ライフサイエンスコーパス: colitis

1 had Crohn's disease, and half had ulcerative colitis.

2 eting casein kinase 2 (CK2) also ameliorated colitis.

3 that Gal2 deficiency ameliorated DSS-induced colitis.

4 eading to high susceptibility to DSS-induced colitis.

5 be of benefit in the prevention/treatment of colitis.

6 permeability and immune responses leading to colitis.

7 ae abundance, with subsequent improvement of colitis.

8 an sodium sulfate (DSS)-, and T-cell-induced colitis.

9 recovery from dextran sulfate sodium-induced colitis.

10 ed Il10(-/-) mice, which develop spontaneous colitis.

11 trol donors into DSS recipients and reducing colitis.

12 required for T(reg)-mediated suppression of colitis.

13 t activation of CD8(+) T cells, resulting in colitis.

14 el disease (IBD) and those with experimental colitis.

15 ntly been successfully applied to ulcerative colitis.

16 ruction, and fulminant Clostridium difficile colitis.

17 while a xusA mutant colonized poorly during colitis.

18 its deficit worsens infectious and chemical colitis.

19 symptoms like diarrhea and pseudomembranous colitis.

20 served in the hippocampus during chronic DSS colitis.

21 % colon cancer cases are closely linked with colitis.

22 out its effects on the gut-brain axis during colitis.

23 arkedly decreased in the colon mucosa during colitis.

24 lls were less able to induce T cell-mediated colitis.

25 ulating the inflammation in the colon during colitis.

26 nging from mild diarrhea to pseudomembranous colitis.

27 lysozyme-sensitive bacteria and exacerbated colitis.

28 ntly attenuated the severity of experimental colitis.

29 ith increased susceptibility to experimental colitis.

30 ferred to Lacc1(-/-)Rag2(-/-) mice to induce colitis.

31 nosuppressive M2 macrophages protect against colitis.

32 ed adults with Crohn's disease or ulcerative colitis.

33 exhibited liver inflammation associated with colitis.

34 Most polyps were in the same location as the colitis.

35 bers of colon tumors in Apc(Min/+) mice with colitis.

36 served resistance of infants to C. difficile colitis.

37 l influences, such as diabetes or ulcerative colitis.

38 s compared with control mice or mice without colitis.

39 inal inflammation after induction of chronic colitis.

40 sociated with future diagnosis of ulcerative colitis.

41 ot wild Treg, were protected from developing colitis.

42 CD4(+) regulatory T cell-mediated control of colitis.

43 reduction in Th17 cells and protection from colitis.

44 patients with Crohn's disease and ulcerative colitis.

45 hemical and genetic models of non-infectious colitis.

46 contribution of claudin-2 to immune-mediated colitis.

47 autoimmune disease with ICI-induced T1D and colitis.

48 signaling in VEOIBD patients with apoptotic colitis.

49 IL-33 during dextran sodium sulfate-induced colitis.

50 sulfate sodium (DSS)-induced mouse model of colitis.

51 unction maintenance and in the prevention of colitis.

52 stinal disease tolerance during experimental colitis.

53 ts hospitalized with acute severe ulcerative colitis.

54 hology in a model of T-cell transfer-induced colitis.

55 zyme (Lyz1) protected mice from experimental colitis.

56 ded hepatitis (0% and 13%, respectively) and colitis (0% and 7%, respectively).

57 At diagnosis, left colitis (61% vs 39%) and proctitis (14% vs 26%) (p = 0.0

58 -cell analysis of immune cell populations in colitis, a common and severe side effect of checkpoint b

59 Activity (sCDAI) or Patient Simple Clinical Colitis Activity Index (P-SCCAI)) and a Food Frequency Q

60 es, N = 627; P = .035), Pediatric Ulcerative Colitis Activity Index score (4 studies, n = 318; P < .0

61 , and one each with constitutional symptoms, colitis, adrenal insufficiency, hyperglycaemia, and hypo

62 suggest distinct selection mechanisms in the colitis-affected colon and that somatic mutations potent

63 is that develops in patients with ulcerative colitis after total proctocolectomy and ileal pouch anal

64 h Crohn disease (CD) and 194 with ulcerative colitis and 68,858 non-IBD mothers.

65 c value for inflammatory disorders including colitis and also for transplantation.

66 to human health due to its ability to induce colitis and cause colon tumor formation in mice through

67 However, the genetic factors regulating colitis and colon tumorigenesis remain elusive.

68 al inflammatory diseases, such as ulcerative colitis and Crohn's disease.

69 lammatory bowel disease including ulcerative colitis and Crohn's disease.

70 ng cause of nosocomial antibiotic-associated colitis and diarrhea in the industrialized world, trigge

71 the effects of wheat and ATIs on severity of colitis and fecal microbiota in mice.

72 oblasts (Rag(-/-)Dr3(DeltaCol1a2)) to induce colitis and fibrosis, assessed by clinical disease activ

73 us ileitis, and exacerbates induced proximal colitis and fibrosis.

74 severe disease outcomes such as hemorrhagic colitis and hemolytic uremic syndrome.

75 increased sensitivity to chemically induced colitis and impaired proliferation in the setting of acu

76 opsy specimens from patients with ulcerative colitis and inactive Crohn's disease have lower levels o

77 III secretion system, leading to infectious colitis and inflammation.

78 against various intestinal diseases such as colitis and intestinal tumorigenesis.

79 he role of the environment in malignancy and colitis and is consistent with Notch-dependent anti-para

80 the gut-brain axis in a model of DSS-induced colitis and its implication on the "secondary" effects a

81 virus model for producing severe vasculitis, colitis and lethal hemorrhagic pneumonia in interferon g

82 ial use in experimental models of ulcerative colitis and lung allograft rejection led us to test the

83 estine tissues from patients with ulcerative colitis and mice with colitis have increased levels of I

84 ult intestinal epithelium causes mild active colitis and mild-to-moderate active enteritis.

85 with quiescent Crohn's disease or ulcerative colitis and persistent gut symptoms at 2 large gastroent

86 ey have shown promise in clinical trials for colitis and psoriasis.

87 e E3 ligase Itch, which leads to spontaneous colitis and rectal prolapse, is associated with alterati

88 studied the association between microscopic colitis and risk of incident IBD using data from a natio

89 related death occurred in one patient due to colitis and sepsis.

90 -deficiency showing increased sensitivity to colitis and skewed composition of fecal microbiota.

91 otective role for PAFR-expressing KCs during colitis and that regulation of PAFR is important for gut

92 ent mice were subject to severe experimental colitis and that such colitis was normalized by administ

93 ic arthritis, Crohn's disease, or ulcerative colitis and who were in commercial health plans from 201

94 y reduces the severity of chemically induced colitis and wild type (WT) mice co-housed with Fam3D(-/-

95 of amebiasis, an infection that manifests as colitis and, in some cases, liver abscess.

96 were given dextran sodium sulfate to induce colitis and/or gavage with an antagonist to MIR200C-3p (

97 with Crohn's disease and 27 with ulcerative colitis) and 30 patients without IBD (control individual

98 disease by IDSA criteria, baseline fulminant colitis, and fever of >38.5 degrees C.

99 n patients (phase 1b study: hospitalization, colitis, and potential drug-induced liver injury) and on

100 f IL-23-driven acanthosis, anti-CD40-induced colitis, and spontaneous lupus, will also be presented.

101 s), including Crohn's disease and ulcerative colitis, are associated with dysbiosis of the gut microb

102 mebic dysentery and Clostridioides difficile colitis as enteric infections profoundly influenced by t

103 reased tolerance to DSS-induced experimental colitis, as judged by the colon length.

104 arding predictors of colectomy, acute severe colitis (ASC), chronically active pediatric UC, cancer a

105 increased sensitivity to chemically induced colitis associated with high incidence of cancer.

106 nto Rag2-deficient mice elicited more severe colitis associated with increased serum concentrations o

107 term exposure to chronic inflammation drives colitis-associated colon cancer (CAC) in patients with i

108 inked to chronic intestinal inflammation and colitis-associated colorectal cancer (CAC).

109 lso promotes tumor development in a model of colitis-associated colorectal cancer, associated with an

110 ry to medical treatment or those who develop colitis-associated colorectal dysplasia or cancer, still

111 vated in tissues from patients with colitis, colitis-associated dysplasia, and CAC as well as in dysp

112 romotes colon tumorigenesis in a preclinical colitis-associated tumor model by upregulating FoxM1 sig

113 r colon tumor formation in a murine model of colitis-associated tumorigenesis and STEAP4 expression c

114 oxygen species and increased development of colitis-associated tumors.

115 t can predict clinical outcome in ulcerative colitis at time of diagnosis.

116 is spanning prediction tasks from ulcerative colitis, atopic dermatitis, diabetes, to many cancer sub

117 on, decreases peristalsis, and protects from colitis because of decreased serotonin.

118 inib is effective in treatment of ulcerative colitis, but there are safety concerns.

119 ed oral pathobionts and cause development of colitis, but they are not activated by gut-resident micr

120 ermeability associated with a mouse model of colitis by maintaining the integrity of the apical junct

121 Colitis caused by Clostridium difficile infection is a g

122 sidual microbiota influences the severity of colitis caused by infection with Clostridioides difficil

123 bowel diseases-Crohn disease and ulcerative colitis-caused by untoward reactivity of the immune syst

124 Collagenous colitis (CC) is an inflammatory bowel disorder with unkn

125 of IRF4 expression in cDC2 in T cell-driven colitis, CD11c-Cre.Irf4 (fl/fl) and Irf4 (fl/fl) mice we

126 quencing in a VEOIBD patient presenting with colitis characterized by colonic apoptosis and no identi

127 were elevated in tissues from patients with colitis, colitis-associated dysplasia, and CAC as well a

128 's disease (CD) in patients with microscopic colitis compared with 94 UC and 42 CD cases in populatio

129 propria from Ffar2(fl/fl)CD11c-Cre mice with colitis compared with control mice or mice without colit

130 n in intestinal tissues of C57BL/6 mice with colitis, compared with mice on control diets.

131 ion as well as a chemically-induced model of colitis, confirmed its predicted regulatory function and

132 by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease r

133 enomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and

134 ommon susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, ce

135 ges; meanwhile Ninj1(-/-) mice showed severe colitis development and impaired recovery, associated wi

136 tion under homeostatic conditions and during colitis development.

137 nd succumb to dextran sulfate sodium-induced colitis due to prolonged intestinal inflammation and imp

138 ilic gastroenteritis (EGE), and eosinophilic colitis (EC), yet these diseases are barely understood c

139 endoscopic Mayo score (eMS) and 1 Ulcerative Colitis Endoscopic Index of Severity (UCEIS) score.

140 We show that acute DSS colitis enhanced neurogenesis but with deficits in cell

141 For patients with ulcerative colitis, Eubacterium rectale and Akkermansia were decrea

142 shows that polyps occur predominantly in the colitis field regardless of colitis type.

143 ults who received a diagnosis of microscopic colitis from 1990 through 2017 in Sweden and risk of inc

144 ght (13%) of 64 patients reporting rash, and colitis, gastritis, pancreatitis and arthritis, and diab

145 Apc(Min/+) mice with colitis given the FFAR2 agonist developed fewer colon tu

146 primary sclerosing cholangitis, longstanding colitis (>10 years), male sex, and younger age at diagno

147 and organoids from patients with ulcerative colitis had increased levels of IL1B mRNA and MIR200C-3p

148 Intestinal tissues from mice with colitis had increased levels of IL1B mRNA and MIR200C-3p

149 Ulcerative Colitis has similar presentation and behaviour in elderl

150 tients with ulcerative colitis and mice with colitis have increased levels of IL1B mRNA and MIR200C-3

151 were pneumonitis (n=2), acute kidney injury, colitis, hypokalaemia, and adrenal insufficiency (n=1 ea

152 diologic manifestations such as pneumonitis, colitis, hypophysitis, thyroiditis, or myocarditis.

153 +) T(reg) cells, which are unable to control colitis in a cell-transfer model of the disease.

154 ells expressing IL-26, which attenuate acute colitis in a humanized IL-26 transgenic mouse model.

155 lls prevented CD45RB(hi)CD4(+) T cell-driven colitis in both Cre(+) and Cre(-) recipients, demonstrat

156 in a trinitro-benzene-sulfonic-acid model of colitis in humanized NOD/scid/gamma mice.

157 -specific RIPK1 deficiency (RIPK1(E-KO)) and colitis in mice with intestinal epithelial-specific FADD

158 erbates dextran sulfate sodium (DSS)-induced colitis in mice.

159 increased disease index of the experimental colitis in mice.

160 ion within cells and reduces the severity of colitis in mice.

161 C7A-deficiency is characterized by apoptotic colitis in milder cases with severe intestinal atresia a

162 ransfer of WT macrophages ameliorated severe colitis in Ninj1(-/-) mice.

163 toxicity (marrow aplasia in one patient and colitis in one patient); no further treatment-related de

164 agonistic antibody significantly alleviated colitis in Rag2(-/-) mice.

165 Likewise, boosting colitis in Rag2(R229Q) mice results in increased frequen

166 ene dose, and the gut, developing ulcerative colitis in response to 1% dextran sulfate sodium (DSS).

167 We induced colitis in Tgr5(ISC-/-) mice by administration of dextra

168 accounts for the accelerated resolution from colitis in the absence of Arg1.

169 e on control diets increased the severity of colitis in these mice.

170 ts hospitalized with acute severe ulcerative colitis included: (5) overall and comparative efficacy o

171 r, administration of GAG protected mice from colitis induced by dextran sulfate sodium in an inflamma

172 brain axis in rats subjected to experimental colitis induced by oral administration of dextran sulfat

173 Notably, we found that acute DSS colitis-induced enhanced infiltration of the hippocampus

174 Following colitis induction, Ninj1 expression was increased in mac

175 icrobiota with NLRs impact the modulation of colitis, inflammatory bowel diseases, and colorectal can

176 Colitis is generally considered a risk factor for colon

177 odel of trinitrobenzenesulfonic acid-induced colitis is re-examined here.

178 hough the TLR2 peptide treatment ameliorated colitis, it allowed recruited monocytes to give rise to

179 In mice with DSS or T-cell-induced colitis, loss of MHCII from IECs reduces but does not el

180 However, in mice with C rodentium-induced colitis, loss of MHCII reduces bacterial clearance by de

181 ible to dextran sulfate sodium (DSS)-induced colitis, manifested by increased weight loss, macrophage

182 Acute severe colitis may be predicted by disease severity at onset an

183 re 93 [IQR 47-156]), and 161 with ulcerative colitis (median P-SCCAI score 1 [IQR 1-3]).

184 demonstrated in cellular assays and a murine colitis model expressing hPXR by a significant reduction

185 e dextran sodium sulfate (DSS)-induced acute colitis model in mice with (WT) or without Lgals2 (Gal2-

186 using a dextran sulfate sodium (DSS)-induced colitis model in mice, we found that GITR-deficiency ren

187 gene expression by Salmonella in the murine colitis model, indicating that the HilD-dependent signal

188 In the dextran sodium sulfate-induced acute colitis model, systemic treatment with MVs prevented col

189 nal permeability in a dextran sulfate sodium colitis model.

190 an sulfate sodium (DSS) and anti-CD40 murine colitis models in response to interleukin-22 immunoglobu

191 In three murine colitis models, SBA supplementation reduces intestinal i

192 These dimers lack efficacy in a colitis mouse model, whereas the monomer reduces disease

193 rleukin-10 and improve colitis symptoms in a colitis mouse model.

194 MV syndrome (n = 1), and CMV pneumonitis and colitis (n = 1).

195 ), normal pouch from patient with ulcerative colitis (n = 10), and normal pouch from patient with fam

196 s of Crohn's disease (n = 200) or ulcerative colitis (n = 199), as well as from 200 healthy individua

197 oratory abnormalities (n = 4), hepatitis and colitis (n = 2).

198 stricture (n = 7), and fulminant C difficile colitis (n = 3).

199 9), Crohn's disease (n = 148), or ulcerative colitis (n = 36) treated with 8 different biopharmaceuti

200 Cases of microscopic colitis (n= 13,957) were identified through Systematized

201 wel disease (IBD) and Non-IBD/Non-Infectious Colitis (NIC).

202 ey effects of acute and chronic experimental colitis on adult hippocampal neurogenesis and innate imm

203 anted to intestines of mice with and without colitis on control or on ATI-containing diets.

204 receptor and dampening signs of DSS-induced colitis on mice, in comparison with reference antagonist

205 T cells lacking caspase-1 failed to induce colitis or confer protection against C. rodentium infect

206 The 14 patients with monogenic ulcerative colitis or IBD-unclassified received their diagnosis at

207 1.88 to 18.1; P = 0.002), baseline fulminant colitis (OR, 84.7; 95% CI, 14.3 to 500; P < 0.001), feve

208 Further, in the DSS-induced mouse model of colitis, oral administration of M2- or M13-loaded NL nan

209 o the micronutrient iron is decreased during colitis, pathogens can scavenge iron by using siderophor

210 More polyps were present in the ulcerative colitis patients when compared to Crohn's disease patien

211 robe, Leonardi et al. demonstrate ulcerative colitis patients with high Candida responded best to fec

212 strategy to reduce the risk of dysplasia in colitis patients.

213 ge of AMT-101 in two mouse models of induced colitis prevented associated pathological events and pla

214 Colitis reduced global PAFR protein expression in mouse

215 d colonic mucosa from patients and mice with colitis released opioids that activated DOPr on nocicept

216 op of an inflamed mucosa (e.g. in ulcerative colitis) remains exceedingly difficult.

217 or Nos2, demonstrating that protection from colitis requires l-arginine.

218 in the mouse intestinal epithelium leads to colitis resistance and substantial changes in gene expre

219 hinery in intestinal epithelial cells in the colitis response and shows how a highly conserved chroma

220 portance of the intestinal epithelium in the colitis response and the potential of microbial species

221 microbiome that elicit a Smarcad1-dependent colitis response, including members of the poorly unders

222 By 7 wk, colitis score and colon CD4(+) T cell numbers were simil

223 Colitis score and innate immune cell influx were reduced

224 e, monocyte ablation was shown to ameliorate colitis scores in preclinical animal models.

225 However, not all types of colitis seem to have equal neoplastic transformation pot

226 inary tract infection, Clostridium difficile colitis, sepsis, or death.

227 orrelation between galectin-9 expression and colitis severity.

228 The anatomic distribution of lesions and colitis shows that polyps occur predominantly in the col

229 C) less vulnerable to dextran sulfate sodium colitis, suggesting the transmission of protective bacte

230 l molecules and was associated with enhanced colitis susceptibility.

231 anti-inflammatory interleukin-10 and improve colitis symptoms in a colitis mouse model.

232 and endothelial cells recovered faster from colitis than Arg1-expressing (Arg1fl/fl) littermates.

233 less severe DSS- or T-cell transfer-induced colitis than control mice.

234 Tgr5(ISC-/-) mice developed more severe colitis than mice without Tgr5 disruption in ISCs.

235 ) mice developed more severe T-cell transfer colitis than wild-type mice and had an increased burden

236 biomarkers of Crohn's disease and ulcerative colitis that can be detected and quantified before diagn

237 ase including Crohn's disease and ulcerative colitis, the arthritis related to anterior uveitis, and

238 In ulcerative colitis, the association was not significant.

239 Further, in patients with ulcerative colitis, the concentration of active IL-18 was inversely

240 diseases such as noninfective enteritis and colitis to be significantly associated with DST shifts i

241 Mean times from diagnosis of microscopic colitis to diagnosis of CD was 3.3 +/- 3.2 years and to

242 that causes disease ranging from hemorrhagic colitis to hemolytic uremic syndrome.

243 We aimed to adapt a model of chronic colitis to pre-pubertal rats and test if a polymeric die

244 ne patient each) in the nivolumab group, and colitis (two patients) in the ipilimumab group.

245 ominantly in the colitis field regardless of colitis type.

246 iagnosis of Crohn disease (CD) or ulcerative colitis (UC) among men and women aged 18-81 years in 201

247 identified 323 incident cases of ulcerative colitis (UC) and 108 incident cases of Crohn's disease (

248 likely impaired in patients with ulcerative colitis (UC) and renders UC-HMA mice more susceptible to

249 standing of prognostic factors in ulcerative colitis (UC) could improve patient management and reduce

250 Patients with ulcerative colitis (UC) experience periods of recurring and episodi

251 Although Crohn's disease (CD) and ulcerative colitis (UC) have been considered as disorders that affe

252 aol and its effectiveness against ulcerative colitis (UC) in a mouse model.

253 Incidence of ulcerative colitis (UC) in elderly population is increasing because

254 Ulcerative colitis (UC) is a chronic inflammatory bowel disease of

255 Ulcerative colitis (UC) is one of the main types of chronic inflamm

256 copic disease activity scoring in ulcerative colitis (UC) is useful in clinical practice but done inf

257 f biologic treatment outcomes for ulcerative colitis (UC) or Crohn's disease (CD) patients are limite

258 rom 16 Crohn's disease (CD) and 6 ulcerative colitis (UC) patients and compared them to samples from

259 A subset of patients with ulcerative colitis (UC) present with, or progress to, moderate to s

260 onic CD8(+) T cells in health and ulcerative colitis (UC) using single-cell transcriptomics with T-ce

261 n colectomy-treated patients with ulcerative colitis (UC) versus controls (familial adenomatous polyp

262 matory responses of patients with ulcerative colitis (UC) vs Crohn's disease (CD).

263 As is known, ulcerative colitis (UC), a chronic inflammatory disease, is closely

264 ween CC and Crohn's disease (CD), ulcerative colitis (UC), and celiac disease.

265 pression in Crohn's disease (CD), ulcerative colitis (UC), and non-inflammatory bowel disease (IBD) c

266 mmatory bowel diseases, including ulcerative colitis (UC), but the causality and mechanisms remain un

267 n to be elevated in patients with ulcerative colitis (UC), Crohn's disease (CD) and colorectal cancer

268 y with 21 patients suffering from ulcerative colitis (UC), in which first-time treatment with vedoliz

269 ncluding Crohn's disease (CD) and ulcerative colitis (UC), is a disease associated with dysbiosis, re

270 tinal microbiota of patients with ulcerative colitis (UC).

271 veloping Crohn's disease (CD) and ulcerative colitis (UC).

272 ith moderately to severely active ulcerative colitis (UC).

273 ogic improvement in patients with ulcerative colitis (UC).

274 mized controlled trial of FMT for ulcerative colitis (UC).

275 colonic Crohn's disease (cCD) and ulcerative colitis (UC).

276 cosa [50 Crohn's disease (CD); 80 ulcerative colitis (UC); 31 controls].

277 ith Crohn's disease [CD], 13 with ulcerative colitis [UC], mean age 45 years [range 19-90], 7 female)

278 clinical studies for treatment of ulcerative colitis, using conditions that mimic the human small int

279 olyps, family history of CRC, and ulcerative colitis versus Crohn's disease was considered moderate.

280 liorates host susceptibility to inflammatory colitis via BA nuclear receptors.

281 creases intestinal inflammation in mice with colitis, via TLR4, and alters their fecal microbiota.

282 Colitis was assessed one week after last dose of TNBS by

283 In multivariable models, microscopic colitis was associated with an aHR of 12.6 (95% CI 8.8-1

284 Chronic DSS colitis was characterized by normal levels of neurogenes

285 Colitis was induced by administration of DSS, transfer o

286 Colitis was induced in 20 five-week-old Sprague-Dawley m

287 Experimental colitis was induced in mice by dextran sulfate sodium sa

288 to severe experimental colitis and that such colitis was normalized by administration of anti-IL-beta

289 TNBS colitis was not associated with growth failure.

290 To examine the role of Gal2 in colitis, we employed the dextran sodium sulfate (DSS)-in

291 then given dextran sodium sulfate to induce colitis; we also studied Il10(-/-) mice, which develop s

292 Features of chronic colitis were confirmed in this model, based on MRC and h

293 Treatment naive-patients with ulcerative colitis were included at time of initial diagnosis from

294 Individuals with microscopic colitis were matched to 5 general population controls (n

295 Rag(-/-) mice developed overt colitis with intestinal fibrostenosis.

296 nalyses, comparing patients with microscopic colitis with their unaffected siblings, the aHRs of CD a

297 etion in mice induced hypersusceptibility to colitis, with increased prevalence of colitogenic Prevot

298 were given dextran sodium sulfate to induce colitis, with or without a FFAR2 agonist or an antibody

299 ients who received a diagnosis of ulcerative colitis within 5 years with an AUROC of only 0.56 and wi

300 ductivity and Activity Impairment-Ulcerative Colitis [WPAI-UC] questionnaire).