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 endent hydrocephalic phenotype in the Wistar polycystic kidney (Wpk) rat.

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

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

6 ll-enriched translated proteins, we identify Polycystic Kidney and Hepatic Disease 1-Like 1 (PKHD1L1)

7 Dominantly inherited polycystic kidney and liver diseases on the ADPKD spectr

8 Autosomal dominant polycystic kidney disease (ADPKD) affects an estimated 1

9 Background Autosomal dominant polycystic kidney disease (ADPKD) affects one in 400 to

10 PKD2 mutations cause Autosomal Dominant Polycystic Kidney Disease (ADPKD) and affect many cellul

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

12 PC-1 and PC-2, result in autosomal dominant polycystic kidney disease (ADPKD) and ultimately renal f

13 idney disease (ARPKD) and autosomal dominant polycystic kidney disease (ADPKD) are genetically distin

14 s and the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD) are not well understoo

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

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

17 assessment is valuable in autosomal dominant polycystic kidney disease (ADPKD) but the reference stan

18 ng molecular pathology of autosomal dominant polycystic kidney disease (ADPKD) by promoting cyst form

19 hether early diagnosis of autosomal dominant polycystic kidney disease (ADPKD) can enable earlier man

20 neys, and often liver, in autosomal dominant polycystic kidney disease (ADPKD) cause progressive incr

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

22 Autosomal dominant polycystic kidney disease (ADPKD) constitutes the fourth

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

24 Patients with autosomal dominant polycystic kidney disease (ADPKD) experience progressive

25 ional group of experts in autosomal dominant polycystic kidney disease (ADPKD) from paediatric and ad

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

27 Autosomal-dominant polycystic kidney disease (ADPKD) induces a secretory ph

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

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

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

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

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

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

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

35 Autosomal dominant polycystic kidney disease (ADPKD) is an inherited monoge

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

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

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

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

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

41 Human autosomal dominant polycystic kidney disease (ADPKD) is characterized by bi

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

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

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

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

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

47 Autosomal dominant polycystic kidney disease (ADPKD) is the leading genetic

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

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

50 Autosomal dominant polycystic kidney disease (ADPKD) is the most common her

51 Autosomal dominant polycystic kidney disease (ADPKD) is the most common her

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

53 Autosomal dominant polycystic kidney disease (ADPKD) is the most common mon

54 Autosomal dominant polycystic kidney disease (ADPKD) is the most common ren

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

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

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

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

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

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

61 imaging classification of autosomal dominant polycystic kidney disease (ADPKD) uses height-adjusted t

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

63 coding for PC2 results in autosomal dominant polycystic kidney disease (ADPKD), a condition character

64 ead to the development of autosomal dominant polycystic kidney disease (ADPKD), a debilitating condit

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

66 Autosomal dominant polycystic kidney disease (ADPKD), caused by mutations i

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

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

69 two main causal genes for autosomal dominant polycystic kidney disease (ADPKD), encode the multipass

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

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

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

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

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

75 KD1 or PKD2 cause typical autosomal dominant polycystic kidney disease (ADPKD), the most common monog

76 human genetic diseases is autosomal dominant polycystic kidney disease (ADPKD), which is caused by mu

77 function deteriorates in autosomal dominant polycystic kidney disease (ADPKD).

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

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

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

81 in-2, respectively, cause autosomal dominant polycystic kidney disease (ADPKD).

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

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

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

85 or polycystin 2 leads to autosomal dominant polycystic kidney disease (ADPKD).

86 loss of renal function in autosomal dominant polycystic kidney disease (ADPKD).

87 or many clinical cases of autosomal dominant polycystic kidney disease (ADPKD).

88 in the polycystins cause autosomal dominant polycystic kidney disease (ADPKD).

89 trarenal manifestation of autosomal dominant polycystic kidney disease (ADPKD).

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

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

92 Autosomal recessive polycystic kidney disease (ARPKD) and autosomal dominant

93 ctomies in patients with autosomal recessive polycystic kidney disease (ARPKD) and long-term clinical

94 cells from patients with autosomal recessive polycystic kidney disease (ARPKD) had significantly lowe

95 Autosomal recessive polycystic kidney disease (ARPKD) is a severe pediatric

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

97 ish an in vitro model of autosomal recessive polycystic kidney disease (ARPKD), the cystic phenotype

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

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

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

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

102 s structure reveals that of the five Ig-like polycystic kidney disease (PKD) domains in AAVR, PKD2 bi

103 sease progression in autosomal-dominant (AD) polycystic kidney disease (PKD) exhibits high intra-fami

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

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

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

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

108 of AQP3 in cyst development, we generated 2 polycystic kidney disease (PKD) mouse models: kidney-spe

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

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

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

112 is challenging for chronic diseases such as polycystic kidney disease (PKD), the most common heredit

113 ouse kidney results in polycystin-1-mediated polycystic kidney disease (PKD).

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

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

116 6A (anoctamin 1), drives cyst enlargement in polycystic kidney disease (PKD).

117 However, in polycystic kidney disease (pkd1)-knockout mice, CFTR was

118 Mutations of polycystic kidney disease 1 (PKD1) account for most ADPK

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

120 otentially deleterious biallelic variants in polycystic kidney disease 1 like 1 (PKD1L1), a gene asso

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

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

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

124 kidney disease [ARPKD] or autosomal dominant polycystic kidney disease [ADPKD]).

125 eral cystic disease (eg, autosomal recessive polycystic kidney disease [ARPKD] or autosomal dominant

126 ve severe ventriculomegaly as well as severe polycystic kidney disease and die during the neonatal pe

127 , emphasizing CKD, transplant rejection, and polycystic kidney disease and discuss strategies to targ

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

129 Roles of autophagy in polycystic kidney disease and kidney cancer have also be

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

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

132 tolvaptan as safe and effective therapy for polycystic kidney disease and reveal a potential new reg

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

134 ascular manifestations of autosomal dominant polycystic kidney disease derive directly from myocardiu

135 Polycystic kidney disease did not result in different SM

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

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

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

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

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

141 iography in patients with autosomal dominant polycystic kidney disease is cost-effective.

142 ssues, the relationship between Hedgehog and polycystic kidney disease is not known.

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

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

145 Autosomal dominant polycystic kidney disease patients develop renal failure

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

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

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

149 Polycystic kidney disease proteins, polycystin-1 and pol

150 manipulations on quantitative parameters of polycystic kidney disease severity.

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

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

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

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

155 originally identified in autosomal dominant polycystic kidney disease where it regulates the calcium

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

157 oding for multiple ciliary proteins underlie polycystic kidney disease, a disorder with numerous card

158 nic kidney diseases after autosomal dominant polycystic kidney disease, accounting for ~5% of monogen

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

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

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

162 nephropathy, albuminuria, autosomal dominant polycystic kidney disease, and ischemia/reperfusion-indu

163 therapeutic targets: TRPC6 in FSGS, PKD2 in polycystic kidney disease, and TRPM6 in familial hypomag

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

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

166 hannel protein PKD2 cause autosomal dominant polycystic kidney disease, but the function of PKD2 in c

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

168 man homologues are associated with autosomal polycystic kidney disease, is an essential protein whose

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

170 vels of the cluster in three disease models: polycystic kidney disease, prostate cancer, and breast c

171 ne that is mutated in the autosomal dominant polycystic kidney disease, regulates a number of process

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

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

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

175 in cysts of patients with autosomal dominant polycystic kidney disease.

176 erimental mouse models of autosomal dominant polycystic kidney disease.

177 sis in the kidney and in the pathogenesis of polycystic kidney disease.

178 ransduction in a model of autosomal dominant polycystic kidney disease.

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

180 in either protein causing autosomal dominant polycystic kidney disease.

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

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

183 Subanalysis explored those with polycystic kidney disease.

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

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

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

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

188 3 control recipients with autosomal dominant polycystic kidney disease.

189 ated with severe developmental disorders and polycystic kidney disease.

190 ease, focal segmental glomerulosclerosis and polycystic kidney disease.

191 henotype associated with autosomal recessive polycystic kidney disease.

192 ic abnormalities in a genetic mouse model of polycystic kidney disease.

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

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

195 Polycystic kidney diseases (PKD) are genetic disorders c

196 Polycystic kidney diseases (PKDs) are genetic disorders

197 Polycystic kidney diseases (PKDs) comprise a subgroup of

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

199 significantly influenced the severity of the polycystic kidney phenotype in mouse models of developme

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

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

202 In Wistar polycystic kidney rats with hydrocephalus, alteration of

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

204 e inflammatory chemokines CCL5 and CXCL10 in polycystic kidneys and cultured tubular cells.

205 Polycystic kidneys are hypoxic, and oxidative stress act

206 ivation is essential and sufficient to cause polycystic kidneys in Tuberous Sclerosis Complex (TSC) a

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

208 on in vitro, the bulk of STAT3 activation in polycystic kidneys occurs through an indirect mechanism

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

210 ogical symptoms, cardiovascular defects, and polycystic kidneys.

211 ma membrane phospholipids in human and mouse polycystic kidneys.

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

213 Polycystic liver disease (PCLD) is characterized by cyst

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

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

216 Liver transplantation (LT) for polycystic liver disease (PLD) is rare, extremely challe

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

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

219 lysis of a randomized trial of patients with polycystic liver disease due to ADPKD, lanreotide for 12

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

221 Polycystic liver disease is a well described manifestati

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

223 Polycystic liver disease is the most common extrarenal m

224 ly unresolved clinical diagnosis of ADPKD or polycystic liver disease to identify a candidate gene, A

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

226 s analysis, we studied the 175 patients with polycystic liver disease with hepatic cysts identified b

227 hen mutated, causes human autosomal dominant polycystic liver disease.

228 presents a potential therapeutic approach in polycystic liver disease.

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

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

231 Polycystic liver diseases (PLDs) are genetic disorders c

232 Mutations in PC2 are associated with polycystic liver diseases.

233 ination of difficult mobilization of a heavy polycystic native liver with narrow access to inferior v

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

235 4 to 52 years consecutively recruited from a polycystic ovarian syndrome (PCOS) clinic between May 18

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

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

238 reported to associate with susceptibility to polycystic ovarian syndrome (PCOS).

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

240 o effect on risk for gestational diabetes or polycystic ovarian syndrome and was associated with a de

241 52 years who met the Rotterdam criteria for polycystic ovarian syndrome rated themselves and were ra

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

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

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

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

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

247 nt was observed for heart failure (0.40) and polycystic ovaries or ovarian cysts (0.27).

248 y androgen excess, ovulatory dysfunction and polycystic ovaries(1), and is often accompanied by insul

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

250 nd is elevated in women with androgen excess polycystic ovary syndrome (AE-PCOS).

251 onfidence interval (95% CI): 1.22-1.53)) and polycystic ovary syndrome (OR = 1.51 (95% CI: 1.33-1.72)

252 eptibility loci that are associated with the polycystic ovary syndrome (PCOS) affection status by scr

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

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

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

256 teristics differed in women with and without polycystic ovary syndrome (PCOS) between a Caucasian and

257 Women with polycystic ovary syndrome (PCOS) commonly suffer from mi

258 Women with polycystic ovary syndrome (PCOS) commonly suffer from mi

259 Polycystic ovary syndrome (PCOS) has been associated wit

260 Women with polycystic ovary syndrome (PCOS) have been shown to be l

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

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

263 Polycystic ovary syndrome (PCOS) is a common, complex ge

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

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

266 Polycystic ovary syndrome (PCOS) is a complex syndrome w

267 Polycystic ovary syndrome (PCOS) is a hypothalamic-pitui

268 Polycystic ovary syndrome (PCOS) is a major reproductive

269 Polycystic ovary syndrome (PCOS) is characterized by and

270 Polycystic ovary syndrome (PCOS) is frequently associate

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

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

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

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

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

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

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

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

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

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

281 rexposure associated with conditions such as polycystic ovary syndrome (PCOS).

282 of healthy women (n = 9), and in women with polycystic ovary syndrome (PCOS; n = 6) or hypothalamic

283 2-1.16; P = 0.007); and genetic liability to polycystic ovary syndrome and endometrioid carcinoma (OR

284 ences in vaginal microbiota between cases of polycystic ovary syndrome and healthy controls.

285 In patients with polycystic ovary syndrome and insulin resistance, piogli

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

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

288 Polycystic ovary syndrome is characterized by an excess

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

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

291 drenal hyperplasia, premature adrenarche and polycystic ovary syndrome, as well as in androgen-depend

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

293 genes associated with spontaneous abortion, polycystic ovary syndrome, myocardial infarction and mel

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 netic liability to 3 factors (endometriosis, polycystic ovary syndrome, type 2 diabetes) scaled to re

297 sex hormone-dependent cancers and diseases (polycystic ovary syndrome, uterine fibroids, endometrios

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

299 based cohort and evaluated the occurrence of polycystic phenotypes in both groups.

300 Treatment of polycystic rats with UDCA-HDAC6i #1 reduced their hepato