ライフサイエンスコーパス: benign prostatic hyperplasia

1 t is not expressed in normal prostate nor in benign prostatic hyperplasia.

2 ed here to differentiate prostate cancer and benign prostatic hyperplasia.

3 tions play a critical role in development of benign prostatic hyperplasia.

4 inary tract symptoms are often attributed to benign prostatic hyperplasia.

5 t of bladder outlet obstruction secondary to benign prostatic hyperplasia.

6 ot improve symptoms or objective measures of benign prostatic hyperplasia.

7 risk than nondaily NSAID users of developing benign prostatic hyperplasia.

8 e most rigorously analyzed interventions for benign prostatic hyperplasia.

9 prostate over other surgical treatments for benign prostatic hyperplasia.

10 SAID use may prevent or delay development of benign prostatic hyperplasia.

11 d with other surgical therapies for men with benign prostatic hyperplasia.

12 (5-ARIs) are widely used in the treatment of benign prostatic hyperplasia.

13 have a potential role in the pathogenesis of benign prostatic hyperplasia.

14 treatment of endometriosis, leiomyomas, and benign prostatic hyperplasia.

15 the appropriate management of a patient with benign prostatic hyperplasia.

16 sk factor for prostate cancer among men with benign prostatic hyperplasia.

17 ion of a patient with symptoms suggestive of benign prostatic hyperplasia.

18 muscle dysfunction, neurological factors and benign prostatic hyperplasia.

19 ases, including prostatic adenocarcinoma and benign prostatic hyperplasia.

20 y on measures of the clinical progression of benign prostatic hyperplasia.

21 role in the etiology of prostate cancer and benign prostatic hyperplasia.

22 of minimally invasive surgical therapies for benign prostatic hyperplasia.

23 line treatment for most men with symptomatic benign prostatic hyperplasia.

24 o be efficacious in reducing the symptoms of benign prostatic hyperplasia.

25 he latter in the context of the aetiology of benign prostatic hyperplasia.

26 lder with or without obstructive symptoms of benign prostatic hyperplasia.

27 r the past year in the medical management of benign prostatic hyperplasia.

28 et obstruction thought to be associated with benign prostatic hyperplasia.

29 ells and a testosterone-induced rat model of benign prostatic hyperplasia.

30 way as it pertains to the pathophysiology of benign prostatic hyperplasia.

31 tatectomy became a widely used treatment for benign prostatic hyperplasia.

32 wing transurethral resection of prostate for benign prostatic hyperplasia.

33 lar transition zone tissue of prostates with benign prostatic hyperplasia.

34 pment of BPSA-specific mAbs for the study of benign prostatic hyperplasia.

35 for alleviating urethral obstruction due to benign prostatic hyperplasia.

36 ved in stromal nodules associated with human benign prostatic hyperplasia.

37 diseases such as myocardial hypertrophy and benign prostatic hyperplasia.

38 e combination of both drugs in 1229 men with benign prostatic hyperplasia.

39 onists will have utility in the treatment of benign prostatic hyperplasia.

40 of the spatial extent of prostate cancer and benign prostatic hyperplasia.

41 a variety of PCA specimens, cell lines, and benign prostatic hyperplasia.

42 ition zone cancers and glandular and stromal benign prostatic hyperplasia.

43 itiation, and to develop novel therapies for benign prostatic hyperplasia.

44 biopsy and improved the outcomes related to benign prostatic hyperplasia.

45 to relieve bladder outlet obstruction due to benign prostatic hyperplasia.

46 ior to other modalities for the treatment of benign prostatic hyperplasia.

47 over other surgical treatments for men with benign prostatic hyperplasia.

48 inflammation may be associated with LUTS and benign prostatic hyperplasia.

49 y used as a therapeutic for the treatment of benign prostatic hyperplasia.

50 ieve lower urinary tract symptoms related to benign prostatic hyperplasia.

51 gonist and ARI was used to treat symptomatic benign prostatic hyperplasia.

52 clearly related to prostatic enlargement or benign prostatic hyperplasia.

53 a-1A blocker prescribed for the treatment of benign prostatic hyperplasia.

54 alues in regions of histologically confirmed benign prostatic hyperplasia (0.61 +/- 0.21 [standard de

55 secrete higher levels of IGF-1 and stimulate benign prostatic hyperplasia-1 cellular proliferation.

56 noma of the prostate (PCA), 15 patients with benign prostatic hyperplasia, 15 normal male subjects, a

57 complete loss of NKX3.1 expression in 5% of benign prostatic hyperplasias, 20% of high-grade prostat

58 was not significantly different from that of benign prostatic hyperplasia (4.8 +/- 2.01 [range, 1.8-8

59 Bacteremic patients were more likely to have benign prostatic hyperplasia (56% vs 19%; P = .04), a hi

60 stained positively in 0 of 12 (0%) cases of benign prostatic hyperplasia, 57 of 63 (90.5%) primary a

61 ry of prostate cancer, age at randomization, benign prostatic hyperplasia, age and stage at diagnosis

62 s frequently misdiagnosed as prostatitis and benign prostatic hyperplasia among men.

63 alpha-reductase inhibitors are used to treat benign prostatic hyperplasia and androgenic alopecia, bu

64 Urinary complications resulting from benign prostatic hyperplasia and bladder outlet obstruct

65 Patients with symptomatic benign prostatic hyperplasia and cataracts requiring a u

66 discussed in relation to the pathogenesis of benign prostatic hyperplasia and future directions for r

67 specificity needed to differentiate PCa from benign prostatic hyperplasia and have high false positiv

68 he authors evaluated the association between benign prostatic hyperplasia and IGF-I and its binding p

69 being extensively used for the treatment of benign prostatic hyperplasia and in experimental setting

70 sely relate in predicting the progression of benign prostatic hyperplasia and in recent years increas

71 en in the United States for the treatment of benign prostatic hyperplasia and is commonly recommended

72 atment failure, or as definitive therapy for benign prostatic hyperplasia and its associated problems

73 cts that have been used for the treatment of benign prostatic hyperplasia and lower urinary tract sym

74 ciated with significantly increased risks of benign prostatic hyperplasia and lower urinary tract sym

75 nd diet - for the prevention or treatment of benign prostatic hyperplasia and lower urinary tract sym

76 ortunity for the prevention and treatment of benign prostatic hyperplasia and lower urinary tract sym

77 alternatives within the context of standard benign prostatic hyperplasia and lower urinary tract sym

78 tor (AR) is associated with prostate cancer, benign prostatic hyperplasia and male infertility.

79 state tissue, with substantial expression in benign prostatic hyperplasia and prominent expression in

80 Both benign prostatic hyperplasia and prostate cancer are com

81 state, EMT processes have been implicated in benign prostatic hyperplasia and prostate cancer progres

82 ve function and/or altered susceptibility to benign prostatic hyperplasia and prostate cancer.

83 previously linked to the development of both benign prostatic hyperplasia and prostate cancer.

84 provide evidence for an association between benign prostatic hyperplasia and serum IGF-I.

85 common problems presenting to urologists are benign prostatic hyperplasia and sexual dysfunction, wit

86 ion in men with lower urinary tract symptoms/benign prostatic hyperplasia and the associated risk of

87 of therapy on the risk of surgery related to benign prostatic hyperplasia and the predictors of disea

88 cts that have been used for the treatment of benign prostatic hyperplasia and voiding dysfunction.

89 mation may play a role in the development of benign prostatic hyperplasia and/or lower urinary tract

90 the referent group after adjustment for age, benign prostatic hyperplasia, and family history.

91 nt for age, race/ethnicity, smoking history, benign prostatic hyperplasia, and family history.

92 rimary tissues derived from normal prostate, benign prostatic hyperplasia, and prostate carcinomas, I

93 n the luminal epithelium of normal prostate, benign prostatic hyperplasia, and prostatic intraepithel

94 the roles of 5 alpha-reductase inhibitors in benign prostatic hyperplasia, and these may expand furth

95 esults Men 60 to 69 years of age, those with benign prostatic hyperplasia, and those with a family hi

96 ars) and evaluated medications used to treat benign prostatic hyperplasia, anti-inflammatory drugs, a

97 known that lower urinary tract symptoms and benign prostatic hyperplasia are definitely related to e

98 ion in men with lower urinary tract symptoms/benign prostatic hyperplasia are few and far between, bu

99 nary tract symptoms that are consistent with benign prostatic hyperplasia are not more likely to harb

100 blockers, commonly used for the treatment of benign prostatic hyperplasia, are associated with prosta

101 In benign prostatic hyperplasia, basal cells and areas of b

102 ergic drugs has been considered hazardous in benign prostatic hyperplasia because of concerns that th

103 pecificity for distinguishing early PCa from benign prostatic hyperplasia, because both PCa and benig

104 CR, while KGF expression was not detected in benign prostatic hyperplasia (BPH) (n = 6).

105 agonists with potential for the treatment of benign prostatic hyperplasia (BPH) (see part 1 of this s

106 were evaluated in relation to development of benign prostatic hyperplasia (BPH) among 29,386 members

107 he presence and progression of components of benign prostatic hyperplasia (BPH) and a clinical outcom

108 Benign prostatic hyperplasia (BPH) and associated lower

109 bladder outlet obstruction (PBOO) caused by benign prostatic hyperplasia (BPH) and in animal models

110 ificantly influence the risks of symptomatic benign prostatic hyperplasia (BPH) and lower urinary tra

111 ormones play prominent roles in the cause of benign prostatic hyperplasia (BPH) and lower urinary tra

112 een the components of metabolic syndrome and benign prostatic hyperplasia (BPH) and lower urinary tra

113 Benign prostatic hyperplasia (BPH) and prostate adenocar

114 examined the association between symptomatic benign prostatic hyperplasia (BPH) and prostate cancer r

115 nes and high-grade clinical CaP (compared to benign prostatic hyperplasia (BPH) and well-differentiat

116 Chronic prostatitis (CPr) and benign prostatic hyperplasia (BPH) are complex inflammat

117 Although surrogate measures of benign prostatic hyperplasia (BPH) are often used in epi

118 Benign prostatic hyperplasia (BPH) as the main cause of

119 utrition seems to modify the pathogenesis of benign prostatic hyperplasia (BPH) effect symptomology i

120 r to discriminate prostatic inflammation and benign prostatic hyperplasia (BPH) from prostate cancer,

121 The understanding and therapy of benign prostatic hyperplasia (BPH) has become more compl

122 y examined dietary risk factors for incident benign prostatic hyperplasia (BPH) in 4,770 Prostate Can

123 Benign prostatic hyperplasia (BPH) is a common cause of

124 Benign prostatic hyperplasia (BPH) is a common disease o

125 , lower urinary tract symptoms (LUTS) due to benign prostatic hyperplasia (BPH) is a common medical p

126 rinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH) is a condition that c

127 Benign prostatic hyperplasia (BPH) is a disease of unkno

128 Lower urinary tract symptoms due to benign prostatic hyperplasia (BPH) is a highly prevalent

129 Benign prostatic hyperplasia (BPH) is a pathologic proli

130 Benign prostatic hyperplasia (BPH) is a progressive age-

131 Benign prostatic hyperplasia (BPH) is an extremely commo

132 Benign prostatic hyperplasia (BPH) is an extremely commo

133 Benign prostatic hyperplasia (BPH) is characterized by i

134 The etiology of benign prostatic hyperplasia (BPH) is multifactorial, an

135 Benign prostatic hyperplasia (BPH) is prevalent in old m

136 umes of interest (VOIs) for prostate tumors, benign prostatic hyperplasia (BPH) nodules, prostatitis,

137 he effect of different treatment options for benign prostatic hyperplasia (BPH) on sexual function or

138 asm and nucleus of PCa samples; in contrast, benign prostatic hyperplasia (BPH) samples presented str

139 tate cancer cell lines, prostate cancer, and benign prostatic hyperplasia (BPH) tissues samples using

140 ofiling of primary human prostate cancer and benign prostatic hyperplasia (BPH) using cDNA microarray

141 Of the 35 benign prostatic hyperplasia (BPH), 25 (71.4%) specimens

142 Current pharmacotherapies for symptomatic benign prostatic hyperplasia (BPH), an androgen receptor

143 roles in the development and progression of benign prostatic hyperplasia (BPH), but the underlying m

144 lower urinary tract symptoms associated with benign prostatic hyperplasia (BPH), the etiology of whic

145 ory drug (NSAID) use and risk of symptomatic benign prostatic hyperplasia (BPH), using data from 4,73

146 inflammatory markers and risk of symptomatic benign prostatic hyperplasia (BPH), using data from the

147 of serum steroid concentrations and risk of benign prostatic hyperplasia (BPH), using data from the

148 h CPI-17 overexpression in BSM from men with benign prostatic hyperplasia (BPH)-induced bladder hyper

149 s a well known approach to the management of benign prostatic hyperplasia (BPH).

150 and differentiation might reduce the risk of benign prostatic hyperplasia (BPH).

151 mation has been suggested as an etiology for benign prostatic hyperplasia (BPH).

152 pecificity for distinguishing early PCa from benign prostatic hyperplasia (BPH).

153 ed with cells derived from normal tissues or benign prostatic hyperplasia (BPH).

154 (1b) are used to treat both hypertension and benign prostatic hyperplasia (BPH).

155 pecificity for distinguishing early PCa from benign prostatic hyperplasia (BPH).

156 1a) antagonists as a potential treatment for benign prostatic hyperplasia (BPH).

157 L-6 in the growth of prostatic carcinoma and benign prostatic hyperplasia (BPH).

158 n higher levels than cells representative of benign prostatic hyperplasia (BPH).

159 adder outlet procedures for the treatment of benign prostatic hyperplasia (BPH).

160 ation in the pathogenesis and progression of benign prostatic hyperplasia (BPH).

161 rovide new viewpoints of hormonal control of benign prostatic hyperplasia (BPH).

162 olization (TAE) as a potential treatment for benign prostatic hyperplasia (BPH).

163 osterone, have been used in the treatment of benign prostatic hyperplasia (BPH).

164 g lower urinary tract symptoms attributed to benign prostatic hyperplasia (BPH); however, recent clin

165 n held as the gold standard for treatment of benign prostatic hyperplasia (BPH); however, there has b

166 0), lymph node metastases (LNMs; n = 8), and benign prostatic hyperplasia (BPH; n = 6) with the use o

167 of the noncancerous disease categories (eg, benign prostatic hyperplasia [BPH], prostatic intraepith

168 gene expression of transformed [tumorigenic benign prostatic hyperplasia (BPH1)(CAFTD)] and parental

169 ow levels in normal prostatic epithelium and benign prostatic hyperplasia but significantly increased

170 nown to improve urinary symptoms in men with benign prostatic hyperplasia, but the extent to which th

171 ing techniques in diagnosis and treatment of benign prostatic hyperplasia by reviewing the most recen

172 Men with benign prostatic hyperplasia can be treated with alpha 1

173 Overactive bladder and benign prostatic hyperplasia commonly cause lower urinar

174 The gold standard for surgical treatment of benign prostatic hyperplasia continues to be transurethr

175 , such as the need for invasive treatment of benign prostatic hyperplasia, development of a clinical

176 portant role in normal prostate development, benign prostatic hyperplasia, established prostate cance

177 o that in studies of dutasteride therapy for benign prostatic hyperplasia, except that in our study,

178 alternative for the treatment of symptomatic benign prostatic hyperplasia for men with prostates of a

179 ral resection of the prostate procedures for benign prostatic hyperplasia from 1983 to 2013 were coll

180 SA levels in the serum may help discriminate benign prostatic hyperplasia from early prostate cancer.

181 ecific antigen marker to better discriminate benign prostatic hyperplasia from early prostate cancer.

182 omy, interest in lasers for the treatment of benign prostatic hyperplasia has been rekindled.

183 cently, much of the available information on benign prostatic hyperplasia has come from randomized co

184 condary to benign prostatic obstruction from benign prostatic hyperplasia has proven to be an effecti

185 samples of normal-appearing prostate tissue, benign prostatic hyperplasia, high-grade prostatic intra

186 ncer progression stages, being detectable in benign prostatic hyperplasia, highly expressed in prosta

187 studies and randomized controlled trials on benign prostatic hyperplasia in order to understand the

188 t largely undetectable in normal prostate or benign prostatic hyperplasia in vivo.

189 some history of intraprostatic injection for benign prostatic hyperplasia including the most recent r

190 oporosis is 1.1% and that for drugs to treat benign prostatic hyperplasia is 1-2%.

191 The surgical treatment of benign prostatic hyperplasia is a dynamic, evolving fiel

192 Although benign prostatic hyperplasia is an important cause of th

193 ey to obtaining optimal outcomes in men with benign prostatic hyperplasia is careful patient selectio

194 Benign prostatic hyperplasia is commonly treated with al

195 Use of 5 mg/day finasteride (Proscar) for benign prostatic hyperplasia is known to affect serum co

196 their application in prostatic pathology and benign prostatic hyperplasia is not as clear.

197 The standard medical therapy for symptomatic benign prostatic hyperplasia is still alpha-blockers and

198 rgo comprehensive clinical evaluation before benign prostatic hyperplasia is treated, if indicated.

199 mportant roles in myocardial hypertrophy and benign prostatic hyperplasia, little is known about acut

200 fferent investigation modalities in men with benign prostatic hyperplasia/lower urinary tract symptom

201 of lower urinary tract symptom suggestive of benign prostatic hyperplasia (LUTS/BPH).

202 eeded before their place in the treatment of benign prostatic hyperplasia/LUTS can be properly assess

203 specific questions and counselling men with benign prostatic hyperplasia/LUTS.

204 Benign prostatic hyperplasia measures included developme

205 antigen (PSCA)in normal urogenital tissues, benign prostatic hyperplasia (n = 21), prostatic intraep

206 ed from 371 formalin-fixed blocks, including benign prostatic hyperplasia (n = 32) and primary tumors

207 ith urination, suggesting an exacerbation of benign prostatic hyperplasia; no other subject reported

208 helium (n = 48), hyperplasticepithelium from benign prostatic hyperplasia nodules (n = 22), PIA (n =

209 The controls (benign prostatic hyperplasias, normal males, and normal

210 s expressed by epithelial cells derived from benign prostatic hyperplasia or prostate cancer; thus, f

211 rinary tract symptom in men with symptomatic benign prostatic hyperplasia over alpha1-adrenergic anta

212 roved medical therapies for the treatment of benign prostatic hyperplasia over the past year, interes

213 high-grade prostate cancer when compared to benign prostatic hyperplasia (P<0.0001).

214 evelopments in the management of symptomatic benign prostatic hyperplasia, particularly the current r

215 ested more imaging studies than expected for benign prostatic hyperplasia patients in recent years, a

216 , inflammation was not related to LUTS or to benign prostatic hyperplasia progression.

217 o apply histotripsy to preclinical models of benign prostatic hyperplasia, prostate cancer, renal mas

218 ride group (5 percent) underwent surgery for benign prostatic hyperplasia (reduction in risk with fin

219 steride has been shown to reduce and control benign prostatic hyperplasia-related haematuria, althoug

220 ute urinary retention or the requirement for benign prostatic hyperplasia-related surgery.

221 prostatic hyperplasia, because both PCa and benign prostatic hyperplasia release PSA into the serum.

222 he prostate (TURP) has dominated symptomatic benign prostatic hyperplasia (s-BPH) surgical treatment

223 or-matched nonneoplastic adjacent tissues or benign prostatic hyperplasia samples.

224 Both proteins were present in benign prostatic hyperplasia samples.

225 ve surgical therapy for LUTS associated with benign prostatic hyperplasia seems attractive and may ha

226 Associations of prostatitis include benign prostatic hyperplasia, sexually transmitted disea

227 minimal initial evaluation of a patient with benign prostatic hyperplasia should include a thorough h

228 the risk of overall clinical progression of benign prostatic hyperplasia significantly more than did

229 an immortalized PrEC line established from a benign prostatic hyperplasia specimen (BPH-1), and in th

230 state, its expression is strongly reduced in benign prostatic hyperplasia suggesting that DAX-1 plays

231 In men with benign prostatic hyperplasia, terazosin was effective th

232 FOXO3a and PUMA is comparable and higher in benign prostatic hyperplasia than in prostate cancer Gle

233 d prevalence of lower urinary tract symptoms/benign prostatic hyperplasia, the incidence of acute uri

234 therapy for lower urinary tract symptoms and benign prostatic hyperplasia, the majority of the data a

235 rial to assess the safety of histotripsy for benign prostatic hyperplasia therapy.

236 tive p27Kip1 expression; acini in epithelial benign prostatic hyperplasia tissue contained more p27Ki

237 ue samples and cultured PC cells compared to benign prostatic hyperplasia tissue samples and normal p

238 atic epithelial cells, derived from tumor or benign prostatic hyperplasia tissue, were studied using

239 ip1-negative basal cells than acini from non-benign prostatic hyperplasia tissue.

240 stromal compartment of normal prostatic and benign prostatic hyperplasia tissue.

241 tissues is significantly higher than that in benign prostatic hyperplasia tissues, and PRMT5 expressi

242 ity of prostate cancer, but not in normal or benign prostatic hyperplasia tissues.

243 ticularly in advanced prostate cancer versus benign prostatic hyperplasia tissues.

244 years who had moderate-to-severe symptoms of benign prostatic hyperplasia to one year of treatment wi

245 For benign prostatic hyperplasia, transperineal and transure

246 ne aminotransferase (nine [6%] vs none), and benign prostatic hyperplasia (two [5%] vs none).

247 een androgen receptor gene polymorphisms and benign prostatic hyperplasia was investigated among 510

248 tionally, the gold standard for treatment of benign prostatic hyperplasia was the electrocautery-base

249 transurethral resection of the prostate for benign prostatic hyperplasia, we assessed serum, urine,

250 x 10(-3) mm(2)/sec) in glandular and stromal benign prostatic hyperplasia were 1.44 and 1.09, respect

251 for men with bladder outlet obstruction from benign prostatic hyperplasia who are deemed high surgica

252 Benign prostatic hyperplasia with associated symptoms an

253 therapy for lower urinary tract symptoms and benign prostatic hyperplasia with either alpha adrenergi

254 sing minimally invasive surgical therapy for benign prostatic hyperplasia with increased attention fr

255 ts groups were (i) histological diagnosis of benign prostatic hyperplasia with no evidence of cancer

256 after prostate artery embolization (PAE) for benign prostatic hyperplasia with spherical particle pol