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 and gingival inflammation appear to act synergistic

3 PCOS AT was determined to have a differentially expresse

4 PCOS groups exhibited a positive correlation among clini

5 PCOS patients with an isolated elevated FAI showed incre

6 PCOS women with both biochemical and clinical hyperandro

7 A controlled, 6-mo trial was conducted in 57 PCOS women.

8 ns in women with (n = 6) and without (n = 8) PCOS.

9 99 PCOS women and 100 healthy controls were recruited.

10 and restricting the simple sugar intake in a PCOS diet.

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

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

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

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

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

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

17 arranted to clarify the relationship between PCOS and gingivitis.

18 to clarify the possible relationship between PCOS and periodontal disease.

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

20 mechanisms for excess androgen synthesis by PCOS theca cells, and 3) identified new candidate genes

21 S theca cells in order to identify candidate PCOS genes.

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

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

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

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

26 e group than the lamotrigine group developed PCOS (9 vs 2%; p = 0.007).

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

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

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

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

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

32 y represent a novel diagnostic biomarker for PCOS.

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

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

35 genism is one of the diagnostic criteria for PCOS.

36 gED(50) 2.53 +/- 0.09, 2.49 +/- 0.09 nm, for PCOS and Control, respectively).

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

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

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

40 Optimal dietary treatment for PCOS is not known.

41 for the development of novel treatments for PCOS.

42 s studies demonstrated that theca cells from PCOS ovaries maintained in long term culture persistentl

43 s were significantly increased in serum from PCOS women (P < 0.01) compared with matched control subj

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

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

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

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

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

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

50 G-VEGF and VEGF mRNA in a series of 13 human PCOS and 13 normal ovary specimens by in situ hybridizat

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

52 In PCOS ovaries, we found strong expression of EG-VEGF mRNA

53 ne expression and intrinsic abnormalities in PCOS theca cells.

54 resistance to insulin's metabolic actions in PCOS.

55 kinase kinase (MEK)1/2 was also activated in PCOS, whereas p38 mitogen-activated protein kinase phosp

56 metabolic abnormalities persist with age in PCOS.

57 f the factor(s) that mediate angiogenesis in PCOS is less clearly understood.

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

59 that both EG-VEGF and VEGF are expressed in PCOS ovaries, but in different cell types at different s

60 cle as it is in cultured skin fibroblasts in PCOS.

61 and metabolic and reproductive functions in PCOS.

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

63 s decreased and Raf-1 abundance increased in PCOS, suggesting that altered mitogenic signaling began

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

65 s balancing selection mechanisms involved in PCOS risk.

66 f metformin treatment on omentin-1 levels in PCOS subjects and effects of omentin-1 on in vitro migra

67 in treatment on circulating vaspin levels in PCOS subjects were also studied.

68 gnificant decrease in serum vaspin levels in PCOS women (P < 0.001).

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

70 Serum omentin-1 was significantly lower in PCOS women (P < 0.05).

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

72 l lead to more judicious use of metformin in PCOS and a more structured approach to research.

73 recommendations for the use of metformin in PCOS can be formalised.

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

75 gED(50), 2.56 +/- 0.09, 2.41 +/- 0.12 nm, in PCOS and Control).

76 en burden and improve metabolic phenotype in PCOS.

77 to the perturbation of ovarian remodeling in PCOS.

78 tokine associated with insulin resistance in PCOS women.

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

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

81 for the improved pregnancy outcomes seen in PCOS patients taking metformin.

82 stress may serve as a therapeutic target in PCOS.

83 We conclude that in PCOS skeletal muscle, 1) mitogenic signaling is enhanced

84 othelial dysfunction is currently unknown in PCOS.

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

86 Currently, no data exists on vaspin in PCOS women.

87 dently related factors to circulating ZAG in PCOS women.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 ression also increased in granulosa cells of PCOS patients.

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

105 cell viability/hyperplasia in the context of PCOS.

106 The varying definitions of PCOS and its heterogeneity confound the interpretation o

107 The primary end point was development of PCOS components (ie, hyperandrogenism or ovulatory dysfu

108 extraovarian mediator in the development of PCOS traits.

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

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

111 t may be involved in the genetic etiology of PCOS.

112 gularity identifies mothers with features of PCOS.

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

114 A hallmark of PCOS is excessive theca cell androgen secretion, which i

115 responsible for ovarian hyperandrogenemia of PCOS have not been identified.

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

117 Gynecologists on the clinical management of PCOS says that there is still no consensus on the "optim

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

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

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

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

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

123 nal roles for DENND1A in the pathogenesis of PCOS.

124 as a potential factor in the pathogenesis of PCOS.

125 lin may contribute to the pathophysiology of PCOS.

126 e 1) defined a stable molecular phenotype of PCOS theca cells, 2) suggested new mechanisms for excess

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

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

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

130 , oligomenorrhea or amenorrhea) suspicion of PCOS.

131 which is directly linked to the symptoms of PCOS.

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

133 m subcutaneous and omental adipose tissue of PCOS women and matched control subjects.

134 tein (P < 0.05) in omental adipose tissue of PCOS women.

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

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

137 ts to know the alternatives for treatment of PCOS.

138 ty confound the interpretation of studies on PCOS.

139 dipose tissue levels of vaspin in overweight PCOS women and ex vivo regulation of vaspin, predominant

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

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

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

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

144 ipants were 401 women referred for suspected PCOS.

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

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

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

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

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

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

151 Polycystic ovary syndrome (PCOS) affects 5% of reproductive aged women and is the l

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

153 bese females with polycystic ovary syndrome (PCOS) and either clinically healthy periodontium or ging

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

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

156 ar-old woman with polycystic ovary syndrome (PCOS) diagnosed after irregular menses, hirsutism, and p

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

158 70% of women with polycystic ovary syndrome (PCOS) have intrinsic insulin resistance (IR) above and b

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

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

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

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

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

164 Polycystic ovary syndrome (PCOS) is associated with insulin resistance and obesity.

165 Polycystic ovary syndrome (PCOS) is associated with the metabolic syndrome.

166 e of metformin in polycystic ovary syndrome (PCOS) is becoming increasingly accepted and widespread,

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

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

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

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

171 Polycystic ovary syndrome (PCOS) recently has been identified as a risk factor asso

172 lin resistance in polycystic ovary syndrome (PCOS) results from a postbinding defect in signaling.

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

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

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

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

177 is usually due to polycystic ovary syndrome (PCOS), a condition in which intrinsic functional ovarian

178 t features of the polycystic ovary syndrome (PCOS), a leading cause of infertility.

179 ted in women with polycystic ovary syndrome (PCOS), and may play a role in the endothelial dysfunctio

180 a is a feature of polycystic ovary syndrome (PCOS), but its pathogenesis remains controversial.

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

182 haracteristics of polycystic ovary syndrome (PCOS), improve with even modest weight loss.

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

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

185 dinal features of polycystic ovary syndrome (PCOS).

186 eir importance in polycystic ovary syndrome (PCOS).

187 a model of human polycystic ovary syndrome (PCOS).

188 the treatment of polycystic ovary syndrome (PCOS).

189 can occur during polycystic ovary syndrome (PCOS).

190 eased severity of polycystic ovary syndrome (PCOS).

191 sociation between polycystic ovary syndrome (PCOS)and endometrial carcinoma was first suggested in 19

192 It has been assumed that PCOS predisposes to endometrial cancer.

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

194 Our analysis revealed that PCOS theca cells have a gene expression profile that is

195 The PCOS + gingivitis group revealed significantly higher GC

196 The PCOS + gingivitis group revealed significantly higher in

197 The PCOS phenotype was induced in mice following prenatal an

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

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

200 involved in excess androgen synthesis by the PCOS theca cells in order to identify candidate PCOS gen

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

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

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

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

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

206 actions that mediate the development of the PCOS phenotype.

207 cantly higher insulin concentration than the PCOS + healthy and control groups (P = 0.014 and P <0.00

208 liva, and serum IL-6 concentrations than the PCOS + healthy group (P <0.0001).

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

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

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

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

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

214 Thus, PCOS may have an impact on gingival inflammation or vice

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

216 genic effects of sera from metformin-treated PCOS women.

217 45 patients with PCOS on medical treatment (PCOS-MT), and 40 systemically healthy controls (control

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

219 nd hyperinsulinaemia are all associated with PCOS as well as with endometrial carcinoma.

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

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

222 ET-B receptor responsiveness associated with PCOS may reflect lower endothelial-mediated vasodilatati

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

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

225 ole in the hyperandrogenemia associated with PCOS.

226 the endothelial dysfunction associated with PCOS.

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

228 ment for PCOS and women newly diagnosed with PCOS.

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

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

231 OS and healthy periodontium, 30 females with PCOS and gingivitis, and 12 systemically and periodontal

232 Thirty-one females with PCOS and healthy periodontium, 30 females with PCOS and

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

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

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

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

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

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

239 Patients with PCOS (n = 28; aged 26 +/- 2 y) were tested with a 5-h or

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

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

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

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

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

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

246 .05) in omental adipose tissue of women with PCOS (P < 0.01).

247 reased plasma omentin-1 levels in women with PCOS (P < 0.05), compared with control subjects, there w

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

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

250 215 non-Hispanic white mothers of women with PCOS and 62 control women.

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

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

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

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

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

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

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

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

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

260 n-1, in omental adipose tissue of women with PCOS and matched control subjects.

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

262 a heritable trait in families of women with PCOS and to investigate the impact of age on reproductiv

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

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

265 Women with PCOS are increasingly aware of the possible risks, and i

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

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

268 lly and in response to insulin in women with PCOS compared with control women.

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

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

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

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

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

274 Women with PCOS had higher androstenedione concentrations than did

275 erformed this study of mothers of women with PCOS to test the hypothesis that dyslipidemia is a herit

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

277 A total of 255 women with PCOS were followed for at least 10 years (mean follow-up

278 to prevent endometrial cancer in women with PCOS".

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

280 ective study of a large cohort of women with PCOS, followed from youth to middle age, aimed at estima

281 88] curve shifted to the right in women with PCOS, suggesting attenuated ET-B receptor mediated vasod

282 evels are increased in mothers of women with PCOS, suggestive of a heritable trait.

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 as male phenotypic equivalents of women with PCOS.

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

289 gh with blunted responsiveness in women with PCOS.

290 this response would be blunted in women with PCOS.

291 levels observed in our overweight women with PCOS.

292 of omentin-1 in adipose tissue of women with PCOS.

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

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

295 function similarly in women with and without PCOS, although with blunted responsiveness in women with

296 s microvasculature in women with and without PCOS.

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

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

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.