ライフサイエンスコーパス: IBD

1 IBD is nevertheless a challenging example for genomic me

2 IBD patients had a higher prevalence of comorbid conditi

3 IBD-AD had poorer psychological functioning and lower PA

4 IBDs identified on the C subgenome were larger than thos

5 Among 112 IBD patients, LOR/drug persistence was 25.9%/74.1%.

6 treated children in 2010 was defined as >/=2 IBD-related visits with one visit and >/=1 dispensed IBD

7 Prevalence was defined as >/=2 IBD-related visits.

8 underwent new ileostomy; 58% had cancer, 31% IBD; 49% underwent LAR, 27% colectomy, and 14% proctocol

9 ntestinal biopsies from patients with active IBD and in preclinical models of intestinal inflammation

10 yptophan degradation in patients with active IBD.

11 e IL23-receptor gene (IL23R) protect against IBD, and, in animals, blocking IL23 reduces the severity

12 Although IBD is dynamic, microbiome studies have primarily focuse

13 d with age at diagnosis, sex, and ductal and IBD subtypes.

14 or which the association between the SNP and IBD were modified by smoking behavior (meta-analysis Wal

15 I1, MAGI2, MAGI3, PARD3, PTEN, and TJP1) and IBD, Crohn's disease (CD), or ulcerative colitis (UC) we

16 rformed 3 meta-analyses each for CD, UC, and IBD (CD and UC combined), comparing data for never vs ev

17 IBD) as well as Mendelian disease-associated IBD.

18 n CLS (19.0) than patients with asymptomatic IBD (7.3; P < .001) or controls (5.9, P < .001).

19 ucosal healing vs patients with asymptomatic IBD in mucosal healing.

20 are discussed, and new models of team-based IBD care are introduced.

21 n patients with and without IBD, and between IBD patients treated with and without biologics.

22 rofiles were significantly different between IBD and healthy subjects.

23 No mean differences were found between IBD-RE and HC.

24 t allelic associations were observed between IBD and SNPs in MAGI2 (rs6962966) and MAGI3 (rs1343126).

25 omparative reAdmix analysis, complemented by IBD sharing, placed their roots in the region of the Nor

26 depth (PD), clinical attachment level (CAL), IBD depth, and percentage defect fill were recorded at b

27 t the hypothesis that reptarenaviruses cause IBD.

28 iruses, now known as reptarenaviruses, cause IBD, there has been no formal demonstration of disease c

29 n levels of MAGI3, PTEN, and TJP1 in colonic IBD as well as UC mucosa, and between inflammation and i

30 nd increased expression of PTPN22 in colonic IBD mucosa, was observed.

31 Randomized controlled trials comparing IBD medical therapies with no restrictions on language,

32 of attachment achieved in infrabony defects (IBDs) by regenerative treatment.

33 Radiologic assessment of intrabony defects (IBDs) and percentage defect depth reduction (DDR%) was d

34 cy of PRF in treatment of intrabony defects (IBDs) in aggressive periodontitis.

35 only in the treatment of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

36 used to fill periodontal intrabony defects (IBDs), resulting in clinically acceptable responses.

37 ing localized periodontal intrabony defects (IBDs).

38 and refine the regulatory framework defining IBD.

39 Identity by descent (IBD) refers to a haplotype segment of a chromosome inher

40 high amount of shared identical-by-descent (IBD) genomic segments between several Siberian populatio

41 n Markov model (HMM) of identity-by-descent (IBD) states along the genome.

42 er 500 million genetic (identity-by-descent, IBD) connections among 770,000 genotyped individuals of

43 l or large-duct disease, and 70.0% developed IBD at some point.

44 factors may modulate the risk of developing IBD including diets, smoking, lifestyle choices, enteric

45 ildren could affect their risk of developing IBD.

46 revealed microbial signatures for different IBD subtypes, including ulcerative colitis, colonic Croh

47 Inclusion body disease (IBD) is an infectious disease originally described in ca

48 ptarenaviruses cause inclusion body disease (IBD), a serious transmissible disease of snakes.

49 nditions such as inflammatory bowel disease (IBD) are associated with a reduced mucus layer, potentia

50 sis of polygenic inflammatory bowel disease (IBD) as well as Mendelian disease-associated IBD.

51 ys a key role in inflammatory bowel disease (IBD) development.

52 individuals with inflammatory bowel disease (IBD) have used data from single centers or CDI administr

53 sive therapy for inflammatory bowel disease (IBD) in pediatric patients is thought to increase the ri

54 ostic workup for inflammatory bowel disease (IBD) in pediatric patients.

55 Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointe

56 Inflammatory bowel disease (IBD) is a chronic inflammatory disorder and is a major r

57 Inflammatory bowel disease (IBD) is associated with altered microbiota composition a

58 Inflammatory bowel disease (IBD) is associated with increased intestinal permeabilit

59 Inflammatory bowel disease (IBD) is characterized by dysregulation in both cytokines

60 Inflammatory bowel disease (IBD) is difficult to diagnose due to nonspecific and var

61 lammation during inflammatory bowel disease (IBD) is poorly defined.

62 by patients with inflammatory bowel disease (IBD) is, "Doctor, what should I eat?" Findings from epid

63 riants linked to inflammatory bowel disease (IBD) not only outperform genetic risk scores (GRSs) in d

64 eal-life data on inflammatory bowel disease (IBD) prevalence and costs are scarce.

65 of patients with inflammatory bowel disease (IBD) receiving anti-TNF therapy.

66 cal therapies of inflammatory bowel disease (IBD) remains controversial.

67 adolescents with inflammatory bowel disease (IBD) report impairments in daily activities, social inte

68 sks conferred by inflammatory bowel disease (IBD) to the development of colorectal cancer gave rise t

69 in patients with inflammatory bowel disease (IBD) who lose response to anti-TNF therapy.

70 tory conditions (inflammatory bowel disease (IBD)) can be identified.

71 hn's disease, an inflammatory bowel disease (IBD), and poor survival in allogeneic hematopoietic stem

72 litis or without inflammatory bowel disease (IBD), and whether expression levels are associated with

73 integral role in inflammatory bowel disease (IBD), as evidenced by the dramatic therapeutic responses

74 isorders such as inflammatory bowel disease (IBD), but the mechanisms of this process are not clear.

75 the severity of inflammatory bowel disease (IBD).

76 ed with risk for inflammatory bowel disease (IBD).

77 protection from inflammatory bowel disease (IBD).

78 el treatment for inflammatory bowel disease (IBD).

79 in patients with inflammatory bowel disease (IBD).

80 ts have comorbid inflammatory bowel disease (IBD).

81 a mouse model of inflammatory bowel disease (IBD).

82 lyposis (FAP) or inflammatory bowel disease (IBD).

83 pathogenesis of inflammatory bowel disease (IBD).

84 pathogenesis of inflammatory bowel disease (IBD).

85 V) infection and inflammatory bowel disease (IBD).

86 es that mediate inflammatory bowel diseases (IBD) in humans and enterocolitis in mice.

87 KGROUND & AIMS: Inflammatory bowel diseases (IBD) increase risk for colorectal cancer.

88 S: Diagnosis of inflammatory bowel diseases (IBD) is increasing among elderly persons (60 years or ol

89 diagnosed with inflammatory bowel diseases (IBD) to learn more about pathogenesis.

90 n patients with inflammatory bowel diseases (IBD), and study their association with clinical and sero

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

92 Inflammatory bowel diseases (IBD), such as Crohn disease and ulcerative colitis, are

93 administered in inflammatory bowel diseases (IBD).

94 Inflammatory bowel diseases (IBDs) are a set of complex and debilitating diseases for

95 Inflammatory bowel diseases (IBDs) are chronic and impose significant, multidimension

96 pathogenesis of inflammatory bowel diseases (IBDs) have provided important information for the develo

97 KGROUND & AIMS: Inflammatory bowel diseases (IBDs) increase the risk of colorectal cancer.

98 central role in inflammatory bowel diseases (IBDs) pathogenesis and propagation.

99 ions, including inflammatory bowel diseases (IBDs), herein we investigate expression and functions of

100 therapies, for inflammatory bowel diseases (IBDs).

101 development of inflammatory bowel diseases (IBDs).

102 ted visits with one visit and >/=1 dispensed IBD-related drug prescription in 2010.

103 stronger patterns of isolation-by-distance (IBD) than females and males in historic populations.

104 ta indicate that IECs undergo changes during IBD development and could be involved in pathogenesis.

105 matching serum and plasma samples from five IBD patients.

106 9 variant proteins to create a blueprint for IBD therapeutics and recapitulated the mechanism of the

107 itamin D also appear to be a risk factor for IBD.

108 identified MAGI3 as a new candidate gene for IBD.

109 a great need for reliable serum markers for IBD.

110 aled that the effects of smoking on risk for IBD depend on genetic variants.

111 fied 64 SNPs whose association with risk for IBD is modified by tobacco smoking.

112 sifiers in processed foods increase risk for IBD.

113 ese genes have been associated with risk for IBD.

114 associations of genome-wide significance for IBD.

115 tential biomarker and therapeutic target for IBD, and has particular relevance for anti-TNF-resistant

116 on conditioning), IL12B,PTGER4, and TNC for IBD; IL23R, PTGER4, and SNX20 (in strong linkage disequi

117 e SIRT1 might be developed as treatments for IBDs.

118 d IFX concentrations in diluted samples from IBD patients.

119 ated factors for CMV colitis in hospitalized IBD patients were that they were elderly in CD and were

120 ical features of CMV colitis in hospitalized IBD patients.

121 nic epithelial cells from patients with IBD, IBD-cancer, FAP-adenoma, and colorectal cancer, but not

122 ting CARD9 illustrate a path toward improved IBD therapeutics.

123 ly induced in mouse models of colitis and in IBD patients.

124 dulation of intestinal epithelial barrier in IBD, and we have identified MAGI3 as a new candidate gen

125 composition of gut microbiota may change in IBD affected individuals, but whether dysbiosis is the c

126 robiota immune targeting as a new concept in IBD diagnotics.

127 or the inhibitor of apoptosis gene family in IBD pathogenesis.

128 lanatory and predictive clinical genomics in IBD.

129 ta-catenin signaling during ulcer healing in IBD.

130 f human CCDC88B RNA and protein is higher in IBD patient colons than in control colon tissue.

131 Costs were higher in IBD patients treated with biologics (OR = 3.98, CI: 3.72

132 ortance of mitochondrial iron homeostasis in IBD and CRC.

133 factor that drives increased inflammation in IBD.

134 rstanding the metabolic pathways involved in IBD.

135 m dynamic behaviour of the gut microbiome in IBD and differentiate this from normal variation.

136 We discuss the key components of PHM in IBD.

137 y event in FAP-adenoma but is not present in IBD-dysplasia.

138 ds a healthy state and maintain remission in IBD.

139 Thus, CD14 plays a protective role in IBD development by enhancing intestinal barrier function

140 of response (LOR) to adalimumab using TDM in IBD patients.

141 CAL-V achieved by regenerative therapy in IBDs may have retained stability over 5 years.

142 and the results are providing insights into IBD pathogenesis and additional strategies for modulatin

143 fantile-onset inflammatory bowel disease (IO IBD) is an invalidating illness with an onset before 2 y

144 The ANKZF1 mutations identified in IO IBD patients with two mutated ANKZF1 alleles result in d

145 y a pathogenic role in the development of IO IBD.

146 range, 0-9 years), elderly patients had less IBD-specific outpatient health care but more IBD-related

147 We searched the University of Manitoba IBD Epidemiology Database and Manitoba Health CDI databa

148 IBD-specific outpatient health care but more IBD-related hospitalizations and overall health care use

149 All subjects met national IBD surveillance inclusion criteria; 27 were assigned ra

150 Many of these genes were located near IBD susceptibility variants.

151 pared to age and gender matched CMV negative IBD patients (81.8% vs. 51.5%).

152 -dependent covariate, Crohn's disease and no IBD (both vs ulcerative colitis) were associated with a

153 h Crohn's disease (HR, 1.56; P < .001) or no IBD (HR, 1.15; P = .002).

154 y rate didn't differ between the IBD and non-IBD population.

155 ncreased ileal MAGI3 expression level in non-IBD controls.

156 The aetiology of IBD is partly attributed to a deregulated immune respons

157 tations, and surgeries in relation to age of IBD onset (pediatric, <18 years; adults, 18-59 years; el

158 predictive model of the immune component of IBD that informs causal relationships among loci previou

159 Assessing the development of IBD as a time-dependent covariate, Crohn's disease and n

160 testinal wound repair and the development of IBD.

161 ambulatory care visits, shorter duration of IBD, and higher comorbidities were associated with an in

162 uld be aware of the changing epidemiology of IBD and environmental factors that modulate the risk of

163 Hypoxia is a feature of IBD and modulates cellular and mitochondrial metabolism.

164 s the importance of studying the genetics of IBD and other complex diseases in populations beyond tho

165 Observations: The increased incidence of IBD can likely be attributed to more than evolving genet

166 A dramatic increase in the incidence of IBD has been observed in the past 2 decades, mainly in d

167 ity populations had a stronger indication of IBD than medium- to high-density populations; however, t

168 gate diet as it relates to the management of IBD.

169 one or in combination, for the management of IBD.

170 in previously published metabolic markers of IBD.

171 Microbiomes of IBD subjects fluctuate more than those of healthy indivi

172 inhibitor MS-444 in AOM/DSS mice, a model of IBD and inflammatory colon cancer, augmented DSS-induced

173 omise for reducing inflammation in models of IBD.

174 of these disorders and in the modulation of IBD clinical phenotypes over time.

175 al iron dysregulation in the pathogenesis of IBD.

176 o the cells, tissues, and pathophysiology of IBD.

177 Patterns of IBD-sharing directly reconnect Albanian-speaking Arberes

178 The prevalence of IBD seems to be increasing in Switzerland.

179 ims data of the Helsana-Group, prevalence of IBD was assessed for 2010, 2012 and 2014.

180 ogical symptoms, and social ramifications of IBD can guide comprehensive care for the whole patient.

181 The overall extrapolated prevalence rates of IBD were 0.32% in 2010, 0.38% in 2012, and 0.41% in 2014

182 hout IBD correctly classified as low risk of IBD increased from 33% to 91%.

183 pattern associated with an increased risk of IBD.

184 tion, with caution advised in the setting of IBD.

185 ildren and adolescents in an active state of IBD seem to be advised in addition to standard treatment

186 In a prospective cross-over study of IBD patients undergoing surveillance colonoscopy, we fou

187 diatric patients with symptoms suggestive of IBD considerably decreased the number of patients in the

188 ated macroscopic and microscopic symptoms of IBD in the TNBS-induced colitis mouse model, indicating

189 rs a promising approach for the treatment of IBD and potentially other chronic inflammatory condition

190 IL18 might be developed for the treatment of IBD and prevention of colitis-associated tumorigenesis.

191 Treatment of IBD is more and more based on biologic therapies.

192 Treatment of IBD with PRF results in significant improvements of clin

193 ave the potential to aid in the treatment of IBD, but further research is needed to validate these ap

194 ht be promising targets for the treatment of IBD.

195 nisms also are emerging for the treatment of IBD.

196 /GCPII inhibitors for the local treatment of IBD.

197 study to estimate incidence and treatment of IBD.

198 tologous PRF versus PRF + HA in treatment of IBDs in patients with chronic periodontitis.

199 when used along with GTR in the treatment of IBDs in patients with CP in terms of both clinical and r

200 included for analysis, each contributing one IBD.

201 CCDC88B maps within one IBD risk locus on human chromosome 11q13.

202 RNASET2 was the only IBD risk-associated gene with >5-fold down-regulation in

203 had Crohn's disease, ulcerative colitis, or IBD-unclassified with 24,543.0 patient-years of follow-u

204 Fifty subjects per group with RA, PsA, OA or IBD and 50 healthy controls were included in the study.

205 The overall prevalence of paediatric IBD in Sweden was similar to that in earlier regional co

206 drugs in treating patients with periodontal IBDs.

207 iating metabolites could potentially predict IBD risk.

208 in only this population; we also replicated IBD, CD, and UC loci identified in European populations.

209 reditary autoinflammatory disease and severe IBD.

210 ase in PD and more CAL gain with significant IBD depth reduction at sites treated with SRP plus local

211 Intriguingly, the microbiomes of some IBD subjects periodically visited the HP then deviated a

212 Patients with symptomatic IBD had a significantly higher median CLS (19.0) than pa

213 al permeability in patients with symptomatic IBD in mucosal healing vs patients with asymptomatic IBD

214 A condition more common than IBD is low-grade inflammation, which correlates with alt

215 Mortality rate didn't differ between the IBD and non-IBD population.

216 Altered functions for the IBD risk locus containing rs7554511, which encompasses t

217 In the IBD group, Firmicutes, Proteobacteria, Verrucomicrobia,

218 Thus, IBD-associated polymorphisms in INAVA modulate PRR-initi

219 duces new regulators of processes central to IBD but also provides the integrated circuits of genetic

220 , CI: 3.72-4.27, p < 0.001) when compared to IBD patients without biologic therapies.

221 lower PA (average steps per day) compared to IBD-RE and HC.

222 n C or antioxidants transport contributes to IBD development.

223 elationships among loci previously linked to IBD through genome-wide association studies (GWAS) using

224 nd corresponding expressions, in relation to IBD.

225 biome changes may be a marker of response to IBD treatment.

226 the gut microbiome may predict responses to IBD therapy, we conducted a prospective study with Crohn

227 reports that pythons are more susceptible to IBD than boas and could reflect the possibility that boa

228 One hundred twelve IBD patients (with 214 TDM measurements, CD/UC 84/28, ma

229 while reconciling the role of XLP-2 and VEO-IBD XIAP mutations in inflammatory cell death and provid

230 wever, the reported effects of XLP-2 and VEO-IBD XIAP mutations on cell death have been inconsistent.

231 Among adults with IBD, the use of thiopurine monotherapy or anti-TNF monot

232 prising 2345 cases of African Americans with IBD (1646 with CD, 583 with UC, and 116 inflammatory bow

233 association study of African Americans with IBD and identified loci associated with UC in only this

234 , then genetic variations may associate with IBD.This study aimed to determine the substrate(s) for t

235 r TNFSF15), CXCR6, and genes associated with IBD at the HLA locus, contained SNPs with unique associa

236 addition, 9 genes previously associated with IBD contained SNPs with significant evidence for replica

237 stry, but few loci have been associated with IBD in other ethnicities.

238 The detection of variants associated with IBD risk in only people of African descent demonstrates

239 te network regulatory states associated with IBD, prioritizing and prospectively validating 12 of the

240 opulation controls (n = 8583), children with IBD had a higher prevalence of dermatologic (4.7% vs. 0.

241 cription profiles of IECs from children with IBD vs controls; some were independent of mucosal inflam

242 n (median age 13 years) newly diagnosed with IBD (43 with Crohn's disease [CD], 23 with ulcerative co

243 solated from boa constrictors diagnosed with IBD.

244 tion for patients of specific genotypes with IBD.

245 e SLC2A14 gene associated independently with IBD.

246 Individuals with IBD had a 4.8-fold increase in risk of CDI than individu

247 Among individuals with IBD, exposure to corticosteroids, infliximab or adalimum

248 no longer increasing among individuals with IBD.

249 Participants with IBD-AD showed higher erythrocyte sedimentation rate (ESR

250 We studied 535 consecutive patients with IBD (211 with ulcerative colitis [UC], 234 with Crohn's

251 psies and resected tissue from patients with IBD (n = 62) and patients without colon inflammation (co

252 ong-term outcomes of pediatric patients with IBD (NCT00606346), from May 31, 2007 through June 30, 20

253 n a population-based cohort of patients with IBD and laboratory confirmation diagnoses of CDI.

254 pendent cohort of 34 pediatric patients with IBD and macroscopic rectal disease and 17 controls from

255 138 treatment-naive pediatric patients with IBD and macroscopic rectal disease, as well as those fro

256 d in the colonic epithelium of patients with IBD and mice with colitis.

257 ptoms were present in 16.3% of patients with IBD and mucosal healing (15.4% of patients with CD, 17.4

258 fied ongoing bowel symptoms in patients with IBD and mucosal healing with 95.2% sensitivity and 97.6%

259 of intestinal permeability in patients with IBD and mucosal healing, we associated impaired intestin

260 on psychological conditions in patients with IBD are chronic abdominal pain, anxiety, and depression.

261 ated from three populations of patients with IBD at different stages of disease.

262 atterns in IECs from pediatric patients with IBD compared with controls.

263 are used by more than half of patients with IBD during some point in their disease course.

264 alignancy and HLH in pediatric patients with IBD exposed to infliximab (IFX) with patients not expose

265 flamed intestinal tissues from patients with IBD express high amounts of the cytokine oncostatin M (O

266 Based on this cutoff, 36.2% of patients with IBD in mucosal healing have increased intestinal permeab

267 ignificant differences between patients with IBD in remission vs controls (P = .261).

268 an were significantly lower in patients with IBD than in controls (P = 5.3 x 10(-6)) with a stronger

269 Ex vivo, in patients with IBD treated with anti-TNF, we found further evidence for

270 d from gut biopsy specimens of patients with IBD were also analyzed along with plasma 25-hydroxy vita

271 irmed low 25D plasma levels in patients with IBD with active inflammation.

272 icial targeting of IL-23/12 in patients with IBD, 1,25D appears as an interesting therapeutic agent t

273 pria cells in colon tissues of patients with IBD, and mice with colitis, had increased expression of

274 colonic epithelial cells from patients with IBD, IBD-cancer, FAP-adenoma, and colorectal cancer, but

275 o an analysis of more than 200 patients with IBD, including two cohorts from phase 3 clinical trials

276 shown definitively to benefit patients with IBD, soluble fiber is the best way to generate short-cha

277 rum samples from more than 500 patients with IBD, we observed a negative correlation between serum le

278 colorectal cancer, but not in patients with IBD-dysplasia.

279 structure or function to treat patients with IBD-either with individual agents, via dietary managemen

280 inflamed intestinal tissues of patients with IBD.

281 all health care use than adult patients with IBD.

282 e between healthy subjects and patients with IBD.

283 ped as a therapeutic agent for patients with IBD.

284 creased in colon biopsies from patients with IBD.

285 unique risk factors for CDI in patients with IBD.

286 malignancy or HLH in pediatric patients with IBD.

287 iated with disease activity in patients with IBD; there was an inverse association between levels of

288 rogated genetic associations of SLC2A14 with IBD.The uptake of radiolabeled substrates into Xenopus l

289 lity among individuals without IBD than with IBD.

290 the detection of dysplasia in patients with IBDs.

291 e compared between patients with and without IBD, and between IBD patients treated with and without b

292 e, as well as those from 49 children without IBD (controls), enrolled in a multicenter prospective ob

293 ative colitis [UC]), and 30 children without IBD (controls).

294 e unclassified) and 5002 individuals without IBD (controls, identified from the Health Retirement Stu

295 rease in mortality among individuals without IBD than with IBD.

296 ease in risk of CDI than individuals without IBD; we found no difference between individuals with ulc

297 entify individuals with CDI, with or without IBD, from July 1, 2005 through March 31, 2014.

298 he model, the proportion of patients without IBD correctly classified as low risk of IBD increased fr

299 en pediatric patients with and those without IBD, when added to evaluation of symptoms.

300 ts with ulcerative colitis (n=10) vs without IBD (n=8, controls).