

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

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

130 rgery during the follicular phase versus the luteal phase.

131 its precursors) were associated with shorter luteal phase.

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

133 ating hormone and luteinizing hormone in the luteal phase.

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

135 ficantly associated with length of the prior luteal phase.

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

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

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

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

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

141 5-1988) of a prospective study, midcycle and luteal-phase estrogens and progestins were measured in 1

142 Luteal-phase females showed diminished subjective drug e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 E1 were determined during the follicular and luteal phases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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