ライフサイエンスコーパス: inflammatory bowel disease

1 s result in gastrointestinal symptoms (e.g., inflammatory bowel disease).

2 atory diseases, such as allergy, asthma, and inflammatory bowel disease.

3 embles ulcerative colitis, one form of human inflammatory bowel disease.

4 se as novel disease-modifying therapeutic of inflammatory bowel disease.

5 treatment with vedolizumab in patients with inflammatory bowel disease.

6 10 receptor (IL10R) develop very early onset inflammatory bowel disease.

7 phages may contribute to the pathogenesis of inflammatory bowel disease.

8 orbidity could affect the natural history of inflammatory bowel disease.

9 al trials as T cell therapy in patients with inflammatory bowel disease.

10 tion (CRD) is suggested as a risk factor for inflammatory bowel disease.

11 elta/Delta)FOXP3(+) mice develop spontaneous inflammatory bowel disease.

12 entified as important therapeutic targets in inflammatory bowel disease.

13 TNF might be more effective in patients with inflammatory bowel disease.

14 , mood, and quality of life in patients with inflammatory bowel disease.

15 lta T cells play a pathogenic role including inflammatory bowel disease.

16 ging tool in the evaluation of patients with inflammatory bowel disease.

17 ded by a locus that has been associated with inflammatory bowel disease.

18 several negative health outcomes, including inflammatory bowel disease.

19 lizumab, is a highly effective treatment for inflammatory bowel disease.

20 immunodeficiencies and rare forms of severe inflammatory bowel disease.

21 diating intestinal inflammatory responses in inflammatory bowel disease.

22 osure is associated with atherosclerosis and inflammatory bowel disease.

23 r detect dysplastic changes in patients with inflammatory bowel disease.

24 thiopurine drugs in paediatric patients with inflammatory bowel disease.

25 eviate chronic inflammatory diseases such as inflammatory bowel disease.

26 to that observed in patients with ileus and inflammatory bowel disease.

27 ffect development of mucosal inflammation or inflammatory bowel disease.

28 ging tool in the evaluation of patients with inflammatory bowel disease.

29 ase models, such as rheumatoid arthritis and inflammatory bowel disease.

30 n may offer a new option in the treatment of inflammatory bowel disease.

31 nded to be associated with increased risk of inflammatory bowel disease.

32 ECs overlapped with susceptibility genes for inflammatory bowel disease.

33 is associated with rheumatoid arthritis and inflammatory bowel disease.

34 ne disorders, such as multiple sclerosis and inflammatory bowel disease.

35 therapeutic approach to treat patients with inflammatory bowel disease.

36 at(+) IL-17-producing Th17 cells, leading to inflammatory bowel disease.

37 g peptide Lipocalin-2 (Lcn2) are observed in inflammatory bowel disease.

38 may represent a novel therapeutic target in inflammatory bowel disease.

39 le in gut homeostasis and mucosal healing in inflammatory bowel disease.

40 colorectal cancers is present in those with inflammatory bowel disease.

41 ss in the colon are the principal factors in inflammatory bowel disease.

42 involved those with rheumatoid arthritis or inflammatory bowel disease.

43 e gut and represents a therapeutic target in inflammatory bowel disease.

44 n a dextran sodium sulfate mediated model of inflammatory bowel disease.

45 ic inflammatory diseases, such as asthma and inflammatory bowel disease.

46 tic disorders such as cholestasis, NASH, and inflammatory bowel disease.

47 disease, chronic heart failure, cancer, and inflammatory bowel disease.

48 scores and quality of life in patients with inflammatory bowel disease.

49 rominent than previously reported cases with inflammatory bowel disease.

50 ovel prevention and treatment strategies for inflammatory bowel disease.

51 ines on the role of TDM in the management of inflammatory bowel disease.

52 target for chemoprevention in patients with inflammatory bowel disease.

53 lammation and contributes to pathogenesis of inflammatory bowel diseases.

54 ment of intestinal fibrosis in patients with inflammatory bowel diseases.

55 eral chronic inflammatory diseases including inflammatory bowel diseases.

56 ne expression patterns associated with human inflammatory bowel diseases.

57 mucosal barrier, and promotes development of inflammatory bowel diseases.

58 lammation and contributes to pathogenesis of inflammatory bowel diseases.

59 be developed as treatments for patients with inflammatory bowel diseases.

60 es of failure to resolve gut inflammation in inflammatory bowel diseases.

61 patic steatosis, cardiovascular disease, and inflammatory bowel diseases.

62 tral pathological feature of colitis and the inflammatory bowel diseases.

63 g of GPBAR1 may offer therapeutic options in inflammatory bowel diseases.

64 , 19.9% were receiving treatment for chronic inflammatory bowel disease, 12.1% of the participants we

65 rheumatoid arthritis, 5 had psoriasis, 6 had inflammatory bowel disease, 2 had systemic lupus erythem

66 that Rag2(R229Q) knock-in mice developed an inflammatory bowel disease affecting both the small bowe

67 olled trials (RCTs) recruiting patients with inflammatory bowel disease aged at least 16 years that c

68 elopment of disease in later life, including inflammatory bowel disease, allergy, and asthma.

69 ated with the presence and risk of new-onset inflammatory bowel disease, although the prevalence rema

70 ocyte infiltration in experimental models of inflammatory bowel disease and acute graft-versus-host d

71 optive-transfer models, including autoimmune inflammatory bowel disease and allogeneic graft-versus-h

72 -mediated mouse models, including a model of inflammatory bowel disease and an inflammatory arthritis

73 testine has been associated with early-onset inflammatory bowel disease and colon cancer.

74 acteroides fragilis (ETBF) is linked to both inflammatory bowel disease and colorectal cancer and, in

75 oides fragilis (ETBF) has been implicated in inflammatory bowel disease and colorectal cancer; howeve

76 Management involves assessment for comorbid inflammatory bowel disease and exclusion of other associ

77 oversy over how to best manage patients with inflammatory bowel disease and flat low-grade dysplasia

78 cells, CD70(-/-) T cells caused more severe inflammatory bowel disease and graft-versus-host disease

79 ght the need for research into prevention of inflammatory bowel disease and innovations in health-car

80 Disorders, such as inflammatory bowel disease and irritable bowel syndrome,

81 pus erythematosus (SLE), Sjogren's syndrome, inflammatory bowel disease and multiple sclerosis.

82 rbate chronic inflammatory disorders such as inflammatory bowel disease and rheumatoid arthritis.

83 autoimmune diseases such as atherosclerosis, inflammatory bowel disease and systemic lupus erythemato

84 umulated in chronic inflammation of the gut (inflammatory bowel disease) and lung (chronic obstructiv

85 otal, 208 healthy controls, 40 controls with inflammatory bowel disease, and 327 consecutive patients

86 irin-exacerbated respiratory disease (AERD), inflammatory bowel disease, and acute respiratory distre

87 ant inflammatory diseases, including asthma, inflammatory bowel disease, and arthritis.

88 e, excluding children with immunodeficiency, inflammatory bowel disease, and juvenile arthritis.

89 FMTs for Clostridium difficile infection or inflammatory bowel disease, and most (87%) were non-rand

90 higher comorbidity burden, previous surgery, inflammatory bowel disease, and procedure type.

91 mune diseases, such as rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythemat

92 a variety of autoimmune disorders, including inflammatory bowel disease, and thus are widely consider

93 uding allergy, diabetes, obesity, arthritis, inflammatory bowel diseases, and even neuropsychiatric d

94 ase and ulcerative colitis are heterogeneous inflammatory bowel diseases, and therapeutic requirement

95 el disease, treatment effects in early-onset inflammatory bowel disease are less certain.

96 Inflammatory bowel diseases are chronic gastrointestinal

97 Strategies for management of inflammatory bowel diseases are shifting from simple con

98 Pathologic states, such as inflammatory bowel disease, are associated with a leaky

99 ess the changing incidence and prevalence of inflammatory bowel disease around the world.

100 for immune-related rheumatoid arthritis and inflammatory bowel disease, as well as neuro-degenerativ

101 nd diagnosis of this serious complication of inflammatory bowel diseases, as well as factors that pre

102 thway is an important therapeutic target for inflammatory bowel disease-associated diarrhea.

103 wide association studies have identified 200 inflammatory bowel disease-associated loci, but few have

104 with duodenal adenocarcinoma, as well as in inflammatory bowel disease-associated SBAs.

105 Inflammatory bowel diseases-associated fibrosis was seen

106 prospective study of 80 pregnant women with inflammatory bowel diseases at tertiary hospitals in Den

107 tal sepsis, pelvic inflammatory disease, and inflammatory bowel diseases-at a concentration range of

108 n, type 1 diabetes mellitus, celiac disease, inflammatory bowel disease, autoimmune thyroid disease,

109 ucocorticoids (GCs) are widely used to treat inflammatory bowel disease but their effect on intestina

110 n the intestinal epithelium of patients with inflammatory bowel disease, but its role in pathogenesis

111 with important roles in human metabolic and inflammatory bowel diseases, but a role in host response

112 therapies and antibiotics for patients with inflammatory bowel diseases, but are these immunotherapi

113 Inflammatory bowel disease causes chronic, relapsing int

114 yzing data from women without a diagnosis of inflammatory bowel disease, celiac disease, or liver dis

115 Moreover, DC-LMP1/CD40 chimeras developed inflammatory bowel disease characterized by massive tran

116 targeted genetic association in the Manitoba Inflammatory Bowel Disease Cohort Study was conducted th

117 antagonists reduce many clinical features of inflammatory bowel disease, complete mucosal healing occ

118 No inflammatory bowel disease control had S-ANT <15.

119 ith autoimmune and other diseases, including inflammatory bowel disease, Crohn's disease and rheumato

120 elvic inflammatory disease) and 30ng/mL (for inflammatory bowel diseases) CRP in 1000-fold diluted bl

121 t of rheumatologic conditions, malignancies, inflammatory bowel disease, dermatologic conditions, or

122 incidence or prevalence of paediatric-onset inflammatory bowel disease (diagnosis at age <16 years)

123 The prevalence of inflammatory bowel disease exceeded 0.3% in North Americ

124 ating variants conferring protection against inflammatory bowel disease exploiting knowledge of commo

125 ents undergoing surveillance colonoscopy for inflammatory bowel disease from 1990 to 2015 at the Univ

126 International Inflammatory Bowel Disease Genetics Consortium members f

127 A minority of patients with SBS and inflammatory bowel diseases had colon-in-continuity (10.

128 RPRETATION: At the turn of the 21st century, inflammatory bowel disease has become a global disease w

129 In small studies, inflammatory bowel disease has been associated with the

130 n and dysplasia management for patients with inflammatory bowel disease has changed since this first

131 The evolving genetic architecture of inflammatory bowel disease has deepened our understandin

132 The study of the genetic underpinnings of inflammatory bowel disease has made great progress since

133 BACKGROUND & AIMS: Diarrhea associated with inflammatory bowel diseases has been associated with inc

134 The intestinal mucosa of patients with inflammatory bowel diseases has reduced expression of so

135 microbial co-occurrence in individuals with inflammatory bowel disease (IBD) and healthy (non-IBD co

136 However, health conditions such as inflammatory bowel disease (IBD) are associated with a r

137 Most children with Inflammatory Bowel Disease (IBD) are diagnosed between 1

138 Obesity and inflammatory bowel disease (IBD) are systemic inflammato

139 nform the complex genetic basis of polygenic inflammatory bowel disease (IBD) as well as Mendelian di

140 er disruption presumably plays a key role in inflammatory bowel disease (IBD) development.

141 ur understanding of genetic underpinnings of inflammatory bowel disease (IBD) has undergone a revolut

142 ile infections (CDIs) among individuals with inflammatory bowel disease (IBD) have used data from sin

143 OUND AND AIMS: Immunosuppressive therapy for inflammatory bowel disease (IBD) in pediatric patients i

144 tectin are used in the diagnostic workup for inflammatory bowel disease (IBD) in pediatric patients.

145 Inflammatory bowel disease (IBD) involves interaction be

146 Inflammatory bowel disease (IBD) is a chronic inflammato

147 Inflammatory bowel disease (IBD) is a chronic inflammato

148 Inflammatory bowel disease (IBD) is an autoimmune condit

149 Inflammatory bowel disease (IBD) is associated with alte

150 Inflammatory bowel disease (IBD) is associated with incr

151 Inflammatory bowel disease (IBD) is associated with risk

152 Inflammatory bowel disease (IBD) is characterized by dys

153 Inflammatory bowel disease (IBD) is characterized by fla

154 Inflammatory bowel disease (IBD) is difficult to diagnos

155 rate aberrant intestinal inflammation during inflammatory bowel disease (IBD) is poorly defined.

156 A major challenge in inflammatory bowel disease (IBD) is the integration of d

157 The role of tobacco smoke in the etiology of inflammatory bowel disease (IBD) is unclear.

158 most common question asked by patients with inflammatory bowel disease (IBD) is, "Doctor, what shoul

159 wide association studies have identified 200 inflammatory bowel disease (IBD) loci, but the genetic a

160 sed on genes regulated by variants linked to inflammatory bowel disease (IBD) not only outperform gen

161 Real-life data on inflammatory bowel disease (IBD) prevalence and costs ar

162 as studied in blood samples of patients with inflammatory bowel disease (IBD) receiving anti-TNF ther

163 ctions due to available medical therapies of inflammatory bowel disease (IBD) remains controversial.

164 Children and adolescents with inflammatory bowel disease (IBD) report impairments in d

165 Conversely, patients with inflammatory bowel disease (IBD) that carried an autoimm

166 Severe forms of inflammatory bowel disease (IBD) that develop in very yo

167 member 9 (CARD9), a susceptibility gene for inflammatory bowel disease (IBD) that functions in the i

168 The increased risks conferred by inflammatory bowel disease (IBD) to the development of c

169 therapeutic decision making in patients with inflammatory bowel disease (IBD) who lose response to an

170 is (OA)) or chronic inflammatory conditions (inflammatory bowel disease (IBD)) can be identified.

171 G16L1 is associated with Crohn's disease, an inflammatory bowel disease (IBD), and poor survival in a

172 s disease (CD)-associated colitis or without inflammatory bowel disease (IBD), and whether expression

173 TNF plays an integral role in inflammatory bowel disease (IBD), as evidenced by the dr

174 ostasis is associated with disorders such as inflammatory bowel disease (IBD), but the mechanisms of

175 In inflammatory bowel disease (IBD), compromised restitutio

176 n algorithms on the prevalence of paediatric inflammatory bowel disease (IBD), Crohn's disease (CD) a

177 Inflammatory bowel disease (IBD), including Crohn diseas

178 3/Th17 pathway is essential for the onset of inflammatory bowel disease (IBD), yet the specific mecha

179 for enhancing its efficacy in patients with inflammatory bowel disease (IBD).

180 approximately 75% of patients have comorbid inflammatory bowel disease (IBD).

181 inflammatory macrophages in a mouse model of inflammatory bowel disease (IBD).

182 hildren has been associated with the risk of inflammatory bowel disease (IBD).

183 ncoded by SNPs that are linked to asthma and inflammatory bowel disease (IBD).

184 of diseases including obesity, diabetes, and inflammatory bowel disease (IBD).

185 rphan hepatobiliary disorder associated with inflammatory bowel disease (IBD).

186 d in ulcerative colitis, a major category of inflammatory bowel disease (IBD).

187 ted among patients receiving thiopurines for inflammatory bowel disease (IBD).

188 Vitamin D deficiency is a risk factor for inflammatory bowel disease (IBD).

189 licated in the initiation and progression of inflammatory bowel disease (IBD).

190 orts the first LANCL2-based therapeutics for inflammatory bowel disease (IBD).

191 athogenesis of rheumatoid arthritis (RA) and inflammatory bowel disease (IBD).

192 to play a role in the pathogenesis of human inflammatory bowel disease (IBD).

193 ablishing a vicious cycle leading to chronic inflammatory bowel disease (IBD).

194 nal antibody used for treating patients with inflammatory bowel disease (IBD).

195 ith familial adenomatosis polyposis (FAP) or inflammatory bowel disease (IBD).

196 tribute to the incidence and pathogenesis of inflammatory bowel disease (IBD).

197 nd to have a key role in the pathogenesis of inflammatory bowel disease (IBD).

198 ncurrent cytomegalovirus (CMV) infection and inflammatory bowel disease (IBD).

199 romote the onset and enhance the severity of inflammatory bowel disease (IBD).

200 led TL1A) have been associated with risk for inflammatory bowel disease (IBD).

201 ed with increased risk of or protection from inflammatory bowel disease (IBD).

202 dioic acid (2-PMPA) as a novel treatment for inflammatory bowel disease (IBD).

203 Atg16l1 is associated with susceptibility to inflammatory bowel disease (IBD); however, it remains un

204 ssue from typically developing children with inflammatory bowel disease (IBD; i.e. Crohn's disease or

205 Inflammatory bowel diseases (IBD) affect over 5 million

206 ion, studying its effects in mouse models of inflammatory bowel diseases (IBD) and intestinal mucosal

207 Inflammatory bowel diseases (IBD) are likely driven by a

208 BACKGROUND & AIMS: Many patients with inflammatory bowel diseases (IBD) have ongoing bowel sym

209 n and effector immune responses that mediate inflammatory bowel diseases (IBD) in humans and enteroco

210 BACKGROUND & AIMS: Inflammatory bowel diseases (IBD) increase risk for colo

211 BACKGROUND & AIMS: Diagnosis of inflammatory bowel diseases (IBD) is increasing among el

212 cells (IEC) of children newly diagnosed with inflammatory bowel diseases (IBD) to learn more about pa

213 BACKGROUND & AIMS: The inflammatory bowel diseases (IBD) ulcerative colitis (UC

214 e been tested for therapeutic application in inflammatory bowel diseases (IBD) yet understanding of t

215 ptophan and its metabolites in patients with inflammatory bowel diseases (IBD), and study their assoc

216 Inflammatory bowel diseases (IBD), including Crohn's dis

217 Inflammatory bowel diseases (IBD), such as Crohn disease

218 ponses are implicated in the pathogenesis of inflammatory bowel diseases (IBD).

219 iciency of MSCs systemically administered in inflammatory bowel diseases (IBD).

220 Inflammatory bowel diseases (IBDs) are a set of complex

221 Inflammatory bowel diseases (IBDs) are chronic and impos

222 Inflammatory bowel diseases (IBDs) are defined as chroni

223 Insights into the pathogenesis of inflammatory bowel diseases (IBDs) have provided importa

224 BACKGROUND & AIMS: Inflammatory bowel diseases (IBDs) increase the risk of

225 The gut microbiome plays a central role in inflammatory bowel diseases (IBDs) pathogenesis and prop

226 f chronic inflammatory conditions, including inflammatory bowel diseases (IBDs), herein we investigat

227 are a key pathogenic factor in patients with inflammatory bowel diseases (IBDs), the molecular pathwa

228 teractions are altered during development of inflammatory bowel diseases (IBDs).

229 ines (CAMs), or nonallopathic therapies, for inflammatory bowel diseases (IBDs).

230 d a well-characterized, spontaneous model of inflammatory bowel disease [ie, SAMP1/YitFc (SAMP) mice]

231 than in the general population, the risk of inflammatory bowel disease in children was 80 times high

232 s reported stable or decreasing incidence of inflammatory bowel disease in North America and Europe.

233 ce of HS, but the data on the concurrence of inflammatory bowel disease in patients with HS are limit

234 fore investigated the prevalence and risk of inflammatory bowel disease in patients with HS compared

235 Inflammatory bowel disease includes ulcerative colitis a

236 occur with other diseases, including asthma, inflammatory bowel disease, infections, cerebral palsy,

237 Inflammatory bowel diseases involve the dynamic interact

238 Infantile-onset inflammatory bowel disease (IO IBD) is an invalidating i

239 These include inflammatory bowel diseases, irritable bowel syndrome, a

240 Inflammatory bowel disease is a global disease in the 21

241 Inflammatory bowel disease is associated with psychologi

242 The management of the pregnant patient with inflammatory bowel disease is complicated by multiple pr

243 Heritability of early-onset inflammatory bowel disease is hypothesised to be between

244 The incidence of early-onset paediatric inflammatory bowel disease is increasing worldwide.

245 Inflammatory bowel disease is thought to arise from inap

246 However, the effect of AS II on inflammatory bowel disease is unknown.

247 The pathology of inflammatory bowel diseases is driven by the inflammator

248 ro-apoptotic function in the pathogenesis of inflammatory bowel disease, ischemia-reperfusion injury,

249 Here we report fine-mapping of 94 inflammatory bowel disease loci using high-density genot

250 3p21) were associated with subphenotypes of inflammatory bowel disease, mainly disease location (ess

251 ation has been established between IL-33 and inflammatory bowel disease, mechanistic studies to date,

252 he risks and benefits of using each class of inflammatory bowel disease medication.

253 colon anatomies), and disease features (with inflammatory bowel disease, mesenteric vascular diseases

254 lammatory diseases (rheumatoid arthritis and inflammatory bowel disease), metabolic diseases (atheros

255 In patients with inflammatory bowel diseases, microbiota-reactive CD4(+)

256 o test the activity of TR1 cells in a murine inflammatory bowel disease model, a model that resembles

257 have identified 163 susceptibility loci for inflammatory bowel disease, mostly shared between Crohn'

258 data support a continuum of disorders within inflammatory bowel disease, much better explained by thr

259 uals (controls, n = 13-30) and patients with inflammatory bowel diseases (n = 119; 59 with ulcerative

260 olitis (UC, n = 74) or from patients without inflammatory bowel diseases (n = 22), to measure levels

261 Because of the heavy burden of severe inflammatory bowel disease on patients' health and quali

262 testinal endoscopy was performed to rule out inflammatory bowel disease or gastrointestinal neoplasm

263 previously investigated in individuals with inflammatory bowel diseases or solid-organ transplants,

264 mitochondria in a mouse model of colitis and inflammatory bowel disease patients, and this results in

265 ons for understanding of heterogeneity among inflammatory bowel disease patients.

266 vely correlated with the histology scores of inflammatory bowel disease patients.

267 1 is downregulated in inflamed biopsies from inflammatory bowel disease patients.

268 Pediatric inflammatory bowel disease (pIBD) is a chronic heterogen

269 Paediatric inflammatory bowel disease (PIBD), comprising Crohn's di

270 ficantly ameliorate rheumatoid arthritis and inflammatory bowel disease provide a path for using elec

271 e primary outcome was quality of life on the Inflammatory Bowel Disease Questionnaire (IBDQ) at 12 mo

272 anges in the bowel component of the modified Inflammatory Bowel Disease Questionnaire (IBDQ) score an

273 nd Crohn's Disease Activity Index (CDAI) and Inflammatory Bowel Disease Questionnaire (IBDQ) scores t

274 fference between groups in the change in the Inflammatory Bowel Disease Questionnaire-Bowel Subset (I

275 he pathogenesis of many disorders, including inflammatory bowel disease, sepsis, and inflammatory art

276 core representing all known risk alleles for inflammatory bowel disease showed strong association wit

277 ion of dysplasia detection and management in inflammatory bowel disease since 1925, the year the firs

278 pplied the Montreal classification system of inflammatory bowel disease subphenotypes to 34,819 patie

279 Increasing incidence of inflammatory bowel diseases, such as Crohn's disease, in

280 In patients with active inflammatory bowel disease the mucosal frequencies of CD

281 effective treatment can alter progression of inflammatory bowel diseases, the importance of examining

282 mising strategy that can be used to optimize inflammatory bowel disease therapeutics.

283 itical barrier function in disorders such as inflammatory bowel disease, there has been long-standing

284 on studies have identified 215 risk loci for inflammatory bowel disease, thereby uncovering fundament

285 egy of reactive TDM (in patients with active inflammatory bowel disease) to guide treatment changes c

286 s had a positive effect in the management of inflammatory bowel disease, treatment effects in early-o

287 ther resolve the genetic architecture of the inflammatory bowel diseases ulcerative colitis and Crohn

288 's disease (CD), ulcerative colitis (UC) and inflammatory bowel disease unclassified (IBDU) is a comp

289 s of Crohn's disease, ulcerative colitis, or inflammatory bowel disease unclassified before the age o

290 with IBD (1646 with CD, 583 with UC, and 116 inflammatory bowel disease unclassified) and 5002 indivi

291 tive syndrome 2 (XLP-2) and very-early-onset inflammatory bowel disease (VEO-IBD).

292 ls and intestinal tissues from patients with inflammatory bowel diseases vs controls, we found that r

293 es of polygenic risk (e.g., genetic risk for inflammatory bowel disease was negatively correlated wit

294 s mostly a protective role in infectious and inflammatory bowel diseases, whereas both beneficial and

295 y cytokines were suppressed in patients with inflammatory bowel disease who were on ARB therapy compa

296 A total of 27 pouch patients with inflammatory bowel diseases, who underwent pelvic MRI-DI

297 The relative risk of relapse of quiescent inflammatory bowel disease with psychological therapy ve

298 ptimizing clinical management strategies for inflammatory bowel disease with the use of EGCG treatmen

299 Isolated inflammatory bowel disease without primary sclerosing ch

300 nd anti-inflammatory properties in models of inflammatory bowel disease, yet the underlying molecular