ライフサイエンスコーパス: menopausal

1 mice and pre- (42.3 +/- 0.5 years) and post-menopausal (61.9 +/- 0.9 years) women.

2 artile range, 5.0-15.2 years), with a median menopausal age of 49 years (47-52 years).

3 portance of lifestyle factors in determining menopausal age.

4 ry of an eating disorder was associated with menopausal age.

5 er risk and that the association may vary by menopausal and ER/PR status.

6 dual SNPs and overall PRS, and stratified by menopausal and receptor status.

7 nder 45) and 173,641 controls (menopause/pre-menopausal at >/= 45 years), in models controlling for p

8 Low estrogen levels undoubtedly underlie menopausal bone thinning.

9 esponse associations in endometrial and post-menopausal breast cancer, and in degree and duration of

10 the most commonly prescribed drugs to treat menopausal conditions, but by non-selectively triggering

11 ABS compared with patients with MI and post-menopausal controls (p < 0.05).

12 ower in patients with ABS compared with post-menopausal controls (p < 0.05).

13 sed in patients with ABS, compared with post-menopausal controls, following acute mental stress testi

14 ental stress in patients with MI versus post-menopausal controls.

15 Breast cancer survivors with menopausal dyspareunia can have comfortable intercourse

16 Menopausal estrogen (E2) replacement therapy increases t

17 against using menopausal estrogen therapy or menopausal estrogen plus progestogen therapy or raloxife

18 commendation 5: ACP recommends against using menopausal estrogen therapy or menopausal estrogen plus

19 ng hospitalized or diagnosed with ABS), post-menopausal female controls (n = 12), and female patients

20 ic paraventricular nucleus (PVN) neurons in "menopausal" female mice.

21 been taking any medication shown to improve menopausal flushes in the preceding 8 weeks.

22 = 0.0491 vs. pre-symptoms) characteristic of menopausal flushing were observed during hot flush episo

23 enopause, perimenopause, and unknown status) menopausal groups (n=2318; HR 1.03, 95% CI 0.89-1.20).

24 on of plant-based and natural therapies with menopausal health.

25 acupuncture for women with moderately severe menopausal HFs.

26 Low OS was associated with menopausal history (P = 0.03), persistent or increased t

27 tive (WHI) in 2002, a precipitous decline in menopausal hormonal therapy (MHT) use in the United Stat

28 ound for the association with current use of menopausal hormone therapy (<0.5 years ago; Pheterogenei

29 isk of tubular cancer in relation to current menopausal hormone therapy (for current use vs. never us

30 studies and randomized controlled trials of menopausal hormone therapy (HT) and chronic disease risk

31 The use of menopausal hormone therapy (HT) continues in clinical pr

32 Estrogen-only menopausal hormone therapy (HT) increases the risk of en

33 nflicting results on the association between menopausal hormone therapy (MHT) and risk of FI.

34 Menopausal hormone therapy (MHT) increases the risk of c

35 Whether menopausal hormone therapy (MHT) protects against cardio

36 Menopausal hormone therapy (MHT) reportedly increases th

37 additionally included estrogen and progestin menopausal hormone therapy (MHT) use, other MHT use, age

38 entation overall and according to the use of menopausal hormone therapy (MHT).

39 , 1.50; 95% CI, 1.04 to 2.17) and any use of menopausal hormone therapy (MHT; HR, 1.16; 95% CI, 1.03

40 ent users of estrogen plus progestin (E + P) menopausal hormone therapy (OR, 2.49; P = 0.0001).

41 The strongest differences were for menopausal hormone therapy (Pheterogeneity < 0.01) and a

42 ograms divided by height in meters squared], menopausal hormone therapy [MHT], alcohol, and smoking).

43 Menopausal hormone therapy continues in clinical use but

44 Use of estrogen-only menopausal hormone therapy did not attenuate the associa

45 Force (USPSTF) recommendation on the use of menopausal hormone therapy for the primary prevention of

46 Menopausal hormone therapy has a complex pattern of risk

47 alth effects in postmenopausal women, use of menopausal hormone therapy has declined.

48 tive that contains the same progestin as the menopausal hormone therapy regimen found to increase bre

49 idence about the benefits and harms of using menopausal hormone therapy to prevent chronic conditions

50 Menopausal hormone therapy to prevent chronic conditions

51 Pheterogeneity = 0.07] and with duration of menopausal hormone therapy use (per five-year increments

52 r type I versus Type II tumors were seen for menopausal hormone therapy use (relative risk (RR) of 1.

53 iparous women, the hazard ratios for current menopausal hormone therapy use (vs. never use), body mas

54 without ovary removal affects risk, whether menopausal hormone therapy use attenuates inverse associ

55 ysical activity level, breastfeeding, and no menopausal hormone therapy use was associated with a PAR

56 physical activity level, breastfeeding, and menopausal hormone therapy use.

57 Increased risks associated with use of menopausal hormone therapy were stronger for LCIS than D

58 usal status, use of oral contraceptives, and menopausal hormone therapy) and these gene variants on g

59 ysical activity, body mass index, menopause, menopausal hormone therapy, and alcohol, bread, coffee,

60 educed among users of oral contraceptives or menopausal hormone therapy, but associations with reprod

61 1 without the disease, none of whom had used menopausal hormone therapy, were included in the analyse

62 al energy intake, and, in women, ever use of menopausal hormone therapy.

63 assessing the efficacy and applicability of menopausal hormone treatment, because they may indicate

64 rom second cancers and other causes, whereas menopausal hormone use was significantly associated with

65 a significant risk factor among women; post-menopausal hormones use was only associated with an incr

66 th placebo resulted in fewer and less severe menopausal hot flashes at 8 weeks of follow-up.

67 vone supplements also consistently alleviate menopausal hot flashes provided they contain sufficient

68 A post-menopausal hot flush consists of profuse physiological e

69 siological symptoms that occur during a post-menopausal hot flush.

70 eurokinin 3 receptor antagonist (MLE4901) on menopausal hot flushes.

71 dies suggest that NKB signalling may mediate menopausal hot flushes.

72 Significance statement: Many aged menopausal individuals experience deficits in working me

73 cortex to women cured of leukemia who became menopausal is currently not performed because of the ris

74 mother Hypothesis to simulate how human post-menopausal longevity could have evolved as ancestral gra

75 Additionally, aged surgically menopausal monkeys experienced a 50% loss of MSBs that w

76 associations with breast cancer according to menopausal or ER status.

77 termediate CVD end points in perimenopausal, menopausal, or postmenopausal women.

78 ial-dose-doxycycline (SDD) treatment of post-menopausal osteopenic women significantly reduced period

79 128 post-menopausal osteopenic women with chronic periodontitis r

80 e both eroded and formative surfaces in post-menopausal osteoporosis patients, and that this absence

81 humanized IL-27 toward the treatment of post-menopausal osteoporosis.

82 deling in a widespread disease, such as post-menopausal osteoporosis.

83 therapeutic agents in the treatment of post-menopausal osteoporosis.

84 p-value = 0.015) and more likely to be post-menopausal (p-value = 0.004; BH-adjusted p-value = 0.015

85 ptake and of 2.38 for the lack of washout in menopausal patients as compared with nonmenopausal patie

86 Lesions in menopausal patients exhibited less suspicious quantitati

87 antly shorter survival, specifically in post-menopausal patients with advanced and terminal stages of

88 c pattern of malignancy being less common in menopausal patients.

89 Also, breast density related to menopausal state (P < 0.05).

90 2) was used to test the relationship between menopausal state and qualitative breast density.

91 Menopausal state had no effect on SUVmax and SUVavg.

92 s the effects of qualitative breast density, menopausal state, and age on SUVmax and SUVavg.

93 was to investigate relationships among age, menopausal state, and breast density and determine wheth

94 according to qualitative breast density and menopausal state.

95 eostatic functions, many of which go awry in menopausal states.

96 anthropometric and biochemical variables, or menopausal status (breast cancer), higher serum iron con

97 gy intake, physical activity, education, and menopausal status (in women).

98 for node status, tumor size, treatment, and menopausal status (P = 0.005 and P < 0.001, respectively

99 s annual screen by 10-year age groups and by menopausal status and current postmenopausal HT use.

100 Overall, associations were homogeneous by menopausal status and ER and PR expression in tumors.

101 regression models and stratified analyses by menopausal status and ER/PR status.

102 Subgroup analyses were performed by menopausal status and estrogen receptor (ER) and progest

103 risk and whether the associations varied by menopausal status and estrogen receptor (ER) and progest

104 ber intake and risk of breast cancer (BC) by menopausal status and hormone receptor expression in tum

105 isk and cancer severity differs according to menopausal status and postmenopausal hormone therapy (HT

106 A significant interaction between menopausal status and treatment group was observed for D

107 intake, smoking status, alcohol intake, and menopausal status as potential covariates.

108 se observations did not vary by adult BMI or menopausal status at blood draw.

109 n, the vascular risk factors increase as the menopausal status changes.

110 Anthropometric measures and menopausal status contribute to a large variability in c

111 ER, stage or menopausal status did not modify the effect of post-diag

112 family history remained significant, whereas menopausal status did not.

113 of asthma and respiratory symptoms differ by menopausal status in a longitudinal population-based stu

114 cross-sectional differences in MD by age and menopausal status in over 11,000 breast-cancer-free wome

115 older adulthood (ages >/=70 years); or 2) by menopausal status in women and stratification by age 50

116 Assessment of menopausal status is critical; ovarian suppression or ab

117 Analyzing data without regard to sex or menopausal status obscured group differences in circuit-

118 interactions between MAF-positive status and menopausal status on efficacy of zoledronic acid.

119 iation, either overall or when stratified by menopausal status or hormone receptor status.

120 etween the two cohorts might be explained by menopausal status or simply by chance.

121 formation on menstrual patterns to determine menopausal status using latent class analysis.

122 Menopausal status was associated with accelerated lung f

123 Menopausal status was defined as nonmenopausal, transiti

124 When matched the participants by age, post-menopausal status was still associated with a higher ris

125 Increasing age and post-menopausal status were associated with the presence of t

126 eptor status and age at diagnosis (proxy for menopausal status) by using conditional logistic regress

127 index (BMI); the endometrial model included menopausal status, age at menopause, BMI, smoking, oral

128 use, other MHT use, age at first live birth, menopausal status, age at menopause, family history of b

129 ments and adjusted for age, education, race, menopausal status, and baseline reading ability, anxiety

130 iate adjustment for baseline age, ethnicity, menopausal status, and changes in comorbidities and life

131 used as risk stratification tools; and age, menopausal status, and medical comorbidities should be c

132 by sensitivity to previous hormonal therapy, menopausal status, and presence of visceral metastasis a

133 nd adjusted for body mass index, parity, and menopausal status, and the area under the receiver opera

134 ontrolled for the age of the patients, their menopausal status, and the orientation of the MR images

135 smoking, use of hormone replacement therapy, menopausal status, baseline menopausal symptoms, and tre

136 inants of calcium absorption efficiency were menopausal status, calcium intake, and serum estradiol a

137 The effects of menopausal status, cyst size and other features, and the

138 Menopausal status, cyst size, and other cyst features si

139 sessed effects of baseline iron status, sex, menopausal status, duration of intervention, iron form,

140 Eligible patients-ie, any menopausal status, Eastern Cooperative Oncology Group pe

141 The authors assessed age, menopausal status, index breast cancer histologic result

142 When stratified by menopausal status, no noteworthy associations were obser

143 s by age, age at menarche, age at menopause, menopausal status, number of pregnancies, breast feeding

144 t differ according to age, CVD risk factors, menopausal status, or anticancer treatment.

145 erences in smoking history, body mass index, menopausal status, or personal or family history of cent

146 not vary by body mass index, smoking status, menopausal status, or time between urine collection and

147 oking, parity and duration of breastfeeding, menopausal status, oral contraceptive use, body mass ind

148 Because choline needs vary by age, sex, and menopausal status, participants were segregated into cor

149 and c-erbB-2 status) and patient parameters (menopausal status, personal history of breast carcinoma)

150 ng, oral contraceptive use, body mass index, menopausal status, postmenopausal hormone therapy use, d

151 oost or no boost, with minimisation for age, menopausal status, presence of extensive ductal carcinom

152 PE demonstrated significant association with menopausal status, prior breast radiation therapy, hormo

153 results were found after adjusting for age, menopausal status, smoking habit, and sexual exposure hi

154 ls; investigated effect modification by sex, menopausal status, smoking, and age; and calculated popu

155 status, type and timing of systemic therapy, menopausal status, statin use, and treating centre.

156 status, type and timing of systemic therapy, menopausal status, statin use, and treatment centre) to

157 years for sociodemographic characteristics, menopausal status, surgeries, body mass index, medicatio

158 In a model that included age, race, obesity, menopausal status, tumor size, nodal status, treatment a

159 ive factors (ages at menarche and menopause, menopausal status, use of oral contraceptives, and menop

160 This association is independent of menopausal status, which remains an independent predicto

161 ast cancer are associated with the patient's menopausal status, with a typical kinetic pattern of mal

162 tion between the kinetic characteristics and menopausal status, with an odds ratio of 2.94 for the la

163 se subjects (n = 1108) and age-, gender- and menopausal status-matched participants in the Framingham

164 , 95% confidence interval: 0.61, 1.33) or by menopausal status.

165 ll reduction in risk of BC, independently of menopausal status.

166 CVD, but most studies retrospectively assess menopausal status.

167 able to assess effects on body iron, sex, or menopausal status.

168 idermal growth factor receptor 2 (HER2), and menopausal status.

169 in analyses stratified by family history or menopausal status.

170 , tumor characteristics, breast density, and menopausal status.

171 lyses, mostly in subgroups defined by age or menopausal status.

172 serologic evaluations were used to determine menopausal status.

173 29% were postmenopausal, and 2% were unknown menopausal status; 49.5% were HmR positive; 33.5% were H

174 body image (EST2 = .45; P = .009) and fewer menopausal symptoms (EST1 = .39; P = .007) than the cont

175 th breast cancer reporting treatment-induced menopausal symptoms (N=422) were randomly assigned to CB

176 these two interventions combined (CBT/PE) on menopausal symptoms (primary outcome), body image, sexua

177 nt of women age >/= 30 years suffered severe menopausal symptoms (three- to four-fold more frequently

178 to be a potential risk factor for vasomotor menopausal symptoms (VMSs), ie, hot flushes and night sw

179 hese results show that women who have severe menopausal symptoms after ovarian cancer treatment can s

180 avone-rich diets are associated with reduced menopausal symptoms and lowered risk of cancers of repro

181 When added to tamoxifen, OFS results in more menopausal symptoms and sexual dysfunction, which contri

182 Menopausal symptoms are significant but are not worse th

183 ted with estrogen and progesterone to manage menopausal symptoms have resulted in its declining use a

184 fects on sexual functioning, body image, and menopausal symptoms in BCSs with a sexual dysfunction.

185 ement therapy (HRT) is widely used to manage menopausal symptoms in women and can be comprised of an

186 She experienced menopausal symptoms including hot flashes, vaginal dryne

187 act of oncologic treatments on fertility and menopausal symptoms is often significant for patients wi

188 al data that young postmenopausal women with menopausal symptoms who use HT for long periods of time

189 ata included health-related quality of life, menopausal symptoms, and sexual function.

190 acement therapy, menopausal status, baseline menopausal symptoms, and treatment.

191 supplements, consumed by women experiencing menopausal symptoms, are suggested to have positive effe

192 For cancer survivors who experience menopausal symptoms, lifestyle changes may be beneficial

193 nts treated with tamoxifen plus OFS had more menopausal symptoms, lower sexual activity, and inferior

194 intimacy (primary outcomes) and body image, menopausal symptoms, marital functioning, psychological

195 as associated with a substantial increase in menopausal symptoms, sexual dysfunction, and diminished

196 dering hormone therapy for the management of menopausal symptoms, such as hot flashes or vaginal dryn

197 rse effects are enhanced in older women with menopausal symptoms.

198 ) and licorice (Glycyrrhiza spec.) to manage menopausal symptoms.

199 ng and aid in developing safer therapies for menopausal symptoms.

200 n memory and mood disorders as well as other menopausal symptoms.

201 replacement therapy (HRT) for alleviation of menopausal symptoms.

202 menopause and were treated for the relief of menopausal symptoms.

203 ctivity and as a dietary supplement reducing menopausal symptoms.

204 ntries use complementary therapies to manage menopausal symptoms.

205 s hormone therapy for preventing or treating menopausal symptoms.

206 ve grandmother effects are also found in non-menopausal taxa, but evidence of their associated fitnes

207 es metabolic physiology, highlighted by post-menopausal temperature dysregulation (hot flashes), gluc

208 ential bias in the understanding of both the menopausal transition and the linkage between the transi

209 hod to 4 alternative proposed markers of the menopausal transition are compared with previous finding

210 terations in serum hormone levels across the menopausal transition are linked to depressive symptoms.

211 Data on the menopausal transition are used to illustrate the problem

212 ps based on menstrual characteristics of the menopausal transition experience.

213 sk of stroke during middle age than men, the menopausal transition is a time when many women develop

214 al atherogenic shift overlapping the time of menopausal transition is observed.

215 Moreover, women undergoing the menopausal transition often complain of problems with me

216 n criteria, most longitudinal studies of the menopausal transition probably include only a subset of

217 ligned with proposed bleeding markers of the menopausal transition, but for some women they are not c

218 gen concentrations decline by 60% during the menopausal transition, leading to a relative androgen ex

219 study that evaluated proposed markers of the menopausal transition, where the markers are measures ba

220 conditions and diseases associated with the menopausal transition.

221 ge in menstrual bleeding patterns during the menopausal transition.

222 tiated within a 'critical window' during the menopausal transition.

223 nopausally, and are most pronounced over the menopausal transition.

224 ute to higher depressive symptoms during the menopausal transition.

225 performed a nutrient tracer study during the menopausal window of vulnerability.

226 hest risk for donation-induced low iron, but menopausal women and high-frequency donors of both sexes

227 iomyopathy that occurs predominantly in post-menopausal women and may be triggered by acute mental st

228 Hot flushes affect 70% of menopausal women and often severely impact physical, psy

229 h ovariectomized mice as a model for UTIs in menopausal women and pinpoint specific events during cou

230 Hot flashes (HFs) affect up to 75% of menopausal women and pose a considerable health and fina

231 l differences in the cognitive outcome among menopausal women and promote a focus on cortical estroge

232 in young women compared with young men, but menopausal women are at greater risk for hypertension co

233 Menopausal women are disproportionally susceptible, sugg

234 ocotyl isoflavone supplementation in healthy menopausal women as a secondary outcome of a trial on bo

235 heart disease (CHD) risk prediction in post-menopausal women compared with assessment using traditio

236 t higher circulating estrogens in young, pre-menopausal women could exert paracrine effects through t

237 Participants were 84,537 post-menopausal women from the WHI (Women's Health Initiative

238 Post-menopausal women have an increased risk of developing a

239 of hormone therapy on cognitive function in menopausal women have been equivocal, in part due to dif

240 , enhanced performances in athletes and post-menopausal women in clinical studies.

241 isk factors for sudden cardiac death in post-menopausal women include African-American race, higher p

242 primary prevention of chronic conditions in menopausal women is associated with some beneficial effe

243 Estrogen withdrawal in menopausal women leads to hot flushes, a syndrome charac

244 eceiving hormone replacement therapy; 3) pre-menopausal women not receiving hormonal contraceptives;

245 rmone status was grouped as: 1) men; 2) post-menopausal women not receiving hormone replacement thera

246 Health across the Nation enrolled 3,302 pre-menopausal women not using hormone therapy between 42 an

247 k of future systemic bone loss in these post-menopausal women not yet on anti-osteoporotic drugs.

248 With the aging U.S. population, post-menopausal women now have the greatest population burden

249 ving hormone replacement therapy; and 5) pre-menopausal women receiving hormonal contraceptives.

250 t receiving hormonal contraceptives; 4) post-menopausal women receiving hormone replacement therapy;

251 py to prevent cardiovascular disease in post-menopausal women remains contentious.

252 Although younger women or more recently menopausal women taking hormone therapy may be at relati

253 omplications are more severe in men and post-menopausal women than in pre-menopausal women.

254 determining potential therapeutic agents for menopausal women to decrease the propensity of diseases

255 ow hypothesis, i.e., that the brains of post-menopausal women ultimately lose their ability to respon

256 In a preference trial, 18 symptomatic post-menopausal women underwent a passive heat stress to indu

257 ated the association between HRT and GORD in menopausal women using validated general practice record

258 51,182 menopausal women were identified using the UK General Pr

259 -blind, double-dummy trial, we enrolled post-menopausal women with at least two moderate or one sever

260 oxide production and lower blood pressure in menopausal women with high normal blood pressure remains

261 itric oxide production and blood pressure in menopausal women with high normal blood pressure.

262 sure and associated vascular hemodynamics in menopausal women with high normal blood pressure.

263 inhibitor administered after surgery to post-menopausal women with hormonally responsive breast cance

264 lf-reported executive functioning in healthy menopausal women with midlife onset of executive difficu

265 One hundred twenty-eight eligible post-menopausal women with periodontitis and systemic osteope

266 anisms and open the door for prophylaxis for menopausal women with recurrent UTIs.

267 uble-blind, placebo-controlled trial of post-menopausal women with serum 25-hydroxyvitamin D concentr

268 INTERPRETATION: Among post-menopausal women with severe osteoporosis, the risk of n

269 reference-controlled trial involving 21 post-menopausal women, 16 weeks of supervised moderate intens

270 Neurokinin B signalling is increased in menopausal women, and has been implicated as an importan

271 -12.5 ml/yr (95% CI, -16.2 to -8.9) in post-menopausal women, compared with women menstruating regul

272 ssociated with decreasing HF risk among post-menopausal women, even in the absence of antecedent coro

273 ned more rapidly among transitional and post-menopausal women, in particular for FVC, beyond the expe

274 ed that hormone treatment benefits memory in menopausal women, several newer studies have shown no ef

275 In post-menopausal women, shorter total reproductive duration wa

276 Among recently menopausal women, significant heterogeneity in CV risk i

277 In hyperlipidemic post-menopausal women, statin therapy induced EAT regression,

278 In post-menopausal women, the attenuation of PP amplification, m

279 otanical estrogens (BEs), widely consumed by menopausal women, we investigated the mechanistic and ce

280 ce of HF hospitalization among healthy, post-menopausal women, whereas multivariable adjustment atten

281 re associated with breast cancer risk in pre-menopausal women, with adjusted odds ratios (aORs) of 2.

282 re associated with breast cancer risk in pre-menopausal women, with aORs of 4.6 (2.3, 9.2), 3.1 (1.6,

283 (and tail) arteries from aged mice and post-menopausal women.

284 k factors for breast cancer in pre- and post-menopausal women.

285 creased bone resorption in osteoporotic post-menopausal women.

286 d cerebral ischemia incidents/impact in post-menopausal women.

287 artery calcium (CAC) in hyperlipidemic post-menopausal women.

288 in men and post-menopausal women than in pre-menopausal women.

289 sed therapies to preserve memory function in menopausal women.

290 and to identify risk factors for SCD in post-menopausal women.

291 d telangiectasias were conducted on 410 post-menopausal women.

292 e-resorption biomarkers in subgroups of post-menopausal women.

293 We included 26,160 healthy, post-menopausal women.

294 arian hormone intervention in peri- and post-menopausal women.

295 eart failure (HF) hospitalization among post-menopausal women.

296 dded to predictive models using TRFs in post-menopausal women.

297 otyl isoflavones has minimal risk in healthy menopausal women.

298 nd -5.2 ml/yr (95% CI, -8.3 to -2.0) in post-menopausal women.

299 n activation during a working memory task in menopausal women.

300 ascular and bone remodelling markers in post-menopausal women.