ライフサイエンスコーパス: PCOS

1 PCOS and ASD were defined from ICD codes through linkage

2 PCOS AT was determined to have a differentially expresse

3 PCOS groups exhibited a positive correlation among clini

4 PCOS is also associated with high androgens, increases t

5 PCOS patients with an isolated elevated FAI showed incre

6 PCOS symptoms most likely result from a disturbance in t

7 PCOS was independently associated with lower age, higher

8 PCOS women with both biochemical and clinical hyperandro

9 in an independent, ungenotyped cohort of 263 PCOS cases (median and IQR: age = 28 [24-33], BMI = 35.7

10 etabolic traits in a genotyped cohort of 893 PCOS cases (median and interquartile range [IQR]: age =

11 99 PCOS women and 100 healthy controls were recruited.

12 NND1A.V2 in normal theca cells resulted in a PCOS phenotype of augmented CYP17A1 and CYP11A1 gene tra

13 roids applied to pregnant sheep programmes a PCOS-like phenotype in female offspring.

14 attenuated ET-1-induced vasodilatation in AE-PCOS is a consequence of androgen receptor-mediated, sup

15 decreased ET-1-induced vasodilatation in AE-PCOS women (logED(50) , 0.64 +/- 0.

16 ndrogen drives endothelial dysfunction in AE-PCOS women and oestradiol (EE) administration reverses t

17 ed vasodilatory responses to ET-1 in lean AE-PCOS (logED(50) , 0.59 +/- 0.08) versus lean controls (l

18 .09, P < 0.05), but not compared to obese AE-PCOS (logED(50) , 0.65 +/- 0.09).

19 Only obese AE-PCOS women were insulin resistant (IR).

20 endothelial dysfunction in lean and obese AE-PCOS.

21 ndrogen excess polycystic ovary syndrome (AE-PCOS).

22 men with (7 lean and 7 obese) and without AE-PCOS (controls, 6 lean, 7 obese).

23 nstrate upregulated miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting

24 a recent meta-analysis of European ancestry PCOS cases found that the genetic architecture of PCOS d

25 d with higher PCOS risk (P=1.6 x 10(-8)) and PCOS-susceptibility alleles are associated with higher s

26 e of periodontitis compared with control and PCOS-MT groups (P </=0.05).

27 lated and propagated from normal cycling and PCOS women, we found that DENND1A variant 2 (DENND1A.V2)

28 fered significantly between normal women and PCOS women.

29 lobulin) may explain the association between PCOS and cardiometabolic diseases.

30 Association between PCOS and diabetes risk was examined in European and Asia

31 NAs differed in the follicular fluid between PCOS and normal control women, correlating with age, FAI

32 and to determine the molecular link between PCOS conditions and placental dysfunction during pregnan

33 arranted to clarify the relationship between PCOS and gingivitis.

34 ascular risk indices were increased for both PCOS cohorts, this may be for different reasons: BMI, wa

35 re further increased among mothers with both PCOS and obesity, a condition common to PCOS that is rel

36 , 622 controls) were compared to a Caucasian PCOS biobank in Hull UK (108 with PCOS, 69 controls).

37 hr 9q22.32 locus previously found in Chinese PCOS.

38 ve as FAI for the diagnosis of the classical PCOS phenotype, and the combination of salT or FAI ident

39 Hyperandrogenism is the most consistent PCOS characteristic; however, it is unclear whether andr

40 A1 mRNA when added to the medium of cultured PCOS theca cells.

41 Women with newly diagnosed PCOS had increased sites with bleeding on probing (BOP),

42 Women with newly diagnosed PCOS may have increased prevalence and likelihood for pe

43 lin resistance (IR) and obesity in different PCOS phenotypes among infertile women (n = 213), of whom

44 The clustering revealed 2 distinct PCOS subtypes: a "reproductive" group (21%-23%), charact

45 glycerides (p < 0.01), whilst Middle Eastern PCOS women showed increased testosterone, free androgen

46 OS patients as well as in a well-established PCOS mouse model.

47 reatment on ovarian function in experimental PCOS, likely via BMP4 signaling.

48 y represent a novel diagnostic biomarker for PCOS.

49 ate MR imaging-based diagnostic criteria for PCOS were OV, FPO-9, and peripheral distribution of foll

50 who did not meet the diagnostic criteria for PCOS, women who met the criteria had higher rates of hir

51 genism is one of the diagnostic criteria for PCOS.

52 ect the molecular mechanisms responsible for PCOS phenotypes.

53 We identify six signals for PCOS at genome-wide statistical significance (P<5 x 10(-

54 reakdown than those on medical treatment for PCOS and systemically healthy females.

55 ion of women receiving medical treatment for PCOS and women newly diagnosed with PCOS.

56 for the development of novel treatments for PCOS.

57 RNA was significantly elevated in urine from PCOS women compared with normal cycling women.

58 g infertile women (n = 213), of whom 159 had PCOS and 54 women without PCOS, recruited as a control g

59 th girls who were highly suspected of having PCOS compared with control subjects as the reference.

60 ria in 50 girls who were suspected of having PCOS to assess reproducibility (kappa and intraclass cor

61 women for the National Institutes of Health PCOS phenotype, which confers the highest risk for metab

62 to later menopause is associated with higher PCOS risk (P=1.6 x 10(-8)) and PCOS-susceptibility allel

63 Genome-wide association studies identified PCOS candidate loci that were replicated in subsequent r

64 In PCOS, miR-382-5p correlated with age and free androgen i

65 In PCOS, no such changes were found, despite similar traini

66 ating with age, FAI, inflammation and AMH in PCOS, and with BMI, fertilization rate (3 miRNA), insuli

67 small non-coding microRNA (miRNA) changes in PCOS and their expression in follicular fluid has been d

68 to prevent cardiometabolic complications in PCOS should focus on women with high-risk features rathe

69 r androgens in cardiovascular dysfunction in PCOS.

70 salT and salA were significantly elevated in PCOS compared to controls (P < 001).

71 and metabolic and reproductive functions in PCOS.

72 V2) protein and mRNA levels are increased in PCOS theca cells.

73 modulation of AKR1C3 activity by insulin in PCOS and in women with INSR mutations.

74 s balancing selection mechanisms involved in PCOS risk.

75 LUT4 expression to be significantly lower in PCOS patients and in control subjects with IR.

76 rculating ZAG and M-value were much lower in PCOS women than in the controls.

77 isms involved in the development of NAFLD in PCOS are not well known.

78 The phenotypic variation observed in PCOS is suggestive of an underlying genetic heterogeneit

79 en burden and improve metabolic phenotype in PCOS.

80 to the perturbation of ovarian remodeling in PCOS.

81 latory dysfunction and insulin resistance in PCOS remains elusive, thus limiting the development of t

82 tokine associated with insulin resistance in PCOS women.

83 ns are hypothesized to play a causal role in PCOS.

84 domization analyses indicate causal roles in PCOS aetiology for higher BMI (P=2.5 x 10(-9)), higher i

85 increases following MVT-602 were similar in PCOS and healthy women, but advanced in HA (P = 0.004).

86 stress may serve as a therapeutic target in PCOS.

87 othelial dysfunction is currently unknown in PCOS.

88 Knock-down of DENND1A.V2 in PCOS theca cells reduced androgen biosynthesis and CYP17

89 dently related factors to circulating ZAG in PCOS women.

90 acebo or dihydrotestosterone (DHT) to induce PCOS-like traits.

91 DHT induced PCOS-like clinical signs in wild type mice as well as si

92 e model of dihydrotestosterone (DHT)-induced PCOS with global and cell-specific AR-resistant (ARKO) m

93 targeting AR-driven mechanisms that initiate PCOS is a promising strategy for the development of nove

94 t first child, higher lifetime parity, lower PCOS risk, and earlier age at menopause.

95 Maternal PCOS increased the odds of ASD in the offspring by 59%,

96 Maternal PCOS increased the odds of offspring ADHD by 42% after a

97 Maternal PCOS was defined by ICD-coded register diagnosis.

98 This study provides evidence that maternal PCOS may subtly influence the neurodevelopment of the of

99 dy, we aimed to investigate whether maternal PCOS increases the risk for ADHD in the offspring.

100 ed miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting for the IR of th

101 n VO(2max) In skeletal muscle of CON but not PCOS, training increased GLUT4 and HKII mRNA and protein

102 ombination of salT or FAI identified 100% of PCOS patients.

103 ombination of salT or FAI identified 100% of PCOS women.

104 cases found that the genetic architecture of PCOS defined by different diagnostic criteria was genera

105 ion study to investigate the associations of PCOS with type 2 diabetes, coronary heart disease (CHD),

106 -sensitive glucose transporter, in the AT of PCOS and matched control subjects.

107 R stress was activated in granulosa cells of PCOS patients as well as in a well-established PCOS mous

108 ression also increased in granulosa cells of PCOS patients.

109 Due to the complexity of PCOS, had it has been challenging to isolate specific ca

110 is treatable, is a cause or a consequence of PCOS.

111 cell viability/hyperplasia in the context of PCOS.

112 extraovarian mediator in the development of PCOS traits.

113 androstenedione (salA) for the diagnosis of PCOS was undertaken in a cross sectional study involving

114 ient biomarker than miR-223 for diagnosis of PCOS.

115 Causal effects of PCOS on risks of CHD and stroke were evaluated in Europe

116 th body fat distribution and the etiology of PCOS, we conducted whole-genome DNA methylation analysis

117 Other features of PCOS (obesity, elevated testosterone, low sex hormone bi

118 is required for all DHT-induced features of PCOS.

119 ased fasting glucose and a family history of PCOS in at least one first degree relative.

120 lthough yet to be defined, role in the IR of PCOS.

121 N are the most reliable cutaneous markers of PCOS and require a comprehensive skin examination to dia

122 miscarriage, but the underlying mechanism of PCOS-induced fetal loss during pregnancy remains obscure

123 ng in the ARN that is enhanced in a model of PCOS and may underpin the neuroendocrine pathophysiology

124 olomic profile in the liver of rat models of PCOS phenotype induced by testosterone or estradiol.

125 a primary pancreatic phenotype in models of PCOS, and that there may be a distinct male and female p

126 As the origins of PCOS remain unknown, mechanism-based treatments are not

127 nal roles for DENND1A in the pathogenesis of PCOS.

128 ota and its metabolites on the regulation of PCOS-associated ovarian dysfunction and insulin resistan

129 nd genotypic factors associated with risk of PCOS and to test for interactions between genotype and v

130 ion between vitamin D deficiency and risk of PCOS in Pakistan, that was not modified by genetic varia

131 genotype of any SNP investigated and risk of PCOS, either as a main effect or in interaction with vit

132 tly attenuated DHT-induced clinical signs of PCOS and alterations in ovarian gene expression.

133 mia and hormonal profile observed in sons of PCOS patients.

134 e perform a genome-wide association study of PCOS in up to 5,184 self-reported cases of White Europea

135 e likely to have the reproductive subtype of PCOS.

136 ere were reproducible phenotypic subtypes of PCOS with subtype-specific genetic associations.

137 there are biologically relevant subtypes of PCOS.

138 cible reproductive and metabolic subtypes of PCOS.

139 ly associated with the level of suspicion of PCOS (P </= .05).

140 , oligomenorrhea or amenorrhea) suspicion of PCOS.

141 unostaining was more intense in the theca of PCOS ovaries.

142 By contrast, treatment of PCOS mice with an ER stress inhibitor, tauroursodeoxycho

143 ms to offer an improved dietary treatment of PCOS women.

144 levels may be of value for the treatment of PCOS.

145 in D pathway (VDR, DBP, CYP27B1, CYP24A1) on PCOS.

146 Limitations of our study were that only PCOS cases of European ancestry diagnosed by National In

147 ising 41 newly diagnosed patients with PCOS (PCOS-N), 45 patients with PCOS on medical treatment (PCO

148 In both populations, PCOS women showed a worse cardiovascular risk profile of

149 ound no association of genetically predicted PCOS with risk of diabetes, CHD, or stroke.

150 kingly similar to those observed in pregnant PCOS patients.

151 are strikingly similar to those in pregnant PCOS patients.

152 nd genotype data from a previously published PCOS genome-wide association study (GWAS), we investigat

153 and October 25, 2012, who met the Rotterdam PCOS criteria.

154 total, 68.8% (276 of 401) met the Rotterdam PCOS diagnostic criteria, while 12.0% (48 of 401) did no

155 The Prostate Cancer Outcomes Study (PCOS) enrolled 3533 men in whom prostate cancer had been

156 ipants were 401 women referred for suspected PCOS.

157 In total, 401 women with suspected PCOS were included in the study.

158 ecruited from a polycystic ovarian syndrome (PCOS) clinic between May 18, 2006, and October 25, 2012,

159 c equivalent of polycystic ovarian syndrome (PCOS) in women, which carries the risk of developing obe

160 Polycystic ovarian syndrome (PCOS) is a hormonal disorder of females of reproductive

161 Polycystic ovarian syndrome (PCOS), the leading cause of female infertility, is assoc

162 vulation due to polycystic ovarian syndrome (PCOS), though her preprocedure body mass index was norma

163 sceptibility to polycystic ovarian syndrome (PCOS).

164 sociated with the polycystic ovary syndrome (PCOS) affection status by screening 731,442 SNP features

165 A]) in women with polycystic ovary syndrome (PCOS) and chronic periodontitis (CP).

166 in patients with polycystic ovary syndrome (PCOS) and systemically healthy controls in the presence

167 egnant women with polycystic ovary syndrome (PCOS) are often overweight or obese.

168 with and without polycystic ovary syndrome (PCOS) between a Caucasian and Middle East population.

169 Women with polycystic ovary syndrome (PCOS) commonly suffer from miscarriage, but the underlyi

170 Women with polycystic ovary syndrome (PCOS) commonly suffer from miscarriage, but the underlyi

171 Women with polycystic ovary syndrome (PCOS) exhibit elevated androgen levels, oligoanovulation

172 Polycystic ovary syndrome (PCOS) has been associated with diabetes and cardiovascul

173 Women with polycystic ovary syndrome (PCOS) have been shown to be less insulin sensitive compa

174 70% of women with polycystic ovary syndrome (PCOS) have intrinsic insulin resistance (IR) above and b

175 for diagnosis of polycystic ovary syndrome (PCOS) in adolescents.

176 Polycystic ovary syndrome (PCOS) is a common problem among Arab women and is the ma

177 Polycystic ovary syndrome (PCOS) is a common, complex genetic disorder affecting up

178 Polycystic ovary syndrome (PCOS) is a common, highly heritable complex disorder of

179 Polycystic ovary syndrome (PCOS) is a complex hormonal disorder characterized by re

180 Polycystic ovary syndrome (PCOS) is a complex syndrome with cardiovascular risk fac

181 Polycystic ovary syndrome (PCOS) is a hypothalamic-pituitary-gonadal (HPG) axis dis

182 Polycystic ovary syndrome (PCOS) is a major reproductive disorder that is responsib

183 Polycystic ovary syndrome (PCOS) is associated with cardiovascular disease.

184 Polycystic ovary syndrome (PCOS) is characterized by androgen excess, ovulatory dys

185 Polycystic ovary syndrome (PCOS) is frequently associated with non-alcoholic fatty

186 spected of having polycystic ovary syndrome (PCOS) is incomplete.

187 Polycystic ovary syndrome (PCOS) is the most common reproductive disorder in women,

188 led the effect of polycystic ovary syndrome (PCOS) on gingival inflammation.

189 lin resistance in polycystic ovary syndrome (PCOS) women.

190 an ovine model of polycystic ovary syndrome (PCOS), (pregnant ewes injected with testosterone propion

191 Maternal polycystic ovary syndrome (PCOS), a common metabolic disorder associated with exces

192 est that maternal polycystic ovary syndrome (PCOS), a condition associated with excess androgens, wou

193 Polycystic ovary syndrome (PCOS), characterized by increased ovarian androgen biosy

194 athophysiology of polycystic ovary syndrome (PCOS), the most common endocrine disorder of reproductiv

195 nce in women with polycystic ovary syndrome (PCOS).

196 eased severity of polycystic ovary syndrome (PCOS).

197 dinal features of polycystic ovary syndrome (PCOS).

198 eir importance in polycystic ovary syndrome (PCOS).

199 onditions such as polycystic ovary syndrome (PCOS).

200 and in women with polycystic ovary syndrome (PCOS; n = 6) or hypothalamic amenorrhea (HA; n = 6).

201 The present findings emphasize that PCOS and gingival inflammation are associated with each

202 This suggests that PCOS in and of itself does not increase the risk of thes

203 The PCOS phenotype was induced in mice following prenatal an

204 The PCOS women with high ZAG had fewer MetS, IGT and polycys

205 io was not significantly different among the PCOS group (n = 37, 23.3%) compared to the control group

206 ey loci of androgen action in generating the PCOS phenotype.

207 ng protein 3, and IL-22 in turn improved the PCOS phenotype.

208 he FGS index was significantly higher in the PCOS + gingivitis group than the PCOS + healthy group (P

209 between the women meeting vs not meeting the PCOS criteria.

210 Women who met the PCOS criteria demonstrated more severe truncal hirsutism

211 Women who met the PCOS criteria had elevated total testosterone levels (40

212 actions that mediate the development of the PCOS phenotype.

213 gher in the PCOS + gingivitis group than the PCOS + healthy group (P = 0.030).

214 We conclude that the PCOS candidate gene, DENND1A, plays a key role in the hy

215 ic regression analysis demonstrated that the PCOS-N group had 2.88 times increased likelihood of havi

216 en with early AGA and to compare it with the PCOS profile; the secondary outcome was to establish a r

217 e endothelin-1-induced vasodilation in these PCOS subject, was dependent on the ET(B) R but was not N

218 or effects on reproductive functions in this PCOS-like mouse model.

219 both PCOS and obesity, a condition common to PCOS that is related to more severe hyperandrogenemia (O

220 in normal pregnant rats, most likely due to PCOS-like endocrine abnormality induced by the treatment

221 ystic ovarian phenotype with similarities to PCOS.

222 45 patients with PCOS on medical treatment (PCOS-MT), and 40 systemically healthy controls (control

223 nsulin or insulin resistance between the two PCOS cohorts.

224 The two PCOS groups exhibited significantly higher saliva TNF-al

225 in resistance did not differ between the two PCOS populations despite differences in BMI.

226 UK PCOS women had a higher body mass index, systolic and di

227 Caucasian PCOS biobank in Hull UK (108 with PCOS, 69 controls).

228 le Eastern women from Qatar Biobank (97 with PCOS, 622 controls) were compared to a Caucasian PCOS bi

229 BB3/HER3 and ERBB4/HER4) are associated with PCOS at or near genome-wide significance.

230 lating ZAG was significantly associated with PCOS even after controlling for anthropometric variables

231 IR was significantly associated with PCOS only among women with central obesity (chi(2) = 35.

232 oping the same complications associated with PCOS, including obesity, metabolic syndrome, IR, cardiov

233 ole in the hyperandrogenemia associated with PCOS.

234 peptide (FSHB) gene strongly associates with PCOS diagnosis and luteinizing hormone levels.

235 ment for PCOS and women newly diagnosed with PCOS.

236 Levels of IL-17E were lowest in females with PCOS and gingivitis who also had the highest FGS.

237 hirty-one females with PCOS, 30 females with PCOS and gingivitis, and 12 systemically and periodontal

238 levels are altered in non-obese females with PCOS and may influence gingival inflammation.

239 saliva, and serum of non-obese females with PCOS and with either a clinically healthy periodontium o

240 Thirty-one females with PCOS, 30 females with PCOS and gingivitis, and 12 system

241 laque index, showed that the two groups with PCOS had higher concentrations of IL-17A, IL-17F, and IL

242 ed in the gut microbiota of individuals with PCOS, accompanied by reduced glycodeoxycholic acid and t

243 reduced levels of IL-22 in individuals with PCOS.

244 for ADHD was higher among obese mothers with PCOS (OR, 1.68; 95% CI, 1.31-2.17) and was highest among

245 17) and was highest among obese mothers with PCOS and other features of metabolic syndrome (OR, 2.59;

246 comprising 41 newly diagnosed patients with PCOS (PCOS-N), 45 patients with PCOS on medical treatmen

247 atients with PCOS (PCOS-N), 45 patients with PCOS on medical treatment (PCOS-MT), and 40 systemically

248 Six women with PCOS (30 +/- 7 years; 31 +/- 6 kg m(-2)) then completed

249 Eleven women with PCOS (age, 29 +/- 7 years; body mass index, 34 +/- 6 kg

250 parate, family-based cohort of 73 women with PCOS (median and IQR: age = 28 [25-33], BMI = 34.3 [27.8

251 A case-control study comparing women with PCOS (n = 25) to age and weight matched controls (n = 24

252 llowing: 1) periodontally healthy women with PCOS (n = 45); 2) women with PCOS and gingivitis (n = 35

253 rrent study, lean hyperandrogenic women with PCOS (n = 9) and healthy CON women (n = 9) completed 14

254 mpared with periodontally healthy women with PCOS (P <0.001; P <0.01; and P <0.0001, respectively).

255 mpared with periodontally healthy women with PCOS (P <0.05).

256 ight and aged matched anovulatory women with PCOS and 30 women without from follicular fluid taken at

257 Differences between women with PCOS and control women and changes with exercise were an

258 ng of the forearm was assessed in women with PCOS and control women, and again in women with PCOS fol

259 INSR mutations after DHEA than in women with PCOS and controls (874.2 [SE 242] vs 425 [136] and 375.2

260 Women with PCOS and CP (n = 60) were randomly divided into two grou

261 treatment alone in management of women with PCOS and CP.

262 lthy women with PCOS (n = 45); 2) women with PCOS and gingivitis (n = 35); 3) systemically and period

263 nd periodontally healthy women or women with PCOS and gingivitis (P <0.05).

264 P-9 and MPO levels were higher in women with PCOS and gingivitis compared with periodontally healthy

265 IR was observed in 133 (83.6%) women with PCOS and in 25 (46.3%) women without PCOS (p < 0.001).

266 markedly elevated in middle-aged women with PCOS and suggests including BMI, glucose, and SHBG-circu

267 ulating ZAG levels are reduced in women with PCOS and ZAG may be a cytokine associated with insulin r

268 In conclusion, children of women with PCOS appear to have a higher risk of developing ASD.

269 A-93 and miRNA-223 were higher in women with PCOS compared to age and weight matched controls indepen

270 y expressed in the circulation of women with PCOS compared to age matched women.

271 scular NO function is impaired in women with PCOS compared with obese matched control women but can b

272 t ER stress in granulosa cells of women with PCOS contributes to the induction of pro-fibrotic growth

273 Our aim was to examine whether women with PCOS demonstrate impaired cutaneous microvascular NO fun

274 S and control women, and again in women with PCOS following exercise training.

275 ing 65 women without PCOS and 110 women with PCOS fulfilling all 3 diagnostic Rotterdam criteria.

276 Women with PCOS had higher androstenedione concentrations than did

277 helial function in lean and obese women with PCOS likely because oestrogen increased NO availability.

278 antation of fecal microbiota from women with PCOS or B. vulgatus-colonized recipient mice resulted in

279 interval, 33.3, 1.7; P = 0.03) in women with PCOS vs. control women.

280 e in whole-body insulin action in women with PCOS with training is caused by an impaired ability to u

281 Similar to in many women with PCOS, DHT exposure led to reduced adiponectin levels, la

282 of exercise training appeared in women with PCOS, including an improvement of the hyperandrogenic st

283 Ten women with PCOS, ten healthy controls, and three women with INSR mu

284 Among women with PCOS, the most common phenotype was type I (50.3%), with

285 Among women with PCOS, the presence of hirsutism (43.9% [54 of 123] vs 30

286 lence of acne was increased among women with PCOS, there were minimal differences in acne types and d

287 igh-risk features rather than all women with PCOS.

288 esemble the well-known profile of women with PCOS.

289 as male phenotypic equivalents of women with PCOS.

290 o a standard-protein (SP) diet in women with PCOS.

291 vasodilatation, but is blunted in women with PCOS.

292 nction) was most profound in lean women with PCOS.

293 and weight matched controls (n = 24) without PCOS was performed.

294 ompared to their respective controls without PCOS.

295 en with PCOS and in 25 (46.3%) women without PCOS (p < 0.001).

296 s sectional study involving 65 women without PCOS and 110 women with PCOS fulfilling all 3 diagnostic

297 UK women without PCOS had higher systolic and diastolic blood pressures,

298 01) compared to Middle Eastern women without PCOS who had higher inflammatory markers (WBC and CRP),

299 ), of whom 159 had PCOS and 54 women without PCOS, recruited as a control group.

300 ycystic ovaries as compared with the low ZAG PCOS women.