ライフサイエンスコーパス: UDCA

1 UDCA (13-15 mg/kg/day) therapy for an average of 40 mont

2 UDCA (up to 100 micromol/L, P <.0001), TUDCA (up to 400

3 UDCA administration significantly decreased ALP and sMet

4 UDCA and SAMe induced the expression of GCL subunits and

5 UDCA and SAMe treatment prevented this fall and combined

6 UDCA and SAMe treatment targets this switch.

7 UDCA and TUDCA inhibited in vivo the cholangiocyte proli

8 UDCA decreases amount of shed TNFalpha, TGFalpha, and sM

9 UDCA did not affect intracellular cAMP levels but increa

10 UDCA had no significant effect on hepatocytes in Fas-L(-

11 UDCA improves peripheral blood flow and is associated wi

12 UDCA increased ATP output in isolated perfused livers fr

13 UDCA is used currently in gastroenterology for several i

14 UDCA is well tolerated in patients with CHF.

15 UDCA potentiated the loss of mitochondrial potential, re

16 UDCA reduced the level of the mature form of ADAM17.

17 UDCA significantly decreases the risk for developing col

18 UDCA significantly inhibited Cox-2 protein and mRNA leve

19 UDCA significantly suppressed the incidence of tumors wi

20 UDCA stimulated apical ATP secretion in WT but not in CF

21 UDCA stimulated fluid secretion and Cl(-) efflux in WT-I

22 UDCA stimulated the translocation of PKC-alpha and PKC-e

23 UDCA therapy had no effect on delaying progression of di

24 UDCA was administered to all patients after 2 years.

25 UDCA was used in 208 pregnancies.

26 UDCA was well tolerated and body weight was stable durin

27 UDCA was well tolerated by pregnant women.

28 UDCA was well tolerated in all patients.

29 UDCA withdrawal resulted in a significant deterioration

30 UDCA, a bile acid used in the treatment of cholestatic l

31 UDCA, a commensal microbial metabolite, abrogates senesc

32 UDCA-LPE ameliorated both HFD- and MCD-induced increases

33 UDCA-stimulated [Ca(2+)]i increase was inhibited by sura

34 UDCA-stimulated secretion was inhibited by 2-bis(2-amino

35 isk scores in an independent cohort of 1,249 UDCA-treated participants.

36 IN-76A chow alone, or supplemented with 0.4% UDCA, and received 20 mg/kg AOM i.p. weekly x 2 weeks.

37 ry variables in a derivation cohort of 1,916 UDCA-treated participants.

38 We identified ursodeoxycholic acid (UDCA) and deoxycholic acid (DCA) as the two most potent

39 and how treatment with ursodeoxycholic acid (UDCA) and/or S-adenosylmethionine (SAMe) affects the exp

40 Ursodeoxycholic acid (UDCA) can protect hepatocytes from apoptosis induced by

41 ycholic acid (CDCA) or ursodeoxycholic acid (UDCA) caused sustained MAPK activation that was dependen

42 arding the efficacy of ursodeoxycholic acid (UDCA) for treating primary sclerosing cholangitis (PSC).

43 Ursodeoxycholic acid (UDCA) has been suggested to be of benefit based on open

44 Ursodeoxycholic acid (UDCA) has shown effectiveness as a colon cancer chemopre

45 BC in combination with ursodeoxycholic acid (UDCA) in adults with an inadequate response to UDCA.

46 the mechanism by which ursodeoxycholic acid (UDCA) inhibits LXR-induced lipogenic gene expression.

47 Ursodeoxycholic acid (UDCA) is a beneficial medical therapy for patients with

48 Ursodeoxycholic acid (UDCA) is a safe and effective medical therapy for most p

49 Ursodeoxycholic acid (UDCA) is a safe and effective medical therapy for most p

50 Ursodeoxycholic acid (UDCA) is no longer recommended for management of adult p

51 Ursodeoxycholic acid (UDCA) is the only approved treatment for primary biliary

52 pite limited benefits, ursodeoxycholic acid (UDCA) is the only Food and Drug Administration-approved

53 Ursodeoxycholic acid (UDCA) is the only known beneficial bile acid with immuno

54 Ursodeoxycholic acid (UDCA) is used for the treatment of cholestatic liver dis

55 Ursodeoxycholic acid (UDCA) is used to treat primary biliary cirrhosis, intrah

56 Ursodeoxycholic acid (UDCA) is widely used for cholangiopathy treatment, but i

57 Standard doses of ursodeoxycholic acid (UDCA) lead to improvements in biochemical abnormalities

58 assess the effects of ursodeoxycholic acid (UDCA) on endothelial function and inflammatory markers i

59 valuate the effects of ursodeoxycholic acid (UDCA) on pruritus, liver test results, and outcomes of b

60 Ursodeoxycholic acid (UDCA) or S-adenosylmethionine (SAMe) prevented the LCA-i

61 e have also shown that ursodeoxycholic acid (UDCA) prevented AOM-induced colon cancer and suppressed

62 Ursodeoxycholic acid (UDCA) prevents the formation of gallstones after bariatr

63 Ursodeoxycholic acid (UDCA) protects cells from the apoptotic effects of hydro

64 IBD and the effect of ursodeoxycholic acid (UDCA) therapy on the course of the liver disease.

65 dose (28-30 mg/kg/day) ursodeoxycholic acid (UDCA) treatment improves serum liver tests in patients w

66 abrogated in vitro by ursodeoxycholic acid (UDCA) treatment.

67 tment with 4-PB and/or ursodeoxycholic acid (UDCA) were assessed.

68 in the follow up with ursodeoxycholic acid (UDCA), eight received during a trial methotrexate (MTX).

69 sponse to therapy with ursodeoxycholic acid (UDCA), laboratory results, and symptom impact (assessed

70 despite treatment with ursodeoxycholic acid (UDCA), the only approved therapy.

71 for these patients is ursodeoxycholic acid (UDCA), which slows the progression of PBC, particularly

72 iochemical response to ursodeoxycholic acid (UDCA)--so-called "treatment response"--strongly predicts

73 incomplete response to ursodeoxycholic acid (UDCA).

74 te pharmacokinetics of ursodeoxycholic acid (UDCA).

75 the natural bile acid ursodeoxycholic acid (UDCA).

76 ted by the hydrophilic ursodeoxycholic acid (UDCA).

77 CP) and treatment with ursodeoxycholic acid (UDCA).

78 h the introduoction of ursodeoxycholic acid (UDCA).

79 After UDCA removal cholestatic parameters, taurine species of

80 ents with stage I to II PBC before and after UDCA treatment.

81 n lithocholic acid and its derivatives after UDCA withdrawal, but no effect on concentrations of prim

82 No significant effect on HRQoL after UDCA withdrawal was observed; however, 42% of patients r

83 as the level of ERK1/2 phosphorylation after UDCA treatment.

84 Although UDCA therapy improves liver biochemistries, it may not d

85 Based on a meta-analysis, UDCA is effective in reducing pruritus and improving liv

86 Furthermore, atRA and UDCA significantly reduced liver messenger RNA and/or pr

87 so seen with treatment with atRA or atRA and UDCA versus PBS and UDCA.

88 tivate the BSEP promoter: CDCA, DCA, CA, and UDCA increased luciferase activity by 25-, 20-, 18-, and

89 50-fold in HepG2 cells, whereas DCA, CA, and UDCA induced BSEP mRNA by 250-, 75-, and 15-fold, respec

90 Inhibition of DCA-, CDCA-, and UDCA-stimulated MAPK activation resulted in approximatel

91 fects of UDCA with those of all controls and UDCA with those of placebos.

92 ereas CA partially activated FXR and DCA and UDCA had negligible activities.

93 partial induction of BSEP mRNA, CA, DCA, and UDCA effectively repressed expression of cholesterol 7al

94 eased, whereas those for CDCA, DCA, LCA, and UDCA were decreased when compared with values in normal

95 Treatment with 4-PB and UDCA partially corrected Bsep mutant targeting.

96 nt with atRA or atRA and UDCA versus PBS and UDCA.

97 ntraction remained normal in the placebo and UDCA-treated groups but was impaired in the CDCA-treated

98 hat are formed in vivo, were as effective as UDCA in promoting PDT phototoxicity.

99 means by which specific bile acids, such as UDCA and DCA, can impact hepatic triglyceride metabolism

100 Because UDCA does not act by enhancing intracellular accumulatio

101 owth factor 19 (FGF19) were collected before UDCA withdrawal and 3 months later.

102 Meta-analysis showed no difference between UDCA and placebo in the incidence of death (odds ratio 1

103 Both UDCA and DCA were able to inhibit LCFA uptake by primary

104 nhibitor of metalloproteinases-1 (TIMP-1) by UDCA was studied using zymography and qRT-PCR.

105 mined the role of Ras in Cox-2 inhibition by UDCA.

106 ble in both HFD and MCD mice, was reduced by UDCA-LPE.

107 and T cells was sharply reduced in vitro by UDCA treatment of the DCs resulting in a remarkable T-ce

108 In pooled analyses that compared UDCA with all controls, UDCA was associated with total r

109 d and switch-over phases of trials comparing UDCA with placebo, obtained from Medline and Embase data

110 In conclusion, UDCA, TUDCA, and TCDCA but not TCA are capable of protec

111 alyses that compared UDCA with all controls, UDCA was associated with total resolution of pruritus (o

112 ine percent of the patients reported current UDCA, therapy, with 80% meeting Paris response criteria.

113 ere randomized to high-dose (20 mg/kg daily) UDCA or placebo.

114 , double-blind controlled trial of high-dose UDCA (28-30 mg/kg/day) versus placebo.

115 High-dose UDCA could result in the production of hepatotoxic bile

116 High-dose UDCA did not influence symptoms, but there was a signifi

117 bo-controlled preliminary study of high-dose UDCA in PSC patients.

118 High-dose UDCA may be of clinical benefit in PSC, but trials with

119 to establish whether the effect of high-dose UDCA on liver biochemistry, histology, and cholangiograp

120 Long-term, high-dose UDCA therapy is associated with improvement in serum liv

121 High-dose UDCA treatment in PSC patients results in marked UDCA en

122 , double-blind controlled trial of high-dose UDCA versus placebo.

123 With low-dose UDCA treatment the obstetric outcome was good.

124 the anti-M2 antibodies they decrease during UDCA and immunosuppressive therapy.

125 dy reactivity significantly decreased during UDCA and MTX-treatment and also after OLT.

126 risk score was noted in all patients during UDCA therapy; however, this improvement was not signific

127 ive, anti-apoptotic, anti-oxidative effects, UDCA was reported to regulate the expression of TNFalpha

128 received daily orogastric gavage with either UDCA or vehicle only.

129 CA and Mitotracker Red were used to evaluate UDCA localization with mitochondria.

130 Immediately after BDL, rats were fed UDCA or TUDCA (both 275 micromol/d) for 1 week.

131 FITC-UDCA and Mitotracker Red were used to evaluate UDCA loca

132 FITC-UDCA colocalized with the mitochondrial probe.

133 DCs expressed the farnesoid X receptor for UDCA.

134 f Ca(2+)-dependent PKC alpha is required for UDCA and TUDCA inhibition of cholangiocyte growth and se

135 Furthermore, UDCA inhibited Cox-2 induction by Ras-dependent and -ind

136 Furthermore, UDCA treatment repressed T7-induced SREBP-1c, FAS, and A

137 Glyco-UDCA and tauro-UDCA, conjugated forms of UDCA that are f

138 ing liver test results in patients with ICP; UDCA therapy might also benefit fetal outcomes.

139 We determined if UDCA and TUDCA activate PKC, increase [Ca(2+)](i), and a

140 ocytes from 1-week BDL rats, we evaluated if UDCA and TUDCA directly inhibit cholangiocyte proliferat

141 ecretion in bile duct-ligated (BDL) rats, if UDCA and TUDCA effects are associated with increased cho

142 howed biochemical improvement (P < 0.001) in UDCA-treated patients, while no significant change occur

143 Serum FGF19 was elevated in UDCA non-responders.

144 scores at 5 min were significantly lower in UDCA group (p < 0.05), but fetal umbilical artery pH val

145 Interestingly, UDCA treatment significantly increased SMILE promoter ac

146 ed by intraperitoneal injections of 30 mg/kg UDCA-LPE three times a week for different time periods.

147 placebo group eventually received open-label UDCA.

148 rsodeoxycholyl lysophosphatidylethanolamide (UDCA-LPE).

149 treatment in PSC patients results in marked UDCA enrichment and significant expansion of the total s

150 Patients received in random order 500 mg UDCA twice daily for 4 weeks and placebo for another 4 w

151 Moreover, UDCA regulates the expression of TIMP-1 and gelatinases

152 patients treated with UDCA (N = 208) vs. no UDCA were compared.

153 uality-adjusted life years with UDCA and OCA+UDCA were 10.74 and 11.78, respectively, and the corresp

154 We found that in comparison with UDCA, OCA+UDCA could decrease the 15-year cumulative incidences of

155 time course of PBC patients treated with OCA+UDCA versus UDCA alone.

156 because of limited small bowel absorption of UDCA and conversion of UDCA by bacteria in the colon.

157 study, we propose that the mode of action of UDCA involves the sensitization of mitochondrial membran

158 To study the mechanism of action of UDCA, we analyzed the effect of UDCA on eosinophils, T c

159 Finally, we studied the capacity of UDCA to influence DC/T cell interaction.

160 l bowel absorption of UDCA and conversion of UDCA by bacteria in the colon.

161 NASH to receive between 13 and 15 mg/kg/d of UDCA or placebo for 2 years.

162 At 3 months, discontinuation of UDCA in patients with PSC causes significant deteriorati

163 and patients continued on the same dosage of UDCA.

164 and patients continued on the same dosage of UDCA.

165 Standard doses of UDCA (8-15 mg/kg daily) have been shown to be ineffectiv

166 The beneficial effect of UDCA appears to be mediated in part by the inhibition of

167 The effect of UDCA on ADAM17 activity was studied using the human live

168 We sought to evaluate the effect of UDCA on colorectal neoplasia in a group of patients with

169 l function of DCs, in essence, the effect of UDCA on DCs through the modulation of the DC/T cell inte

170 of action of UDCA, we analyzed the effect of UDCA on eosinophils, T cells, and dendritic cell (DCs).

171 with concomitant UC to assess the effect of UDCA on the development of colorectal dysplasia and canc

172 echanism explaining the choleretic effect of UDCA.

173 have assessed the anti-apoptotic effects of UDCA and other bile acids in a novel coculture model whe

174 number of cholecystectomies, side-effects of UDCA and quality of life.

175 pposite result when assessing the effects of UDCA on the apoptotic response to mitochondrial photodam

176 resent study examined the in vivo effects of UDCA or CDCA on gallbladder muscle dysfunction caused by

177 siology, our understanding of the effects of UDCA remains unclear.

178 im was to determine the long-term effects of UDCA therapy on histological stage and progression to ci

179 double blinded) that compared the effects of UDCA to other drugs, placebo, or no specific treatment (

180 pooled analyses that compared the effects of UDCA with placebo, UDCA reduced pruritus (OR, 0.21; 95%

181 pooled analysis that compared the effects of UDCA with those of all controls and UDCA with those of p

182 Here we investigated the effects of UDCA-LPE in two nutritional mouse models of NAFLD.

183 of this study was to clarify the efficacy of UDCA in primary biliary cirrhosis.

184 of this study was to clarify the efficacy of UDCA in primary biliary cirrhosis.

185 We undertook a prospective evaluation of UDCA withdrawal in a group of consecutive patients with

186 The immunosuppressive features of UDCA were studied in vivo, in mice, in an ovalbumin (OVA

187 yco-UDCA and tauro-UDCA, conjugated forms of UDCA that are formed in vivo, were as effective as UDCA

188 Furthermore, hepatocytes of UDCA-treated animals retained their metabolic activity a

189 (norUDCA), the C(23) (C(24)-nor) homolog of UDCA.

190 and alkaline phosphatase, after 12 months of UDCA.

191 represents an additional beneficial path of UDCA treatment.

192 CA significantly decreased the percentage of UDCA in bile.

193 In contrast, the potentiation of UDCA-induced apoptosis weakly correlated with procaspase

194 we have investigated around the structure of UDCA, a clinically used bile acid devoid of FXR agonist

195 mized, placebo-controlled crossover study of UDCA in 17 clinically stable male patients with CHF (New

196 ior, randomized, placebo-controlled trial of UDCA therapy in PSC at our center, we followed-up patien

197 Published randomised controlled trials of UDCA do not show evidence of therapeutic benefit in PBC

198 , 16 women, median age of 50 who had been on UDCA (13-15 mg/kg/d) for a mean of 46 months (range 6-10

199 enty-seven patients with PBC who had been on UDCA (13-15 mg/kg/day) therapy for 7 to 221 months and h

200 dose 20 mg) once a week while continuing on UDCA.

201 dpoint was 2.3 times greater for patients on UDCA than for those on placebo (P < 0.01) and 2.1 times

202 and changes in composition after 2 years on UDCA were similar in patients with varying severity of P

203 ed data from 454 patients: 207 received only UDCA, 70 received only placebo, 42 received cholestyrami

204 S), UDCA, all-trans retinoic acid (atRA), or UDCA and atRA by gavage.

205 served for patients taking UDCA plus MTX, or UDCA plus placebo.

206 Pretreatment with oral UDCA prevented the defective contraction in response to

207 In parallel, UDCA upregulates TIMP-1 that in turn inhibits matrix met

208 As for metabolic parameters, UDCA-LPE reduced elevated serum triglyceride and cholest

209 reated with phosphate-buffered saline (PBS), UDCA, all-trans retinoic acid (atRA), or UDCA and atRA b

210 Compared with placebo, UDCA improved peak post-ischemic blood flow in the arm (

211 t compared the effects of UDCA with placebo, UDCA reduced pruritus (OR, 0.21; 95% CI, 0.07-0.62; P <

212 Guinea pigs were treated with placebo, UDCA, or CDCA for 2 weeks before sham operation or induc

213 In conclusion, neither colchcine plus UDCA nor methotrexate plus UDCA improved survival beyond

214 lar in both groups: 0.57 for colchicine plus UDCA and 0.44 for methotrexate plus UDCA, results that a

215 er colchcine plus UDCA nor methotrexate plus UDCA improved survival beyond that predicted by the Mayo

216 ine plus UDCA and 0.44 for methotrexate plus UDCA, results that are similar to those predicted by the

217 enter trial compared the effects of MTX plus UDCA to UDCA alone on the course of primary biliary cirr

218 ke no definite statement about postoperative UDCA prophylaxis and most bariatric centers do not presc

219 and most bariatric centers do not prescribe UDCA.

220 For PSC, UDCA therapy does not improve survival, and recommendati

221 Those originally assigned to receive UDCA had a relative risk of 0.26 for developing colorect

222 The intervention group will receive UDCA 900 mg once daily for six months.

223 Mothers receiving UDCA had ICP diagnosed five weeks earlier than mothers w

224 LE shRNA (Ad-shSMILE) significantly reversed UDCA-mediated repression of SREBP-1c, FAS, and ACC prote

225 rum albumin 3 g/dL or greater, who had taken UDCA 15 mg/kg daily for at least 6 months, were stratifi

226 atment failures observed for patients taking UDCA plus MTX, or UDCA plus placebo.

227 Glyco-UDCA and tauro-UDCA, conjugated forms of UDCA that are formed in vivo,

228 pid and cholesterol secretion into bile than UDCA.

229 but also release granule proteins, and that UDCA treatment inhibits this eosinophil activation/degra

230 Collectively, these results demonstrate that UDCA activates SMILE gene expression through adenosine m

231 These data demonstrate that UDCA is a useful scaffold to generate novel and selectiv

232 The current study demonstrates that UDCA-LPE improves hepatic injury at different stages of

233 We hypothesized that UDCA modulates ADAM17 activity, resulting in amelioratio

234 Our data indicate that UDCA stimulates a CFTR-dependent apical ATP release in c

235 ion qRT-PCR of liver specimens revealed that UDCA-LPE strongly down-regulated inflammatory genes and

236 d placebo-controlled studies have shown that UDCA improves transplant-free survival in primary biliar

237 mmary, we have shown for the first time that UDCA suppressed the development of tumors with Ras mutat

238 were not significantly different between the UDCA and placebo groups.

239 mistries were stable or improved in both the UDCA and placebo-treated groups.

240 At enrollment, the UDCA (n = 76) and placebo (n = 74) groups were similar w

241 By the end of the study, 30 patients in the UDCA group (39%) versus 19 patients in the placebo group

242 micromol/L) were significantly higher in the UDCA group (n = 29) versus the placebo group (n = 27) wh

243 creased (0.22 versus 0.01 micromol/L) in the UDCA group compared to the placebo group (P = 0.001).

244 rious adverse events were more common in the UDCA group than the placebo group (63% versus 37% [P < 0

245 ine phosphatase levels decreased more in the UDCA group than the placebo group (P < 0.01), but improv

246 Patients (n = 9) in the UDCA group who reached clinical endpoints of disease pro

247 The mean changes in the UDCA level (16.86 versus 0.05 micromol/L) and total bile

248 Assigning these patients to the UDCA group from the time they began active therapy did n

249 Thus, UDCA-LPE represents a promising compound suitable for th

250 In conclusion, methotrexate when added to UDCA for a median period of 7.6 years had no effect on t

251 o add minimal, if any, additional benefit to UDCA, and it is associated with a significant worsening

252 he addition of colchicine or methotrexate to UDCA would improve survival free of liver transplantatio

253 findings indicate that the addition of RA to UDCA reduces the bile salt pool size and liver fibrosis

254 significantly more likely not to respond to UDCA therapy, based on alanine aminotransferase and aspa

255 gnificantly less likely to have responded to UDCA than women (72% vs 80% response rate; P < .05); mal

256 tients do not have a biochemical response to UDCA and would benefit from new therapies.

257 some patients have an incomplete response to UDCA therapy, whereas other, more advanced cases often r

258 some patients show an incomplete response to UDCA therapy.

259 Among patients with PBC, response to UDCA, treatment and symptoms are related to sex and age

260 ents with PBC with an incomplete response to UDCA.

261 CA) in adults with an inadequate response to UDCA.

262 h PBC who had shown a suboptimal response to UDCA.

263 PBC, who have shown a suboptimal response to UDCA.

264 strongly and independently with response to UDCA; response rates ranged from 90% among patients who

265 atients with PBC and incomplete responses to UDCA to be treated with 2 doses of 1000 mg rituximab sep

266 patients with PBC responding suboptimally to UDCA.

267 pplementation of RA with UDCA is superior to UDCA alone for treating cholestasis, male Sprague-Dawley

268 ial compared the effects of MTX plus UDCA to UDCA alone on the course of primary biliary cirrhosis (P

269 e (DCA), cholate (CA), and ursodeoxycholate (UDCA), act as selective FXR agonists in a gene-specific

270 study was to determine if ursodeoxycholate (UDCA) or tauroursodeoxycholate (TUDCA) chronic feeding p

271 s analysed and data of the patients who used UDCA during pregnancy was analysed separately and compar

272 al BA and ALT were higher in the group using UDCA compared to the group without medication.

273 of PBC patients treated with OCA+UDCA versus UDCA alone.

274 In vitro UDCA and TUDCA inhibition of cholangiocyte growth and se

275 These effects were not observed when UDCA was added after irradiation.

276 slices, norUDCA was glucuronidated, whereas UDCA was conjugated with glycine or taurine.

277 GRADE trial will answer the question whether UDCA reduces the incidence of symptomatic gallstone dise

278 It is unknown whether UDCA would also modulate eosinophilic inflammation outsi

279 total BA > 40 mumol/l at diagnosis, 24 with UDCA and 6 without medication and those deliveries were

280 atRA alone or in combination with UDCA greatly repressed CYP7A1 expression in human hepato

281 We found that in comparison with UDCA, OCA+UDCA could decrease the 15-year cumulative inc

282 test whether the supplementation of RA with UDCA is superior to UDCA alone for treating cholestasis,

283 ease in total bile acids and saturation with UDCA >70% confirmed patient compliance.

284 In conclusion, 2 years of therapy with UDCA at a dose of 13 to 15 mg/kg/d, although safe and we

285 ht be an effective supplemental therapy with UDCA for cholestatic diseases.

286 Twenty six patients, all treated with UDCA (dose range: 10-15 mg/kg/day) were included.

287 = 307) was studied and patients treated with UDCA (N = 208) vs. no UDCA were compared.

288 no effect on the course of PBC treated with UDCA alone.

289 ced the death response of cells treated with UDCA and MEK1/2 inhibitor to that observed for DCA and M

290 Treatment with UDCA also prevented the expected increase in the levels

291 Treatment with UDCA and atRA substantially improved animal growth rates

292 who responded incompletely to treatment with UDCA and colchicine.

293 Treatment with UDCA caused the proportion of all endogenous bile acids

294 Treatment with UDCA enriched gallbladder bile acids with its conjugates

295 thermore it will determine if treatment with UDCA is cost-effective.

296 IU (range, 155-467 IU) after treatment with UDCA plus colchicine, and 120 IU (range, 66-351 IU) afte

297 In conclusion, oral treatment with UDCA prevents gallbladder muscle damage caused by BDL, w

298 a receptor 1 were lower after treatment with UDCA than after placebo (all p < 0.05).

299 discounted quality-adjusted life years with UDCA and OCA+UDCA were 10.74 and 11.78, respectively, an

300 g human ADAM17 were cultured with or without UDCA and further activated using phorbol-12-myristate-13