ライフサイエンスコーパス: IBD

1 IBD and IBD + CDI have overlapping symptoms but respond

2 IBD has so far been overlooked as a contributor to the b

3 IBD is associated with a variety of musculoskeletal mani

4 IBD is thought to develop as a result of interactions be

5 IBD leads to a breakdown in the integrity of the intesti

6 IBD mother with low PPDS was associated with significant

7 IBD patients were younger than NIC patients (median age

8 IBD phenotype and complications during pregnancy and del

9 In all, 107 patients with CRC, 113 IBD patients with colonic lesions, and 96 participants w

10 485 patients were included in the study: 70 IBD and 415 NIC based on a thorough review of colonoscop

11 The median time from last active IBD episode to immunotherapy initiation was 5 years (int

12 atures were only found in the original adult IBD patient cohort.

13 cted in either a pediatric or a second adult IBD cohort.

14 flecting in part substantially lower African IBD case-control reference sizes.

15 irst-step towards a multi-factorial amenable IBD platform that could be scaled up to assess compound

16 Increasing African American IBD case-collections should be prioritized to reduce hea

17 We develop FastSMC, an IBD detection algorithm that combines a fast heuristic s

18 potential to shift gut microbiota towards an IBD-like composition.

19 ared molecular networks between COVID-19 and IBD.

20 reciation of the confluence of COVID-19- and IBD-associated inflammation and provide mechanistic insi

21 evidence for an association between CeD and IBD.

22 fill in the two questionnaires IBD Disk and IBD-DI at baseline, then between 3 and 12 months later,

23 IBD and IBD + CDI have overlapping symptoms but respond to disti

24 , we studied pediatric patients with IBD and IBD + CDI, comparing longitudinal data on the gut microb

25 reduced risk of SGA compared to non-IBD and IBD mothers with high PPDS.

26 ng the risk of CeD in patients with IBD, and IBD in patients with CeD, compared with controls of any

27 d associations between specific microbes and IBD.

28 y lower risk of SGA than non-IBD mothers and IBD mothers with high PPDS (aOR = 0.19, 95% CI: 0.07, 0.

29 etic risk factors are shared between SpA and IBD, and changes in the composition of gut microbiota ar

30 eeded to assess the risk of CeD-specific and IBD-specific biomarkers in patients with IBD and CeD.

31 etween nutritional manganese (Mn) status and IBD patients.

32 e evaluate hap-IBD and four state-of-the-art IBD segment detection methods (GERMLINE, iLASH, RaPID, a

33 The median age at IBD diagnosis was 55 years (range 29-85 years).

34 onal threads detects 231.5 billion autosomal IBD segments with length >=2 cM in 24.4 h.

35 lf-siblings-using the locations of autosomal IBD segments shared between the pair.

36 discusses the epidemiological links between IBD and ASCVD and potential mechanisms underlying these

37 9 UK Biobank samples and detect ~214 billion IBD segments transmitted by shared ancestors within the

38 antify endpoint uncertainty for 77.7 billion IBD segments from 408,883 individuals of white British a

39 Variants believed to cause IBD were validated using Sanger sequencing.

40 IBIS is also accurate, inferring >=7 cM IBD segments at quality comparable to Refined IBD and GE

41 accurately detect short 2-4 centiMorgan (cM) IBD segments in the full UK Biobank data.

42 We found that the common IBD-associated rs1517352 C risk allele increased both ST

43 information for the differentiation of CRC, IBD and NTC on CT, particularly in PVP images.

44 used to prevent, manage, and eventually cure IBD.

45 ABG in the management of intrabony defects (IBDs).

46 s for fast detection of identity by descent (IBD) segments report identity by state segments without

47 CREST utilizes identity by descent (IBD) segments shared between a pair of samples and their

48 nship coefficients from identity by descent (IBD) segments.

49 Identity-by-descent (IBD) segments are a useful tool for applications ranging

50 Here we describe IBD as a model disease in the context of leveraging huma

51 e UK Biobank who share at least one detected IBD segment with length >= 4 cM.

52 We show that hap-IBD detects IBD segments faster and more accurately than competing m

53 acid (AA), which entails risk for developing IBD.

54 These were associated with different IBD phenotypes, and 1% of the patients had variants that

55 population with inflammatory bowel disease (IBD) and Non-IBD/Non-Infectious Colitis (NIC).

56 gh prevalence of inflammatory bowel disease (IBD) and the even higher occurrence of subclinical gut i

57 in patients with inflammatory bowel disease (IBD) and those with experimental colitis.

58 Patients with inflammatory bowel disease (IBD) are at increased risk of invasive pneumococcal infe

59 uman cohorts: an inflammatory bowel disease (IBD) cohort, an obese cohort and two population-based co

60 is (UC), and non-inflammatory bowel disease (IBD) controls.

61 sed incidence of inflammatory bowel disease (IBD) has become a global phenomenon that could be relate

62 with cancer and inflammatory bowel disease (IBD) has not been well described.

63 Patients with inflammatory bowel disease (IBD) have an increased risk of colorectal cancer (CRC).

64 Studies of inflammatory bowel disease (IBD) have been inconclusive in relating microbiota with

65 ndrome (IBS) and inflammatory bowel disease (IBD) intersect to form a scantily defined overlap syndro

66 Inflammatory bowel disease (IBD) is a chronic disorder characterized by inflammation

67 Inflammatory bowel disease (IBD) is a chronic immune-mediated disease affecting the

68 Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with i

69 Inflammatory bowel disease (IBD) is a common chronic inflammatory condition, and the

70 Inflammatory bowel disease (IBD) is a complex genetic disease that is instigated and

71 Inflammatory bowel disease (IBD) is a debilitating chronic disease with limited trea

72 Inflammatory bowel disease (IBD) is associated with the production of reactive speci

73 ically suspected inflammatory bowel disease (IBD) is not well defined, and its correlation with clini

74 gnant women with inflammatory bowel disease (IBD) may require biologic or thiopurine therapy to contr

75 ations (EIMs) in inflammatory bowel disease (IBD) patients, and they are responsible for a relevant r

76 ction of Arg1 in inflammatory bowel disease (IBD) remains poorly characterized.

77 used to predict inflammatory bowel disease (IBD) risk in prevention efforts.

78 hronic relapsing inflammatory bowel disease (IBD) that may be marked by debilitating symptoms of abdo

79 the severity of inflammatory bowel disease (IBD)(2,5), the diverse immunomodulatory phenotypes remai

80 esions caused by inflammatory bowel disease (IBD), and normal thickened colon wall (NTC) on computed

81 cal challenge in inflammatory bowel disease (IBD), due, in part, to insufficient understanding of dis

82 stine, including inflammatory bowel disease (IBD), graft-versus-host disease (GVHD), and cancer.

83 Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative coli

84 or patients with inflammatory bowel disease (IBD), who have failed azathioprine (AZA) or mercaptopuri

85 in patients with inflammatory bowel disease (IBD).

86 nd patients with inflammatory bowel disease (IBD).

87 e development of inflammatory bowel disease (IBD).

88 in patients with inflammatory bowel disease (IBD).

89 oms in quiescent inflammatory bowel disease (IBD).

90 pathogenesis of inflammatory bowel disease (IBD).

91 (Mphis) leads to inflammatory bowel disease (IBD).

92 ibility gene for inflammatory bowel disease (IBD).

93 om patients with inflammatory bowel disease [IBD]) or mouse macrophages, respectively.

94 Inflammatory Bowel Diseases (IBD) affect psychological, family, social and profession

95 Inflammatory bowel diseases (IBD) are associated with alterations in gut microbial ab

96 Children with inflammatory bowel diseases (IBD) are particularly vulnerable to infection with Clost

97 of adults with inflammatory bowel diseases (IBD).

98 n patients with inflammatory bowel diseases (IBDs) and differences in inflammatory responses of patie

99 emiology of the inflammatory bowel diseases (IBDs) is changing.

100 a treatment for inflammatory bowel diseases (IBDs), but there are no established associations between

101 Inflammatory bowel diseases (IBDs), including Crohn's disease and ulcerative colitis,

102 iseases such as inflammatory bowel diseases (IBDs), is often associated with dysbiosis, particularly

103 arly evident in inflammatory bowel diseases (IBDs), where clinical trials of fecal microbiota transpl

104 or treatment of inflammatory bowel diseases (IBDs).

105 1.8) for UC, and 16.8 (95% CI 13.9-20.3) for IBD.

106 sk of infections after immunosuppression for IBD.

107 g extensive dysbiosis, with implications for IBD prevention and therapy.

108 nflammatory responses, with implications for IBD.

109 preventive agent and therapeutic target for IBD.

110 oral steroids and the underlying therapy for IBD can reduce or cut out at all the recurrence of these

111 starches may represent a novel treatment for IBD.

112 prophylactic and therapeutic treatments for IBDs.

113 Although proteomics data from IBD mouse models exist, data and phenotype discrepancies

114 Our method, called hap-IBD, combines a compressed representation of haplotype d

115 We evaluate hap-IBD and four state-of-the-art IBD segment detection meth

116 An attractive feature of hap-IBD is its simplicity: the input parameters clearly and

117 46 UK Biobank samples through the use of hap-IBD with 12 computational threads detects 231.5 billion

118 We show that hap-IBD detects IBD segments faster and more accurately than

119 urately than competing methods, and that hap-IBD is the only method that can rapidly and accurately d

120 at VEO-IBD patients have, on average, higher IBD polygenic risk scores than population controls (99 p

121 Human IBD is modeled by administering dextran sulfate sodium (

122 cantly increased in inflamed mucosa of human IBD patients and in human colorectal adenocarcinoma, acc

123 t a novel approach to the treatment of human IBD.

124 rt of the integrative human microbiome (iHMP-IBD) project.

125 In IBD + CDI, we detect both metabolites associated with in

126 ccess of therapies blocking TNF and IL-23 in IBD and in some forms of SpA.

127 Adenoma prevalence was 4.3% (3/70) in IBD patients and 3.9% (16/415) in the NIC patients (p =

128 abolites that are differentially abundant in IBD on the growth and physiology of gut bacteria that ar

129 ria that are also differentially abundant in IBD.

130 y targeting molecules such as alpha4beta7 in IBD can lead to onset or flares of SpA.

131 that inflammatory polyps are more common in IBD patients when compared to NIC patients.

132 le in daily practice to assess disability in IBD patients.

133 a class of metabolites that are elevated in IBD and have the potential to shift gut microbiota towar

134 COVID-19 infection that are also enriched in IBD, pointing to shared molecular networks between COVID

135 Compromised barrier is a key event in IBD pathogenesis.

136 o the lowest PPDS group was twice as high in IBD mothers compared to non-IBD mothers (aOR = 2.02, 95%

137 Disease activity was higher in IBD participants with a more pro-inflammatory diet with

138 stinal microbiota in driving inflammation in IBD, the gut microbiome composition was not altered by c

139 rve as a target for clinical intervention in IBD patients.

140 duced SB but elevated colonic ACE2 levels in IBD are associated with inflammation and severe disease,

141 ws that intake of dairy products is lower in IBD mothers than in non-IBD mothers, and further, that l

142 tinal inflammation, such as that observed in IBD.

143 ll gene transcription and disease outcome in IBD.

144 ger correlated with dysregulated pathways in IBD patients.

145 d race, odds ratio of inflammatory polyps in IBD patients was 6.0 (P = 0.016).

146 mmunogenicity of PCV13 followed by PPSV23 in IBD patients by measuring serotype-specific pneumococcal

147 urther, that low intake of dairy products in IBD mothers is associated with reduced risk of SGA compa

148 s) newly included in the targets to reach in IBD patients.

149 s, and improvements in clinical remission in IBD patients.

150 mutations potentially play a causal role in IBD pathogenesis.

151 ositively associated with the risk of SGA in IBD mothers.

152 (GWG) or small for gestational age (SGA) in IBD compared to non-IBD in the population-based Norwegia

153 The production of reactive species in IBD is reflected by a reduction in systemic free thiols,

154 or therapeutic modulation of redox status in IBD.

155 RC risk stratification-based surveillance in IBD.

156 fficacy and safety of low-dose TG therapy in IBD patients failing AZA and MP.

157 s, including amelioration of inflammation in IBDs.

158 r the treatment of patients with co-incident IBD and SpA and for the repurposing of therapeutics from

159 een microscopic colitis and risk of incident IBD using data from a nationwide cohort study.

160 through 2017 in Sweden and risk of incident IBD.

161 t completes this analysis in 2.8 h including IBD detection in eight threads.

162 f TNBS, 10 rats were fed exclusively MODULEN IBD(R) powder, while remaining rats were fed breeding ch

163 Treatment with MODULEN IBD(R) was associated with growth failure, increased col

164 Monogenic IBD is rare, but should be considered in analysis of all

165 Features associated with monogenic IBD, compared to cases of IBD not associated with a sing

166 ermeability and neutrophil activity in mouse IBD models using near infrared (NIR) detection.

167 d 194 with ulcerative colitis and 68,858 non-IBD mothers.

168 nic cohorts; n = 495; n = 387 UC; n = 94 non-IBD), we analyzed the relationship between ACE2 with dem

169 ith inflammatory bowel disease (IBD) and Non-IBD/Non-Infectious Colitis (NIC).

170 products is lower in IBD mothers than in non-IBD mothers, and further, that low intake of dairy produ

171 with IBD in the 2 cohorts that included non-IBD controls.

172 ith significantly lower risk of SGA than non-IBD mothers and IBD mothers with high PPDS (aOR = 0.19,

173 Surprisingly, and in opposition to the non-IBD mothers, PPDS was positively associated with the ris

174 ted with reduced risk of SGA compared to non-IBD and IBD mothers with high PPDS.

175 gestational age (SGA) in IBD compared to non-IBD in the population-based Norwegian Mother, Father and

176 twice as high in IBD mothers compared to non-IBD mothers (aOR = 2.02, 95% CI: 1.53, 2.67).

177 and elevated in colonic UC compared with non-IBD controls.

178 model the human intestine and key aspects of IBD.

179 ted with monogenic IBD, compared to cases of IBD not associated with a single variant, were age of on

180 We identified incident cases of IBD, with PSC (PSC-IBD) and without, from April 2006 to

181 ts in the development and clinical course of IBD, and strategies by which microbiome-based therapies

182 iminated by the use of unbiased estimates of IBD segment endpoints and a pedigree-based genetic map.

183 enic, and thus beneficial in the majority of IBD patients, those receiving immunosuppressive agents,

184 leritis are common defined as a good mark of IBD activity.

185 charomyces antibodies, a serologic marker of IBD, in patients with CeD vs controls (RR 6.22; 95% CI 2

186 tabolites to a major immunological marker of IBD.

187 ease (VEOIBD) denotes children with onset of IBD before six years of age.

188 ysis of all patients with pediatric onset of IBD.

189 Forty six percent of IBD and 41% of NIC cases were male.

190 validate this tool in a large population of IBD patients and to compare it to the already validated

191 derstand the epidemiology and progression of IBD in different racial and ethnic groups, and the effec

192 macrophages contribute to the progression of IBD whereas immunosuppressive M2 macrophages protect aga

193 meta-analysis, we found an increased risk of IBD in patients with CeD and increased risk of CeD in pa

194 The role of IBD in current primary prevention guidelines is evaluate

195 Nowadays, in the setting of IBD-related arthritides, different drugs are available a

196 al therapeutic strategy for the treatment of IBD but also a model through which S-palmitoylation regu

197 n, and gene manipulation in the treatment of IBD.

198 ree patients were not receiving treatment of IBD.

199 One hundred forty-one IBD patients were included, of whom 37 were controls.

200 ed in genes associated with very early-onset IBD (VEO-IBD), by estimating genetic penetrance in each

201 PSCs) were generated from an infantile-onset IBD patient lacking a functional IL10RB gene.

202 atients with monogenic ulcerative colitis or IBD-unclassified received their diagnosis at a younger a

203 ates mitochondrial activity, ameliorated pre-IBD symptoms.

204 exacerbate inflammation and distinguish pre-IBD from IBS.

205 ance distinguish the fecal microbiota of pre-IBD patients from IBS patients.

206 actors resulted in conditions resembling pre-IBD and impaired mitochondrial bioenergetics in the colo

207 cantily defined overlap syndrome, termed pre-IBD.

208 As with patients, mice with pre-IBD exhibited notable expansions of Enterobacteriaceae t

209 ease of their implementation in preclinical IBD research.

210 s which combination of scores best predicted IBD status in European, AJ, Hispanic, and African Americ

211 Preexisting IBD increases the risk of severe GI adverse events in pa

212 flammatory Bowel Disease-Specific Programme (IBD-DSP) were used.

213 ntified incident cases of IBD, with PSC (PSC-IBD) and without, from April 2006 to April 2016 and coll

214 e study, we confirmed that patients with PSC-IBD have increased risks of CRC, hepatopancreatobiliary

215 Among patients with PSC-IBD we observed 173 first liver transplants.

216 utationally efficient method for quantifying IBD segment endpoint uncertainty is implemented in the o

217 patient will fill in the two questionnaires IBD Disk and IBD-DI at baseline, then between 3 and 12 m

218 s of inflammation in patients with quiescent IBD.

219 tent gut symptoms in patients with quiescent IBD.

220 biobank to define effects of common and rare IBD variants on disease prediction and pathophysiology.

221 kes 4.3 CPU days, followed by either Refined IBD or GERMLINE segment detection in 2.9 or 1.1 h, respe

222 BD segments at quality comparable to Refined IBD and GERMLINE.

223 cies and 1,050 pathway co-abundances showing IBD-specific effects and 281 pathway co-abundances showi

224 supporting further investigation of specific IBD drugs in the treatment of COVID-19.

225 microscopic ileitis in clinically suspected IBD is associated with increased risk of future diagnosi

226 s part of a diagnostic work-up for suspected IBD.

227 meta-analyses of cohort studies suggest that IBD is an independent risk factor for ASCVD.

228 The IBD group shows increased concentrations of markers of i

229 parameters clearly and precisely define the IBD segments that are reported, so that program correctn

230 co-abundances in longitudinal data from the IBD cohort of the integrative human microbiome (iHMP-IBD

231 However, the IBD Disk has not been validated yet in clinical practice

232 all types of polyps was 15.7 and 8.2% in the IBD and NIC groups, respectively (P = 0.045).

233 nce of inflammatory polyps was higher in the IBD group (55%) compared to the NIC group (12%).

234 Other psychometric criteria of the IBD Disk will also be analysed as its reliability or its

235 t will allow to evaluate the validity of the IBD Disk with respect to the IBD-DI in order to generali

236 e percent of the NIC patients and 81% of the IBD patients were African Americans.

237 ertainty in the endpoints and lengths of the IBD segments.

238 validity of the IBD Disk with respect to the IBD-DI in order to generalize its use for clinical pract

239 study is the study designed to validate the IBD Disk, a visual tool easily useable in daily practice

240 patients (27% vs. 5%, P < 0.001) within the IBD group.

241 We can also replicate these IBD microbial co-abundances in longitudinal data from th

242 ancestry in the UK Biobank, and we use these IBD segments to find regions showing evidence of recent

243 on and impaired host defense contributing to IBD pathogenesis.

244 issecting pathological mechanisms underlying IBD has led to the development of transformative approac

245 at among similar patients without underlying IBD who were treated at centers participating in the stu

246 Commonly used IBD medications, both biologic and nonbiologic, do not s

247 s and to compare it to the already validated IBD-DI.

248 We also present a case study of a VEO-IBD patient with a mosaic de novo, pathogenic allele in

249 es associated with very early-onset IBD (VEO-IBD), by estimating genetic penetrance in each BioMe pop

250 s that a polygenic component operates in VEO-IBD pathogenesis.

251 this finding in an independent cohort of VEO-IBD cases and controls (117 patients and 2,603 controls;

252 Finally, we show that VEO-IBD patients have, on average, higher IBD polygenic risk

253 We replicated associations for two VEO-IBD genes, ADAM17 and LRBA, with high dominant model pen

254 f the 485 patients, 415 were NIC and 70 were IBD.

255 l comprising 136 patients with PSC (58% with IBD), 158 HCs, and 93 patients with IBD without PSC, wer

256 ne transcription was clearly associated with IBD in the 2 cohorts that included non-IBD controls.

257 nic genes among 31 of the 1005 children with IBD (including 5 variants in XIAP, 3 in DOCK8, and 2 eac

258 m an unselected cohort of 1005 children with IBD, aged 0-18 years (median age at diagnosis, 11.96 yea

259 Twenty-four patients with IBD (11 with Crohn's disease [CD], 13 with ulcerative co

260 Colon biopsy specimens from patients with IBD (30 with Crohn's disease and 27 with ulcerative coli

261 cancers, and death compared to patients with IBD alone.

262 and IBD-specific biomarkers in patients with IBD and CeD.

263 Here, we studied pediatric patients with IBD and IBD + CDI, comparing longitudinal data on the gu

264 ping prognostic biomarkers for patients with IBD and the importance of their validation in large, ind

265 s in the mucosa and blood from patients with IBD and without IBD (controls) at single-cell resolution

266 hanced ASCVD risk reduction in patients with IBD are outlined.

267 Macrophages from patients with IBD carrying a single-nucleotide polymorphism associated

268 estimate the risk of polyps in patients with IBD compared to those with NIC after adjusting for age a

269 gut microbiome is different in patients with IBD compared with that in healthy control subjects.

270 Intestinal mucosa from patients with IBD exhibited reduced levels of both HuR and ATG16L1.

271 Patients with IBD had a slight decrease in risk of anti-endomysial ant

272 s, colonic mucosa samples from patients with IBD had increased abundances of HLA-DR+CD38+ T cells, in

273 Colon tissues from patients with IBD had reduced levels of CRT messenger RNA compared wit

274 ASCVD risk management of patients with IBD is challenging because of their young age and the in

275 e in risk of HLA-DQ2 or DQ8 in patients with IBD vs controls (RR 1.04; 95% CI 0.42-2.56), and very lo

276 nti-tissue transglutaminase in patients with IBD vs controls (RR 1.52; 95% CI 0.52-4.40).

277 abundances of some bacteria in patients with IBD vs controls, but we cannot make conclusions due to i

278 decreased or not different in patients with IBD vs controls.

279 intestinal tissue samples from patients with IBD vs controls.

280 58% with IBD), 158 HCs, and 93 patients with IBD without PSC, were subjected to metagenomic shotgun s

281 s assessing the risk of CeD in patients with IBD, and IBD in patients with CeD, compared with control

282 D and increased risk of CeD in patients with IBD, compared with other patient populations.

283 evels in mucosal biopsies from patients with IBD.

284 ferric carboxymaltose (FCM) in patients with IBD.

285 sease in a cohort of pediatric patients with IBD.

286 g health equity among minority patients with IBD.

287 might reduce infection risk in patients with IBD.

288 gh-grade dysplasia, or CRC) in patients with IBD.

289 d barrier function observed in patients with IBD.

290 es) among patients (adult or pediatric) with IBD vs healthy individuals (controls).

291 Uveitis are unrelated with IBD activity and they even precede the onset of the inte

292 Between 2007 and 2019, pregnant women with IBD were enrolled in a prospective, observational, multi

293 and blood from patients with IBD and without IBD (controls) at single-cell resolution.

294 rvational study of patients with and without IBD evaluated serum phosphate for 28 days following intr

295 rom 3 adult patient cohorts with and without IBD were included in data analyses.

296 ifferences between patients with and without IBD were seen, but patients with CD had greater decline

297 y sources (PPDS) in mothers with and without IBD, and to explore the impact of PPDS on inadequate ges

298 d between patients with PSC with and without IBD.

299 ulcerative colitis) and 30 patients without IBD (control individuals) and colon tissues from mice (w

300 e 19-90], 7 female), and 20 patients without IBD (mean age 56 [22-88] y, 11 female), were included.