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 300 mg tablets and capsules were developed and manu

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 decreases amount of shed TNFalpha, TGFalpha, and sM

8 UDCA did not affect intracellular cAMP levels but increa

9 UDCA improves peripheral blood flow and is associated wi

10 UDCA increased ATP output in isolated perfused livers fr

11 UDCA inhibited OATP4A1 activity in placental villous fra

12 UDCA inhibition of OATP4A1 suggests it will protect the

13 UDCA is well tolerated in patients with CHF.

14 UDCA may protect the fetus in ICP by inhibiting OATP4A1-

15 UDCA orientation within the UDCA-HDAC6i structure was de

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 stimulated apical ATP secretion in WT but not in CF

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

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

22 UDCA therapy had no effect on delaying progression of di

23 UDCA was administered to all patients after 2 years.

24 UDCA was used in 208 pregnancies.

25 UDCA was well tolerated and body weight was stable durin

26 UDCA was well tolerated by pregnant women.

27 UDCA was well tolerated in all patients.

28 UDCA withdrawal resulted in a significant deterioration

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

30 UDCA, a commensal microbial metabolite, abrogates senesc

31 UDCA-HDAC6i #1 was actively transported into cells throu

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 UDCA-treatment increased serum FGF19, and reduced C4 (re

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

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 Ursodeoxycholic acid (UDCA) and histone deacetylase 6 inhibitors (HDAC6is) hav

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

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

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

43 Ursodeoxycholic acid (UDCA) has previously been shown to be antiarrhythmic in

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

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

46 Whereas ursodeoxycholic acid (UDCA) is a commonly used treatment for ICP, no studies h

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

48 Ursodeoxycholic acid (UDCA) is one of the first-line therapeutic medications u

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

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

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

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

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

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

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

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

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

58 iochemical response to ursodeoxycholic acid (UDCA) therapy in early patients with PBC was associated

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

60 g the effect of adding Ursodeoxycholic acid (UDCA) to CBD stenting alone in order to reduce the size

61 t salvage therapy with ursodeoxycholic acid (UDCA) to prevent rCDI in 16 high-risk patients.

62 Ursodeoxycholic acid (UDCA) treatment can reduce itch and lower endogenous ser

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

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

65 the use and effect of ursodeoxycholic acid (UDCA) treatment.

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

67 Treatment includes ursodeoxycholic acid (UDCA), but it is not clear if UDCA protects the fetus.

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

69 available treatment is ursodeoxycholic acid (UDCA), however, direct and indirect treatment costs are

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

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

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

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

74 levels in this largely ursodeoxycholic acid (UDCA)-responding, early-disease stage cohort.

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

76 h the introduoction of ursodeoxycholic acid (UDCA).

77 incomplete response to ursodeoxycholic acid (UDCA).

78 ted by the hydrophilic ursodeoxycholic acid (UDCA).

79 te pharmacokinetics of ursodeoxycholic acid (UDCA).

80 the natural bile acid ursodeoxycholic acid (UDCA).

81 he secondary bile acid ursodeoxycholic acid (UDCA; ursodiol) inhibits the life cycles of various stra

82 jugates presented selective HDAC6i activity, UDCA-HDAC6i #1 being the most promising candidate.

83 iarrhythmic effect was observed in the acute UDCA administration group.

84 Adding UDCA to CBD stenting, due to decrease in the stone size

85 After UDCA removal cholestatic parameters, taurine species of

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

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

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

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

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

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

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

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

94 50-fold in HepG2 cells, whereas DCA, CA, and UDCA induced BSEP mRNA by 250-, 75-, and 15-fold, respec

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

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

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

98 ) received standard endoscopic therapies and UDCA + CBD stenting (group B) and controls only received

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

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

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

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

103 and rat vasculature, which was attenuated by UDCA.

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

105 ular function, and how these are modified 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 c conjugates with selective HDAC6i capacity (UDCA-HDAC6i).

109 In cystic cholangiocytes UDCA-HDAC6i #1 restored primary cilium length and exhibi

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

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

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

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

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

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

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

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

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

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

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

123 DCs expressed the farnesoid X receptor for UDCA.

124 Four UDCA-HDAC6i conjugates presented selective HDAC6i activi

125 cholestatic liver disease might benefit from UDCA with respect to periodontal health.

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

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

128 During ICP, UDCA treatment can be associated with enrichment of the

129 d profile of fetal serum from untreated ICP, UDCA-treated ICP and uncomplicated pregnancies and found

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

131 xycholic acid (UDCA), but it is not clear if UDCA protects the fetus.

132 This study was performed to investigate if UDCA protects against ischaemia-induced and reperfusion-

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

134 Serum FGF19 was elevated in UDCA non-responders.

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

136 lar activity, which were reversed in part in UDCA responders.

137 eir hepatomegaly and cystogenesis, increased UDCA concentration, and inhibited HDAC6 activity in live

138 Interestingly, UDCA treatment significantly increased SMILE promoter ac

139 opus laevis oocytes were used to investigate UDCA transport.

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

141 placebo group eventually received open-label UDCA.

142 rsodeoxycholyl lysophosphatidylethanolamide (UDCA-LPE).

143 In RAW 264.7 macrophages, UDCA attenuated the expression of IL1alpha, IL1beta, and

144 significant difference between manufactured UDCA (capsule and tablet) and standard UDCA.

145 costs was based on price of the manufactured UDCA and standard UDCA price of the hospital.

146 e PBC treatment costs using the manufactured UDCA by the university hospital.

147 % the PBC treatment costs using manufactured UDCA.

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

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

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

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

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

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

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

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

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

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

158 Immunoassay confirmed the capacity of UDCA to reduce inflammation-induced production of IL6 in

159 equence (A and B) and tablets or capsules of UDCA formulations applied in the treatment of PBC.

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

164 The antiarrhythmic effect of UDCA may be partially mediated by an increase in cardiac

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

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

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

168 echanism explaining the choleretic effect of UDCA.

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

170 We then investigated the effects of UDCA in a mouse model of hypercholanemic pregnancy and s

171 on that support anti-inflammatory effects of UDCA on three different periodontium-related cell types.

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

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

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

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

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

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

178 was to assess if the therapeutic efficacy of UDCA manufactured by the university hospital is equivale

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

180 gn, synthesis, and validation of a family of UDCA synthetic conjugates with selective HDAC6i capacity

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

182 gesting that the FDA-approved formulation of UDCA, known as ursodiol, may be able to restore coloniza

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

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

185 Increasingly precocious initiation of UDCA treatment did not change the incidence of severe CF

186 Understanding the physiologic mechanisms of UDCA may allow better therapeutic interventions to be de

187 and alkaline phosphatase, after 12 months of UDCA.

188 represents an additional beneficial path of UDCA treatment.

189 CA significantly decreased the percentage of UDCA in bile.

190 iltered human saliva also in the presence of UDCA.

191 urther support the anti-inflammatory role of UDCA.

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

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

194 factors for CFLD development; earlier use of UDCA over the last 20 years has not changed the incidenc

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

196 Patients on UDCA had a low observed recurrence rate (12.5%).

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

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

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

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

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

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

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

204 onged (2 weeks pre-treatment plus perfusion) UDCA administration.

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

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

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

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

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

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

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

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

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

214 and most bariatric centers do not prescribe UDCA.

215 Prolonged UDCA administration reduced the incidence of acute ischa

216 Neither acute nor prolonged UDCA treatment altered the incidence of reperfusion arrh

217 otential antiarrhythmic effects of prolonged UDCA administration merit further investigation.

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

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

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

221 ed pregnancies and 21 with ICP, 17 receiving UDCA).

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

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

224 price of the manufactured UDCA and standard UDCA price of the hospital.

225 tured UDCA (capsule and tablet) and standard UDCA.

226 y hospital is equivalent to that of standard UDCA and treatment cost reduction in patients with PBC.

227 hirty patients under treatment with standard UDCA, in stable doses were randomized in sequence A and

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

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

230 Women taking UDCA had higher faecal lithocholic acid (p < 0.0001), wi

231 pid and cholesterol secretion into bile than UDCA.

232 We therefore conclude that UDCA can be used as an intervention in pregnancy to redu

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

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

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

236 and uncomplicated pregnancies and found that UDCA ameliorates ICP-associated fetal dyslipidemia.

237 We report here that UDCA significantly reduced the IL1beta and TNFalpha-indu

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

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

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

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

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

243 ups were treated for 12 weeks and after, the UDCA formulation was changed, following for another 12 w

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

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

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

247 fter a two-month period were assessed in the UDCA + CBD stenting group.

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

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

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

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

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

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

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

255 UDCA orientation within the UDCA-HDAC6i structure was determinant for HDAC6i activit

256 These UDCA-HDAC6i conjugates open a therapeutic avenue for PLD

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

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

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

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

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

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

263 , immunosuppression, biochemical response to UDCA and elevated IgG-levels confirmed MRS (p = 0.03), D

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

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

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

267 ents with PBC with an incomplete response to UDCA.

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

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

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

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

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

273 Taken together, UDCA can attenuate the provoked expression of inflammato

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

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

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

277 liver diseases, the question arises weather UDCA holds anti-inflammatory properties on periodontal h

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

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

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

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

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

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

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

285 Treatment of polycystic rats with UDCA-HDAC6i #1 reduced their hepatomegaly and cystogenes

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

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

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

289 rmicutes were more likely to be treated with UDCA (Fisher's exact test p = 0.0178) than those with a

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

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

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

293 Treatment with UDCA and atRA substantially improved animal growth rates

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

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

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

297 e, history of meconium ileus, treatment with UDCA, and respiratory and nutritional status.

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

299 necrosis factor (TNF)alpha with and without UDCA.

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