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 strual status, age at last menstruation, and menopausal aetiology) information available.

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

4 portance of lifestyle factors in determining menopausal age.

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

6 span were more generally associated with pre-menopausal AMH levels.

7 e-scale population and explore the impact of menopausal and HER2 status on CTS5 model.

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

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

10 0 symptoms (abnormal mole, breast lump, post-menopausal bleeding, rectal bleeding, lower urinary trac

11 Low estrogen levels undoubtedly underlie menopausal bone thinning.

12 the response of Estrogen Receptor (ER)+ post-menopausal breast cancer tumors to aromatase inhibitors

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

14 ratios (OR) <= 3] for (mostly peri- and post-menopausal) breast cancer.

15 lth-related, and demographic factors in post-menopausal, but not pre-menopausal, women, with biologic

16 and cortical parameters consistent with post-menopausal disease, and negative phosphorus balance comp

17 Breast cancer survivors with menopausal dyspareunia can have comfortable intercourse

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

19 Whether health outcomes of menopausal estrogen therapy differ between women with an

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

21 om baseline serum/plasma samples of 191 post-menopausal female liver cancer cases (HCC n=83, ICC n=56

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

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

24 = 0.0491 vs. pre-symptoms) characteristic of menopausal flushing were observed during hot flush episo

25 130 000 and 490 000 deaths occurring in each menopausal group, respectively.

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

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

28 acupuncture for women with moderately severe menopausal HFs.

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

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

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

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

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

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

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

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

37 Whether menopausal hormone therapy (MHT) protects against cardio

38 Menopausal hormone therapy (MHT) reportedly increases th

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

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

41 , 1.50; 95% CI, 1.04 to 2.17) and any use of menopausal hormone therapy (MHT; HR, 1.16; 95% CI, 1.03

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

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

44 conducted to assess the association between menopausal hormone therapy and cardiovascular disease.

45 Menopausal hormone therapy continues in clinical use but

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

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

48 Menopausal hormone therapy has a complex pattern of risk

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

50 The influence of menopausal hormone therapy on breast cancer remains unse

51 to obtain further insight into influences of menopausal hormone therapy on chronic disease.

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

53 ted the model to account for smoking status, menopausal hormone therapy status, body-mass index, and

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

55 Menopausal hormone therapy to prevent chronic conditions

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

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

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

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

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

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

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

63 nicity, education, income, smoking, alcohol, menopausal hormone therapy, and hysterectomy status, hig

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

65 ave been promoted as natural alternatives to menopausal hormone therapy, but their potential effect o

66 1 without the disease, none of whom had used menopausal hormone therapy, were included in the analyse

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

68 rdiovascular disease risk factors and use of menopausal hormone therapy.

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

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

71 , smoking, diet, alcohol, physical activity, menopausal hormone use, Body Mass Index (BMI), diabetes,

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

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

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

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

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

77 of an open-label placebo (OLP) treatment for menopausal hot flushes.

78 os may be an effective, safe alternative for menopausal hot flushes.

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

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

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

82 tudies in preclinical models showed that pre-menopausal levels of estradiol (E2) promote TNBC-BM thro

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

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

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

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

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

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

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

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

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

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

93 Lesions in menopausal patients exhibited less suspicious quantitati

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

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

96 The female climacteric or menopausal process characterised by reduced estrogen, as

97 ence of the grandmother effect in a nonhuman menopausal species.

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

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

100 Furthermore, apart from age and menopausal status a statistically significant positive c

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

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

103 Subgroup analyses were performed 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 A significant interaction between menopausal status and treatment group was observed for D

106 Tests of an interaction between menopausal status and treatment were nonsignificant.

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

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

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

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

111 interaction between history of migraine and menopausal status for the prediction of VMS was also ide

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

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

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

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

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

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

118 act with hormonal birth control use and with menopausal status on risk of YOBC.

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

120 not observe any significant interactions by menopausal status or other participant characteristics.

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

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

123 Menopausal status was associated with accelerated lung f

124 Menopausal status was defined as nonmenopausal, transiti

125 Menopausal status was defined using age as a proxy, wher

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

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

128 ty, age at first birth, age at menarche, and menopausal status with percent density and dense area as

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

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

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

132 nsideration of sex differences, sex hormones/menopausal status, age, and other reproductive informati

133 ysical activity, dyslipidemia, hypertension, menopausal status, and adiposity.

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

135 ontinue to investigate links between parity, menopausal status, and biological age using targeted phy

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

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

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

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

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

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

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

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

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

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

146 The lifestyle extended model included menopausal status, family history of breast cancer, body

147 , stage, grade, treatments, body mass index, menopausal status, hormone therapy use, family history o

148 ndomisation was stratified by disease stage, menopausal status, hormone-receptor status, and intentio

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

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

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

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

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

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

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

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

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

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

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

160 Age, menopausal status, prior UTI, and host genetics were top

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

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

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

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

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

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

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

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

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

170 serologic evaluations were used to determine menopausal status.

171 , 95% confidence interval: 0.61, 1.33) or by menopausal status.

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

173 CVD, but most studies retrospectively assess menopausal status.

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

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

176 in analyses stratified by family history or menopausal status.

177 global burden and trends in breast cancer by menopausal status.

178 n terms of both BCSS and OS, irrespective of menopausal status.

179 redicts poor clinical outcomes regardless of menopausal status.

180 In addition, we examined associations by menopausal status.

181 omen and lower than in whites, regardless of menopausal status.

182 significant improvement in overall levels of menopausal symptoms (ES, .33; P = .003), and NS frequenc

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

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

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

186 d night sweats (HF/NS) and overall levels of menopausal symptoms (primary outcomes), sleep quality, H

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

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

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

190 Full hGnRH-R blockade, however, results in menopausal symptoms and affects bone mineralization, thu

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

192 Menopausal symptoms are significant but are not worse th

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

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

195 She experienced menopausal symptoms including hot flashes, vaginal dryne

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

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

198 ct and frequency of HF/NS, overall levels of menopausal symptoms, and sleep quality.

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

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

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

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

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

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

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

206 diovascular disease, autoimmune disease, and menopausal symptoms, that affect >200 million individual

207 ctivity and as a dietary supplement reducing menopausal symptoms.

208 ntries use complementary therapies to manage menopausal symptoms.

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

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

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

212 the self-managed group on overall levels of menopausal symptoms.

213 east cancer survivors with treatment-induced menopausal symptoms.

214 uently have significant side effects such as menopausal symptoms.

215 s hormone therapy for preventing or treating menopausal symptoms.

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

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

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

219 osis who were assessed longitudinally during menopausal transition as part of the Study of Women's He

220 n with depressive syndromes during and after menopausal transition but associated with a higher risk

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

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

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

224 f decreasing estradiol concentrations during menopausal transition may explain the increased frequenc

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

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

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

228 essants in depressive women during and after menopausal transition, PubMed, Cochrane Library, EMBASE

229 pitulating fundamental features of the human menopausal transition, results of transcriptomic analysi

230 conditions and diseases associated with the menopausal transition.

231 ge in menstrual bleeding patterns during the menopausal transition.

232 eased frequency of VMS in migraineurs during menopausal transition.

233 quency of VMS but not vaginal dryness during menopausal transition.

234 n increased frequency of VMS in women during menopausal transition.

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

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

237 ciation between the PRS and YOBC risk in pre-menopausal women (OR = 2.46 versus 1.23).

238 individual-level data from 558,709 naturally menopausal women across 20 prospective cohorts, among wh

239 1) levels and pericardial fat volume in post-menopausal women and high cardiovascular disease (CVD) r

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

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

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

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

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

245 Menopausal women are disproportionally susceptible, sugg

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

247 out a genome-wide meta-analysis in 3344 pre-menopausal women from five cohorts (median age 44-48 yea

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

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

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

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

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

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

254 , with attenuated sex differences among post-menopausal women not taking hormone replacement therapy.

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

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

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

258 cal age acceleration being lowest among post-menopausal women reporting between three and four live b

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

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

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

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

263 er profiles were most pronounced between pre-menopausal women versus men, with attenuated sex differe

264 51,182 menopausal women were identified using the UK General Pr

265 histological composition of the USL in post-menopausal women with and without POP at various stages.

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

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

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

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

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

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

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

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

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

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

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

277 -12.5 ml/yr (95% CI, -16.2 to -8.9) in post-menopausal women, compared with women menstruating regul

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

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

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

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

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

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

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

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

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

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

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

289 risk of development of late onset asthma in menopausal women.

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

291 creased bone resorption in osteoporotic post-menopausal women.

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

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

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

295 sed therapies to preserve memory function in menopausal women.

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

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

298 ely and effectively reduce memory decline in menopausal women.

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

300 phic factors in post-menopausal, but not pre-menopausal, women, with biological age acceleration bein