ライフサイエンスコーパス: polycystic

1 , and activation of XBP1 can protect against polycystic disease in the setting of impaired biogenesis

2 definition of the spectrum of dominant human polycystic diseases.

3 In the polycystic kidney (PCK) rat model, activation of STAT3 i

4 ession was analyzed in livers of control and polycystic kidney (PCK) rats, control and polycystic kid

5 nd polycystic kidney (PCK) rats, control and polycystic kidney 2 (Pkd2(ws25/-)) mice, healthy individ

6 duced levels of Cdc25A) were cross-bred with polycystic kidney and hepatic disease 1 (Pkhd1(del2/del2

7 ted from the unaffected parent, or biallelic polycystic kidney and hepatic disease 1 (PKHD1) mutation

8 e 1 region that includes a novel mutation in polycystic kidney and hepatic disease 1 (Pkhd1).

9 and comparing with IgAN, autosomal dominant polycystic kidney disease (ADPKD) and diabetic nephropat

10 ps early in patients with autosomal dominant polycystic kidney disease (ADPKD) and is associated with

11 Hypertension is common in autosomal dominant polycystic kidney disease (ADPKD) and is associated with

12 Autosomal-dominant polycystic kidney disease (ADPKD) and von Hippel-Lindau

13 Prenatal forms of autosomal dominant polycystic kidney disease (ADPKD) are rare but can be re

14 -Biedl syndrome (BBS) and autosomal dominant polycystic kidney disease (ADPKD) are two genetically di

15 l epigenetic regulator of autosomal dominant polycystic kidney disease (ADPKD) but also as a novel cl

16 a cohort of patients with autosomal dominant polycystic kidney disease (ADPKD) compared with a contro

17 Autosomal dominant polycystic kidney disease (ADPKD) constitutes the most i

18 elegans and mammals, the autosomal dominant polycystic kidney disease (ADPKD) gene products polycyst

19 ation and modification in autosomal dominant polycystic kidney disease (ADPKD) have helped to explain

20 Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of E

21 Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of r

22 Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited

23 Autosomal-dominant polycystic kidney disease (ADPKD) is a common life-threa

24 Autosomal-dominant polycystic kidney disease (ADPKD) is a common, progressi

25 Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder

26 Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of

27 Autosomal dominant polycystic kidney disease (ADPKD) is a progressive genet

28 Autosomal dominant polycystic kidney disease (ADPKD) is an important cause

29 Autosomal dominant polycystic kidney disease (ADPKD) is associated with pro

30 Autosomal dominant polycystic kidney disease (ADPKD) is caused by inactivat

31 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

32 Autosomal-dominant polycystic kidney disease (ADPKD) is caused by mutations

33 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

34 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

35 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

36 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by in

37 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by re

38 Autosomal dominant polycystic kidney disease (ADPKD) is driven by mutations

39 Autosomal dominant polycystic kidney disease (ADPKD) is heterogeneous with

40 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most com

41 Autosomal dominant polycystic kidney disease (ADPKD) is the most common gen

42 Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inh

43 Autosomal dominant polycystic kidney disease (ADPKD) is the most common lif

44 Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent g

45 Autosomal dominant polycystic kidney disease (ADPKD) often results in ESRD

46 gression in patients with autosomal dominant polycystic kidney disease (ADPKD) remains untested.

47 etic nephropathy (DN) and autosomal-dominant polycystic kidney disease (ADPKD) served as "external" n

48 Novel therapies in autosomal dominant polycystic kidney disease (ADPKD) signal the need for ma

49 Patients with autosomal dominant polycystic kidney disease (ADPKD) typically carry a muta

50 The course of autosomal dominant polycystic kidney disease (ADPKD) varies among individua

51 lycystin-1 (PC1) leads to autosomal dominant polycystic kidney disease (ADPKD), a disorder characteri

52 ed Pkd1 protein result in autosomal dominant polycystic kidney disease (ADPKD), a serious inherited s

53 Autosomal dominant polycystic kidney disease (ADPKD), characterized by the

54 In autosomal dominant polycystic kidney disease (ADPKD), cysts accumulate and

55 compared with those with autosomal dominant polycystic kidney disease (ADPKD), in which the native k

56 idely among patients with autosomal dominant polycystic kidney disease (ADPKD), necessitating optimal

57 Autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

58 (Pkd2) gene is mutated in autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

59 cally identified cases of autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

60 Autosomal dominant polycystic kidney disease (ADPKD), the most common form

61 rgement of renal cysts in autosomal dominant polycystic kidney disease (ADPKD).

62 nsion and cystogenesis in autosomal dominant polycystic kidney disease (ADPKD).

63 PKD2 gene, which leads to autosomal dominant polycystic kidney disease (ADPKD).

64 ssion to renal failure in autosomal dominant polycystic kidney disease (ADPKD).

65 n genetic kidney disorder autosomal dominant polycystic kidney disease (ADPKD).

66 uses ciliopathies such as autosomal dominant polycystic kidney disease (ADPKD).

67 ain cause of mortality in autosomal-dominant polycystic kidney disease (ADPKD).

68 t for almost all cases of autosomal dominant polycystic kidney disease (ADPKD).

69 the genes responsible for autosomal dominant polycystic kidney disease (ADPKD).

70 ses, including cancer and autosomal dominant polycystic kidney disease (ADPKD).

71 polycystin-1 (PC1), cause autosomal-dominant polycystic kidney disease (ADPKD).

72 ng pathway is aberrant in autosomal-dominant polycystic kidney disease (ADPKD).

73 escribed manifestation of autosomal dominant polycystic kidney disease (ADPKD).

74 ed to the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD).

75 olycystin-2 (PC2) lead to autosomal dominant polycystic kidney disease (ADPKD).

76 lving patients with early autosomal dominant polycystic kidney disease (ADPKD; estimated creatinine c

77 th refractory symptoms of autosomal dominant polycystic kidney disease (APKD) in need of a renal tran

78 Autosomal recessive polycystic kidney disease (ARPKD) is an important childh

79 rmation and expansion in autosomal recessive polycystic kidney disease (ARPKD) is poorly understood,

80 Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio

81 BACKGROUND & AIMS: Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio

82 Autosomal recessive polycystic kidney disease (ARPKD), usually considered to

83 Caroli disease (CD), and autosomal recessive polycystic kidney disease (ARPKD).

84 ectomies exist for patients with symptomatic polycystic kidney disease (PCKD).

85 ious studies report a cross-talk between the polycystic kidney disease (PKD) and tuberous sclerosis c

86 insulinemic hypoglycemia (HI) and congenital polycystic kidney disease (PKD) are rare, genetically he

87 denosine monophosphate (cAMP) drives genetic polycystic kidney disease (PKD) cystogenesis.

88 s to drive the aggregation of the downstream polycystic kidney disease (PKD) domain into a melanosoma

89 ncluding the leucine-rich repeats, the first polycystic kidney disease (PKD) domain, and the C-type l

90 nd their disruption has been associated with polycystic kidney disease (PKD) genes, the majority of w

91 Polycystic kidney disease (PKD) is a leading cause of ES

92 Polycystic kidney disease (PKD) is a life-threatening di

93 Polycystic kidney disease (PKD) is one of the most commo

94 and interstitial fibrosis, similar to known polycystic kidney disease (PKD) models.

95 olysis Site (GPS) of cell-adhesion GPCRs and polycystic kidney disease (PKD) proteins constitutes a h

96 ptor potential channel polycystin (TRPP) and polycystic kidney disease (PKD) proteins, play key roles

97 eracts predominantly with the second Ig-like polycystic kidney disease (PKD) repeat domain (PKD2) pre

98 be an underlying cause of autosomal dominant polycystic kidney disease (PKD), and ciliary-EV interact

99 ney disease (ADPKD), the most common form of polycystic kidney disease (PKD), is a disorder with char

100 In polycystic kidney disease (PKD), renal parenchyma is des

101 Polycystic kidney disease (PKD), the most common genetic

102 P signaling contribute to the development of polycystic kidney disease (PKD).

103 tro and in vivo models of autosomal dominant polycystic kidney disease (PKD).

104 is an important mediator of cystogenesis in polycystic kidney disease (PKD).

105 indicates the importance of elevated cAMP in polycystic kidney disease (PKD).

106 ding the kidney, liver and pancreas features polycystic kidney disease (PKD).

107 on to the familial mutation, variation(s) in polycystic kidney disease 1 (PKD1) or HNF1 homeobox B (H

108 ng from inherited mutations in the genes for polycystic kidney disease 1 (PKD1) or polycystic kidney

109 or potential (TRP) channels Trpm, NompC, and Polycystic kidney disease 2 (Pkd2) are expressed in CIII

110 The Polycystic Kidney Disease 2 (Pkd2) gene is mutated in au

111 olved in osteoblast differentiation and that polycystic kidney disease 2 (Pkd2) was a downstream targ

112 es for polycystic kidney disease 1 (PKD1) or polycystic kidney disease 2 (PKD2).

113 Here, we show that disruption of the polycystic kidney disease 2-like 1 (Pkd2l1 or Pkdl), enc

114 ociated with higher 16:1n-7, whereas PKD2L1 (polycystic kidney disease 2-like 1; P=5.7x10(-15)) and a

115 allele significantly ameliorated the severe polycystic kidney disease and consequent runting caused

116 sing for the treatment of autosomal dominant polycystic kidney disease and have been approved in Japa

117 d Safety in Management of Autosomal Dominant Polycystic Kidney Disease and Its Outcomes) trial, tolva

118 vels of this eicosanoid are also elevated in polycystic kidney disease and may contribute to cyst for

119 It has a critical role in polycystic kidney disease and nephronophthisis.

120 weights and cyst growth in animal models of polycystic kidney disease and PLD, and might be develope

121 In polycystic kidney disease and polycystic liver disease (

122 The first case is a 67-year-old man with polycystic kidney disease and recipient of a zero-antige

123 mbryonic development to adult progression of polycystic kidney disease and some cancers.

124 acterized internal domain is a member of the polycystic kidney disease domain family but also how the

125 ozygous mutations in the autosomal recessive polycystic kidney disease gene PKHD1, indicating that ad

126 Knockout of the polycystic kidney disease genes PKD1 or PKD2 induces cys

127 uires lov-1 and pkd-2 (homologs of the human polycystic kidney disease genes, PKD1 and PKD2), which a

128 or down-regulation of PKD1 or PKD2 leads to polycystic kidney disease in animal models, but their in

129 Autosomal dominant polycystic kidney disease is a genetic disorder associat

130 Autosomal dominant polycystic kidney disease is caused by mutations in the

131 Recent evidence suggests that polycystic kidney disease is characterized by defects in

132 Autosomal dominant polycystic kidney disease is the most common inherited k

133 Using human ADPKD tissues and polycystic kidney disease mouse models, we show that the

134 The most severe form of autosomal dominant polycystic kidney disease occurs in patients with mutati

135 fective for patients with autosomal dominant polycystic kidney disease or polycystic liver disease; e

136 m that may play a role in autosomal dominant polycystic kidney disease pathogenesis.

137 ls (NL, 42 vs. 17; US, 40 vs. 13 points) and polycystic kidney disease patients without PLD (22 point

138 es of PLD patients with general controls and polycystic kidney disease patients without PLD.

139 Cysts and aneurysms from polycystic kidney disease patients, Pkd mouse, and zebra

140 in a disruption of renal ciliogenesis and a polycystic kidney disease phenotype in zebrafish and mic

141 unction by re-expressing survivin can rescue polycystic kidney disease phenotypes.

142 may predict and/or effect autosomal dominant polycystic kidney disease progression.

143 Furthermore, the polycystic kidney disease protein IFT88 binds IFT52281-3

144 GPS is also shared by polycystic kidney disease proteins and it precedes the f

145 who participated in the Halt Progression of Polycystic Kidney Disease Study A were categorized on th

146 For patients with autosomal dominant polycystic kidney disease that progressed more slowly, t

147 rize for Advancement in the Understanding of Polycystic Kidney Disease to participate in a forward-th

148 enal disease secondary to autosomal dominant polycystic kidney disease was referred to a quaternary c

149 , recipient employment, and the diagnosis of polycystic kidney disease were significantly associated

150 to identify patients with autosomal dominant polycystic kidney disease who are most likely to benefit

151 om GPCRs and fibrocystin (also implicated in polycystic kidney disease), we demonstrate these motifs

152 linical manifestations seen in patients with polycystic kidney disease, a cilia-associated pathology

153 a role in the pathogenesis of hypertension, polycystic kidney disease, AKI, and CKD.

154 stin-1 (PC1) give rise to autosomal dominant polycystic kidney disease, an important and common cause

155 iseases such as ischemia/reperfusion injury, polycystic kidney disease, and congenital solitary kidne

156 C and PKD), identified in linkage studies of polycystic kidney disease, are candidate channels divide

157 ed in cancer cells, ciliopathies such as the polycystic kidney disease, as well as in the genetic dis

158 laying an important role in the formation of polycystic kidney disease, but not for Rab8 another cili

159 s the juvenile cystic kidneys (jck) model of polycystic kidney disease, but the functions of Nek8 are

160 dentical to those seen in autosomal dominant polycystic kidney disease, but without clinically releva

161 APK activation, all of which are features of polycystic kidney disease, especially nephronophthisis.

162 Deletion of Lgr4 in mouse led to aniridia, polycystic kidney disease, genitourinary anomalies, and

163 a suspected diagnosis of autosomal dominant polycystic kidney disease, medullary cystic kidney disea

164 In contrast to many models of polycystic kidney disease, precystic Ift140-deleted coll

165 f a 21-year-old man with autosomal recessive polycystic kidney disease, presenting with subarachnoid

166 tin 2 are responsible for autosomal dominant polycystic kidney disease, the most common heritable hum

167 To gain insights into autosomal dominant polycystic kidney disease, we performed yeast two-hybrid

168 ferral before dialysis were the diagnosis of polycystic kidney disease, white recipient race, referra

169 Furthermore, autosomal dominant polycystic kidney disease-associated TRPP2 mutant T448K

170 G protein-coupled receptors (GPCRs) and the polycystic kidney disease-causing polycystin 1/2 complex

171 ithelial pancreatic neoplasia, and 1 case of polycystic kidney disease.

172 in either protein causing autosomal dominant polycystic kidney disease.

173 Dysfunction of renal primary cilia leads to polycystic kidney disease.

174 umerous disease models, including cancer and polycystic kidney disease.

175 have utility in diagnosis and monitoring of polycystic kidney disease.

176 s on renal function and favor cyst growth in polycystic kidney disease.

177 as a possible therapy for heart failure and polycystic kidney disease.

178 3 control recipients with autosomal dominant polycystic kidney disease.

179 arget in the treatment of autosomal dominant polycystic kidney disease.

180 trarenal manifestation in autosomal dominant polycystic kidney disease.

181 g therapeutic strategy in autosomal dominant polycystic kidney disease.

182 ions to human PC2 (hPC2) are associated with polycystic kidney disease.

183 hannel that is mutated in autosomal dominant polycystic kidney disease.

184 2), respectively, lead to autosomal dominant polycystic kidney disease.

185 plains both renal and vascular phenotypes in polycystic kidney disease.

186 l diseases, such as diabetic nephropathy and polycystic kidney disease.

187 pathway result in deranged ciliogenesis and polycystic kidney disease.

188 humans and mice, nephronophthisis (NPHP) and polycystic kidney disease.

189 st, urine podocyte mRNAs did not increase in polycystic kidney disease.

190 a Ca(2+)-dependent channel with relevance to polycystic kidney disease.

191 obulin A nephropathy, and autosomal dominant polycystic kidney disease.

192 Persons with early autosomal dominant polycystic kidney disease.

193 2, the protein mutated in autosomal dominant polycystic kidney disease.

194 d to preserve renal function in experimental polycystic kidney disease.

195 Ectopic cAMP signaling is pathologic in polycystic kidney disease; however, its spatiotemporal a

196 s of inherited disorders, autosomal dominant polycystic kidney diseases (ADPKD), a significant cause

197 Polycystic kidney diseases (PKD) are genetic disorders c

198 Polycystic kidney diseases (PKDs) are genetic disorders

199 Polycystic kidney diseases (PKDs) comprise a subgroup of

200 Genetic forms of polycystic kidney diseases (PKDs), including nephronopht

201 Polycystic kidney diseases are characterized by numerous

202 Polycystic kidney diseases are the most common genetic d

203 ation of both SEC63 and XBP1 exacerbated the polycystic kidney phenotype in mice by markedly suppress

204 examined hepatic cystogenesis in OA-treated polycystic kidney rats and after genetic elimination of

205 OA increased cystogenesis in polycystic kidney rats by 35%; in contrast, hepatic cyst

206 In Wistar polycystic kidney rats with hydrocephalus, alteration of

207 All patients received general health and polycystic kidney symptom surveys.

208 However, automatic segmentation of polycystic kidneys is a challenging task due to severe a

209 Polycystic kidneys of Pkd2WS25/- mice, an orthologous mo

210 neal injection is preferentially targeted to polycystic kidneys whereas injected IgG is not.

211 mutant alleles of IFT complex B genes cause polycystic kidneys, but the influence of IFT complex A p

212 ogical symptoms, cardiovascular defects, and polycystic kidneys.

213 EM2 that had previously been associated with polycystic lipomembranous osteodysplasia with sclerosing

214 In polycystic liver (PLD) and kidney (PKD) diseases, increa

215 one of the genes causing autosomal dominant polycystic liver disease (ADPLD).

216 seen in the rare inherited disorder isolated polycystic liver disease (PCLD) and are recognized as th

217 Dominantly inherited isolated polycystic liver disease (PCLD) consists of liver cysts

218 Polycystic liver disease (PCLD) is characterized by cyst

219 hepatocystin (80K-H, PRKCSH), gives rise to polycystic liver disease (PCLD).

220 Treatment of polycystic liver disease (PLD) focuses on symptom improv

221 Polycystic liver disease (PLD) is a member of the cholan

222 ical trials have shown that in patients with polycystic liver disease (PLD), short-term treatment wit

223 In polycystic kidney disease and polycystic liver disease (PLD), the normally nonprolifer

224 ncreased level of intracranial aneurysms and polycystic liver disease (PLD), which can be severe and

225 in vitro key features of Alagille syndrome, polycystic liver disease and cystic fibrosis (CF)-associ

226 Mutations in the gene encoding SEC63 cause polycystic liver disease in humans; however, it is not c

227 Genetically, polycystic liver disease is a heterogeneous disorder wit

228 Polycystic liver disease is a well described manifestati

229 Hepatic cystogenesis in polycystic liver disease is associated with increased le

230 d from healthy individuals and patients with polycystic liver disease to reproduce the effects of the

231 presents a potential therapeutic approach in polycystic liver disease.

232 d in livers of animal models and humans with polycystic liver disease.

233 osomal dominant polycystic kidney disease or polycystic liver disease; efficacy does not depend on si

234 ficant cause of ESRD, and autosomal dominant polycystic liver diseases (ADPLD), which result in signi

235 Mutations in PC2 are associated with polycystic liver diseases.

236 er volume, and diagnosis (autosomal dominant polycystic liver or kidney disease).

237 old or younger) had the greatest increase in polycystic liver volume (4.8%; 95% confidence interval:

238 ase; efficacy does not depend on size of the polycystic liver.

239 l mutations in three unrelated families with polycystic livers (p.V454M, p.R1529S, and p.D1551N), aga

240 Polycystic livers are seen in the rare inherited disorde

241 in androgen levels, ovarian dysfunction, and polycystic ovarian morphology but is also associated wit

242 4 to 52 years consecutively recruited from a polycystic ovarian syndrome (PCOS) clinic between May 18

243 tly reported as the phenotypic equivalent of polycystic ovarian syndrome (PCOS) in women, which carri

244 Polycystic ovarian syndrome (PCOS) is a hormonal disorde

245 Polycystic ovarian syndrome (PCOS), the leading cause of

246 ory was relevant only for anovulation due to polycystic ovarian syndrome (PCOS), though her preproced

247 re potential therapeutic agents for treating polycystic ovarian syndrome and other ovarian disorders.

248 52 years who met the Rotterdam criteria for polycystic ovarian syndrome rated themselves and were ra

249 For patients with polycystic ovarian syndrome showing follicle arrest, ova

250 A 30-year-old woman with polycystic ovarian syndrome who was undergoing hormone r

251 ductive and metabolic programming leading to polycystic ovarian syndrome, insulin resistance and hype

252 herpeticum, gram-negative folliculitis, and polycystic ovarian syndrome.

253 women with high ZAG had fewer MetS, IGT and polycystic ovaries as compared with the low ZAG PCOS wom

254 n disease (primary ovarian insufficiency and polycystic ovaries) were increased in the F3 generation

255 (anovulation with either hyperandrogenism or polycystic ovaries).

256 elopment of dysfunctional ovulation, classic polycystic ovaries, reduced large antral follicle health

257 isease, ovarian primordial follicle loss and polycystic ovary disease were increased in F1 generation

258 emales, ovarian primordial follicle loss and polycystic ovary disease were increased in F3 generation

259 tatic model assessment [HOMA]) in women with polycystic ovary syndrome (PCOS) and chronic periodontit

260 tor of MMP-1 (TIMP)-1 ratio in patients with polycystic ovary syndrome (PCOS) and systemically health

261 Pregnant women with polycystic ovary syndrome (PCOS) are often overweight or

262 Women with polycystic ovary syndrome (PCOS) exhibit elevated androg

263 Approximately 70% of women with polycystic ovary syndrome (PCOS) have intrinsic insulin

264 an morphologic measurements for diagnosis of polycystic ovary syndrome (PCOS) in adolescents.

265 Polycystic ovary syndrome (PCOS) is a common problem amo

266 Polycystic ovary syndrome (PCOS) is a common, highly her

267 Polycystic ovary syndrome (PCOS) is a complex hormonal d

268 Polycystic ovary syndrome (PCOS) is associated with card

269 Polycystic ovary syndrome (PCOS) is frequently associate

270 nostic criteria in women suspected of having polycystic ovary syndrome (PCOS) is incomplete.

271 Polycystic ovary syndrome (PCOS) is the most common repr

272 ly, some studies have revealed the effect of polycystic ovary syndrome (PCOS) on gingival inflammatio

273 d androgen excess with insulin resistance in polycystic ovary syndrome (PCOS) women.

274 Using an ovine model of polycystic ovary syndrome (PCOS), (pregnant ewes injecte

275 Maternal polycystic ovary syndrome (PCOS), a common metabolic dis

276 This would suggest that maternal polycystic ovary syndrome (PCOS), a condition associated

277 Polycystic ovary syndrome (PCOS), characterized by incre

278 oxidative stress, in the pathophysiology of polycystic ovary syndrome (PCOS), the most common endocr

279 ciated with insulin resistance in women with polycystic ovary syndrome (PCOS).

280 yperandrogenism are the cardinal features of polycystic ovary syndrome (PCOS).

281 s increasing evidence of their importance in polycystic ovary syndrome (PCOS).

282 fertility and thus serve as a model of human polycystic ovary syndrome (PCOS).

283 levels correlate with increased severity of polycystic ovary syndrome (PCOS).

284 s for the analysis of a previously described polycystic ovary syndrome gene expression dataset.

285 MI 33 kg/m(2)), insulin-resistant women with polycystic ovary syndrome had aberrant skeletal muscle m

286 Polycystic ovary syndrome is characterized by an excess

287 the University of California, San Francisco, Polycystic Ovary Syndrome Multidisciplinary Clinic over

288 nificant benefit when including metformin in polycystic ovary syndrome treatment regimens.

289 The polycystic ovary syndrome was defined according to modif

290 ons, linking dementia with bone development, polycystic ovary syndrome with cardiovascular developmen

291 g obesity, type 2 diabetes, hepatitis C, and polycystic ovary syndrome, and is a primary feature of m

292 line infertility treatment in women with the polycystic ovary syndrome, but aromatase inhibitors, inc

293 56), after adjustment for education, parity, polycystic ovary syndrome, energy intake, and physical a

294 eted educational qualification, nulliparity, polycystic ovary syndrome, physical activity, and body m

295 rched PubMed using a string of variations of polycystic ovary syndrome, therapy/treatment, and adoles

296 ulation rates among infertile women with the polycystic ovary syndrome.

297 seen in diseases of excess androgens such as polycystic ovary syndrome.

298 lays a key role in the early pathogenesis of polycystic ovary syndrome.

299 ND1A) previously shown to be associated with polycystic ovary syndrome.

300 fferentiation as an exclusion criterion, TRP polycystic (P)3, and TPR melastatin (M)8 were found to b