ライフサイエンスコーパス: RA

1 RA and SA CMCs were isolated from mouse hearts, expanded

2 RA classification using metabolic profiles shows a sensi

3 RA currently focuses on monomers and additives used in t

4 RA deformation properties are significantly altered in p

5 RA focuses on management of a toxicological hazard in a

6 RA induced loss of PR binding only at the proximal site.

7 RA reservoir, pump function, the rate of RA filling, and

8 RA synovial tissue and synovial fluid macrophages expres

9 RA was associated with increased numbers of neutrophils

10 RA, produced by newly generated mesodermal cells, provid

11 e- and sex-matched RA-normotensive (n = 13), RA-hypertensive patients (RA-HTN; n = 17), normotensive

12 Among 2334 RA patients who had available hepatitis B surface antige

13 We further recruited another cohort of 3,353 RA patients and confirmed the findings.

14 analysis studies to date using a score of 62 RA risk SNPs (p < 5 * 10(-8)) as instrumental variable (

15 eyes (67.5%), and >/=20/40 in 76 eyes (95%); RA averaged 3.10+/-1.30 diopters (D), with 73 eyes (91%)

16 r -130 bp that contains PRE half-sites and a RA response element (RARE).

17 ng histone methyltransferase Ehmt2/G9a, as a RA coactivator controlling somite symmetry.

18 It remains unclear whether radial access (RA), compared with femoral access (FA), mitigates the ri

19 on of two targeted therapies: retinoic acid (RA) and arsenic.

20 mitogenesis symmetry requires retinoic acid (RA) and its coactivator Rere/Atrophin2.

21 and RALDH3 establish dynamic retinoic acid (RA) landscapes in feather mesenchyme, which modulate GRE

22 min D3 (VD3) and/or all-trans retinoic acid (RA) on wild-type mouse skin induces a human atopic derma

23 embryonic bilateral symmetry.Retinoic acid (RA) regulates the maintenance of somitogenesis symmetry.

24 as well as the involvement of retinoic acid (RA) signaling in the entire process.

25 Retinoic acid (RA) treatment blocked the P4 increase in CK5+ cells and

26 All-trans-retinoic acid (RA), a bioactive derivative of vitamin A, exhibits diver

27 ir origin unless treated with retinoic acid (RA), which results in proximodistal (PD) limb duplicatio

28 ibe light-inducible polymeric retinoic acid (RA)-containing nanoparticles (NPs) with the capacity to

29 In all-trans retinoic acid (RA)-induced differentiation of acute promyelocytic leuka

30 lated by enzymes that degrade retinoic acid (RA).

31 rk the aggregation behavior of Rumenic acid (RA) is presented for the first time.

32 adhering (SA) but not from rapidly adhering (RA) fractions of cardiac mesenchymal cells (CMCs) are ef

33 All these changes facilitate ADP-RA to bind ARH1.

34 After RA SF and peripheral blood (PB) CD14+ monocytes were tre

35 sk of nonischemic HF increased rapidly after RA onset, in contrast to the risk of ischemic HF.

36 Full-term pups developed in room air (RA) or an oxygen-induced retinopathy (OIR) model.

37 e arginyl dipeptides: Ala-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER); and t

38 o reflected in the expression patterns of an RA-responsive gene, STRA8; RA levels were low before the

39 lysis included 2737 patients who received an RA graft (RA group; n=632) or SVG only (SVG group; n=210

40 This association was present when an RA graft was used to supplement both SITA and BITA graft

41 l policy and decision-making: risk analysis (RA) and life-cycle assessment (LCA).

42 (n = 188), control individuals (n = 83) and RA (n = 168) patients.

43 Combined systemic distribution of AZA and RA impedes tumor growth and prolongs survival.

44 ood from individuals from the NBS cohort and RA patients from 2 independent cohorts.

45 erved in individuals from the NBS cohort and RA patients from the Nijmegen cohort homozygous for the

46 ighlight an essential role for both GCN5 and RA signaling in early diencephalic development, and eluc

47 We imaged the LA and RA of all subjects using short axis and long axis slices

48 r and age have considerable impact on LA and RA size and function.

49 interrelationship between periodontitis and RA remains unclear.

50 ions between exposure to some pesticides and RA in male farmers.

51 und most of the significant genes of T1D and RA were also located within the MHC region.

52 rting a direct link between GCN5, TACC1, and RA signaling in the developing diencephalon.

53 AR, RA, and RP significantly increased the number of cell re

54 ns in the robust nucleus of the arcopallium (RA) regulate variability in phonology but not syntax.

55 gion, the robust nucleus of the arcopallium (RA), controls syllable and trill bandwidth stereotypy, w

56 r cortex (robust nucleus of the arcopallium, RA) in Bengalese Finches.

57 , Av; the Robust nucleus of the Arcopallium, RA; the Uvaeform nucleus, Uva).

58 Whether the use of the radial artery (RA) can improve clinical outcomes in coronary artery byp

59 From 277 patients with rheumatoid arthritis (RA) and 141 healthy individuals, we also identify N-glyc

60 systemic inflammatory rheumatoid arthritis (RA) and AD.

61 riodontal disease with rheumatoid arthritis (RA) and ankylosing spondylitis (AS).

62 Current treatments for rheumatoid arthritis (RA) do not reverse underlying aberrant immune function.

63 ls in individuals with rheumatoid arthritis (RA) infiltrate non-lymphoid tissue sites, maneuver throu

64 ABSTRACT: Rheumatoid arthritis (RA) is a chronic inflammatory condition associated with

65 Rheumatoid arthritis (RA) is a progressive disease that affects both pediatric

66 heart failure (HF) in rheumatoid arthritis (RA) is independent of ischemic heart disease (IHD).

67 Rheumatoid arthritis (RA) is the most common inflammatory arthropathy.

68 TRAIL in experimental rheumatoid arthritis (RA) models.

69 HDs) and patients with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE).

70 Rheumatoid arthritis (RA) patients have been observed to be at a lower risk of

71 l fluid (SF) from four rheumatoid arthritis (RA) patients.

72 y in various stages of rheumatoid arthritis (RA) progression is unknown.

73 " (SE) associated with rheumatoid arthritis (RA), especially more severe cyclic-citrullinated peptide

74 Disease activity of rheumatoid arthritis (RA), evaluated as Disease Activity Score (DAS), is assoc

75 In rheumatoid arthritis (RA), immunological triggers at mucosal sites, such as th

76 nt forms of arthritis (rheumatoid arthritis (RA), psoriatic arthritis (PsA), osteoarthritis (OA)) or

77 cytokine implicated in rheumatoid arthritis (RA).

78 togenic role of H4R in rheumatoid arthritis (RA).

79 in the pathogenesis of rheumatoid arthritis (RA).

80 c arthritis (PsA), and rheumatoid arthritis (RA).

81 hirds of patients with rheumatoid arthritis (RA).

82 atory signaling in the rheumatoid arthritis (RA).

83 n patients with active rheumatoid arthritis (RA).

84 s been associated with rheumatoid arthritis (RA); pesticides may account for this association, but th

85 76) and patients with rheumatoid arthritis (RA, n = 244).

86 ents with cirrhosis with refractory ascites (RA).

87 is evaluated using chemical risk assessment (RA).

88 have poorly controlled or refractory asthma (RA).

89 sual acuity (BSCVA), refractive astigmatism (RA), and topographic astigmatism (TA), central corneal t

90 eatment, WHHERE and Ehmt2 become enriched at RA target genes to promote RNA polymerase II recruitment

91 Rotational atherectomy (RA) is an important interventional tool for heavily calc

92 any evidence of a causal association between RA and AD (OR = 1.012, 95% CI 0.98-1.04).

93 There were significant associations between RA function with invasive hemodynamics (P<0.01).

94 sm of RA by identifying correlations between RA-associated metabolites.

95 F(ab')2 targets better discriminated between RA and HDs or SLE, with significantly higher AHA levels

96 establish if there is a causal link between RA and AD.

97 The causal relationship between RA and AD was assessed using Mendelian Randomization (MR

98 than the other ANA staining patterns in both RA and healthy population (p < 0.0001).

99 he premeiotic transitions are coordinated by RA from Sertoli (somatic) cells.

100 ulbar block) with Monitored Anesthesia Care (RA-MAC) or General Anesthesia (GA) for open globe injury

101 Among anti-CCP+ RA women, SE alleles were not related to age-adjusted ri

102 inated peptide antibody-positive (anti-CCP+) RA.

103 ferroni correction) associated with T1D, CD, RA and T2D.

104 nsfected with light-inducible NPs containing RA can engraft into bone marrow in vivo in the proximity

105 DC-RA expression of IL-27 was important to their induction

106 DC-RAs displayed a mature yet tolerogenic phenotype, expres

107 IL-27 (Ebi)(-/-) (ie, IL-27-incompetent) DC-RAs were ineffective in inducing food allergen tolerance

108 Delivery of specific allergen-presenting DC-RAs to half-maximally sensitized mice with ovalbumin or

109 encephalic expansion, decreased diencephalic RA signaling, and increased diencephalic WNT and SHH sig

110 medication, selection bias and differential RA diagnosis.

111 OPLS-DA was used to discriminate RA patients from controls.

112 Forty-five individuals with documented RA (n = 15), spondyloarthropathy (n = 15), and calcium p

113 cid receptors (RARs) to either PD duplicate (RA treatment or RARgamma agonist) or truncate (RARbeta a

114 em, is the target of autoantibodies in early RA.

115 lgia, undifferentiated arthritis (UA), early RA, and established RA cohorts in comparison with health

116 enriched in synovial tissues from UA, early RA, and established RA patients.

117 Several factors hamper effective RA for many FCMs, including a lack of information on che

118 yzed HPbetaCD was the best for encapsulating RA.

119 etes mellitus, systemic lupus erythematosus, RA, and celiac disease, these results suggest a general

120 ed arthritis (UA), early RA, and established RA cohorts in comparison with healthy donors.

121 l tissues from UA, early RA, and established RA patients.

122 fficacious not only in early and established RA, but also in inhibiting the progression of the diseas

123 Mice diseased from experimental RA exhibited a 3-fold enhancement in hypoxia tracer upta

124 The pKa determined for RA was 4.31.

125 epigenome-wide association study (EWAS) for RA with three different replication cohorts, to identify

126 d the effect of therapeutic intervention for RA on periodontal disease.

127 e a novel molecular regulatory mechanism for RA signaling that is specific to the developing forebrai

128 udy indicates that CD38 is not necessary for RA-induced differentiation.

129 njuries, there are equal selection ratio for RA-MAC and GA.

130 that Wdr5, Hdac1, and Hdac2 are required for RA signaling in vitro and in vivo.

131 We review regulatory requirements for RA of FCMs in the United States and Europe, identify gap

132 Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which re

133 t) ) mutants can be rescued with gestational RA supplementation, supporting a direct link between GCN

134 EE and rates of glucose appearance (glucose RA) during three separate infusion protocols in healthy

135 uded 2737 patients who received an RA graft (RA group; n=632) or SVG only (SVG group; n=2105) in addi

136 neurons, about half of these being other HVC(RA) cells.

137 In RA patients, reported pain was positively correlated wit

138 Raynaud's phenomenon (p = 6.8 x 10(-11)) in RA.

139 total cells in vehicle and 19.3 +/- 1.8% in RA CMCs; p < 0.05).

140 s increased prevalence of atherosclerosis in RA and provides data to support the hypothesis that pati

141 ened sympathetic outflow and reduced cBRS in RA that can be independent of hypertension.

142 drive the pathogenic activity of B cells in RA and suggest shared methylation patterns with SLE.

143 luence functional properties of key cells in RA, especially synovial fibroblasts.

144 gly, and these responses were more common in RA patients with SE alleles.

145 This bias is gradually consolidated in RA, a motor cortex analogue downstream of LMAN.

146 agement may resolve autonomic dysfunction in RA.

147 flammatory cytokines that can be elevated in RA evoke pathogenic increases in sympathetic activity an

148 17, and IL-22 stimulated RANKL expression in RA monocytes and JNJ7777120 reduced the RANKL expression

149 as potent inhibitors of IL-34 expression in RA synovial fibroblasts.

150 -TNF-alpha agents on endothelial function in RA patients.

151 reatment may improve endothelial function in RA patients.

152 beneficial effect on endothelial function in RA.

153 e United States and Europe, identify gaps in RA, and highlight opportunities for improving the protec

154 ent (LBH) gene as a key dysregulated gene in RA and other autoimmune diseases.

155 rum concentration of histamine was higher in RA, compared with osteoarthritis and healthy controls.

156 apies to ameliorate pain and inflammation in RA restores autonomic balance and reduces cardiovascular

157 hways were also differentially methylated in RA B cells.

158 alleles, the transcriptome and methylome in RA FLS, we recently identified the limb bud and heart de

159 sion of H4R was increased in PB monocytes in RA patients.

160 valence of plaque calcification was noted in RA, despite similar plaque size (73.3% vs 20%, p = 0.04)

161 her such autonomic dysfunction is present in RA is not known.

162 ymorphism (SNP) in IL32 on lipid profiles in RA patients and individuals, suggesting a possible prote

163 The most discriminatory AHA reactivity in RA was against pepsin-cleaved IgG4, with a 35% prevalenc

164 ), whereas cardiac BRS (cBRS) was reduced in RA, RA-HTN and HTN patients [5(3-8), 4 (2-7), 6 (4-9) ms

165 B cells are highly relevant in RA, since patients express autoantibodies and depleting

166 explain the increased cardiovascular risk in RA, and raises the possibility that optimizing pain mana

167 ve bias from LMAN given a plasticity rule in RA.

168 e initiation and propagation of synovitis in RA patients.

169 Incident RA cases (n=220), confirmed by physicians or by self-rep

170 Incident RA was associated with ever use of fonofos (OR = 1.70; 9

171 RCT, before-after cohort study; 2) including RA patients; 3) treatment with anti-TNF-alpha medication

172 Apart from increased RA-induced CD11b expression, ablation of all but the fir

173 Intriguingly, RA signaling defects caused by in vitro inhibition of GC

174 on (MR), using summary data from the largest RA and AD Genome Wide Association (GWA) and meta-analysi

175 6 mice were exposed to LG-IH or room air (LG-RA) during days 13-18 of gestation.

176 on of RA required for tight control of local RA concentrations, is significantly downregulated in emb

177 patients who underwent invasive management, RA was associated with a reduced risk of AKI compared wi

178 e (HR) were recorded in age- and sex-matched RA-normotensive (n = 13), RA-hypertensive patients (RA-H

179 We measured RA concentrations and found that they changed periodical

180 effector memory T cells and effector memory RA T cells.

181 effector memory T cells < T effector memory RA(+) cells).

182 and phenotypic analysis revealed that murine RA and SA CMCs are indistinguishable; nevertheless, tran

183 rheumatoid factor (RF)-positive and negative RA patients, as well as anti-citrullinated protein antib

184 tein antibodies (ACPA)-positive and negative RA patients.

185 iency is potentially causal of sero-negative RA and provide new insights into the pathogenesis of the

186 tudy (vGWAS) of six cohorts of sero-negative RA recruited in Europe and the US that were genotyped wi

187 rst six amino acids of CD38 affected neither RA-induced differentiation nor associated signalling.

188 Infection-negative neutrophilic RA was associated with an increase in levels of select b

189 up of patients with noninfected neutrophilic RA was associated with systemic inflammation.

190 he -130 bp PRE/RARE regions with P4, but not RA alone or RA plus P4.

191 % in vehicle-treated mice; p < 0.05) but not RA CMCs (11.7 +/- 1.7%), which was associated with reduc

192 f 99) of SLE patients, and 81% (79 of 97) of RA patients.

193 oic acid response elements in the absence of RA.

194 s and leads to transcriptional activation of RA target genes.

195 Using an integrative analysis of RA risk alleles, the transcriptome and methylome in RA F

196 idemiological evidence for an association of RA with lower AD incidence, this association does not ap

197 We evaluated the association of RA with the use of 46 pesticides and across 4 levels (ne

198 Incremental changes of RA gradient slopes establish a continuum of asymmetric f

199 ylation450 BeadChip in a discovery cohort of RA patients (N = 50) and controls (N = 75).

200 TFE-covered stent leads to better control of RA secondary to portal hypertension in patients with cir

201 embryos with a preexisting genetic defect of RA metabolism.

202 emia (AML) and induce the differentiation of RA-low sensitive leukaemia cells.

203 xpressing Cyp26a1 show reduced efficiency of RA clearance.

204 y the intracellular metabolic environment of RA T cells-specifically, by reduced glycolytic flux that

205 Notably, patterned expression of RA signaling components was also found in humans, sugges

206 t represents a bold vision for the future of RA therapeutics.

207 patients with RA and to assess the impact of RA disease factors.

208 s a key enzyme for catabolic inactivation of RA required for tight control of local RA concentrations

209 t is now clear that a further integration of RA and LCA based on dataset completion will remain futil

210 nthesis corrected the tissue-invasiveness of RA T cells in vivo and reversed their proarthritogenic b

211 egrin function and therefore invasiveness of RA-FLSs.

212 ephalic morphogenesis and the involvement of RA signaling in this process are poorly understood.

213 Transient manipulation of RA signaling, or reduction of Fgf8 expression, disrupted

214 Our chemical manipulations of RA levels in mouse testes now reveal that RA also regula

215 found that pharmacological manipulations of RA's inhibitory circuitry drove large shifts in learned

216 CN5 in a previously undescribed mechanism of RA signaling in the developing forebrain that is require

217 njection in an adjuvant-induced rat model of RA induces apoptosis of FLS, leading to significant decr

218 ng the wing, while switch-like modulation of RA signalling confers distinct vane shapes between feath

219 shown to be involved in the pathogenesis of RA and might be linked to the development of atheroscler

220 reover, to investigate the pathomechanism of RA by identifying correlations between RA-associated met

221 at allows cells to maintain a stable rate of RA biosynthesis by utilizing a biological circuit genera

222 hese features of ROC ensure that the rate of RA biosynthesis in whole cells is largely independent of

223 RA reservoir, pump function, the rate of RA filling, and atrial minimum volume predicted adverse

224 It is a critical regulator of RA-FLS migration and invasion and therefore represents a

225 ents an attractive target for the therapy of RA.

226 significant implications in the treatment of RA patients with anti-TNF-alpha drugs and in the potenti

227 romising candidate drug for the treatment of RA.

228 ence from confounding factors such as use of RA medication, selection bias and differential RA diagno

229 Progressive worsening of RA reservoir and conduit functions is related to changes

230 A systematic literature review on RA incidence and its link to AD was carried out accordin

231 RE/RARE regions with P4, but not RA alone or RA plus P4.

232 , the influence of SF from osteoarthritis or RA patients on total Th cells or different Th cell subse

233 ohort study among patients with PsO, PsA, or RA and matched controls in The Health Improvement Networ

234 have reported that anti-TNF-alpha therapy or RA itself can modulate AD pathology, although the underl

235 otensive (n = 13), RA-hypertensive patients (RA-HTN; n = 17), normotensive (NC; n = 17) and hypertens

236 There is limited data on phasic RA function (reservoir, conduit, and pump) in pediatric

237 ith a bimodal distribution, and ACA-positive RA may constitute a distinct subset with specific clinic

238 basis for a new mouse model of ACPA-positive RA.

239 hereas cardiac BRS (cBRS) was reduced in RA, RA-HTN and HTN patients [5(3-8), 4 (2-7), 6 (4-9) ms mmH

240 Here, we demonstrate that KCa1.1 regulates RA-FLS adhesion through controlling the plasma membrane

241 with noncases (n=26,134) who did not report RA.

242 on patterns of an RA-responsive gene, STRA8; RA levels were low before the four transitions, increase

243 In this pilot study, RA patients and age/sex-matched controls were evaluated

244 toid arthritis fibroblast-like synoviocytes (RA-FLSs) isolated from the synovium of patients with RA.

245 especially owing to number of missing teeth (RA = 6.0 +/- 5.4, HC = 3.1 +/- 3.3; P <0.01).

246 More so than RA, PsO and PsA are associated with liver disease, parti

247 Here we found that RA T cells abundantly express the podosome scaffolding p

248 of RA levels in mouse testes now reveal that RA also regulates the two postmeiotic transitions: initi

249 ion of pachytene spermatocytes revealed that RA from pachytene spermatocytes was required for the two

250 Meta-analysis of the literature showed that RA was associated with lower AD incidence (OR = 0.600, 9

251 ts was also found in humans, suggesting that RA also plays a role in setting up the human fovea.

252 Steroid levels show variation among the RA patients according to the corticosteroid treatment; l

253 hicle-treated mice; p < 0.05) but not in the RA CMC group (24.1 +/- 1.2%).

254 Plaque was more prevalent in the RA group (53.1% vs 37.0%, p = 0.038) and was independent

255 ite end point was significantly lower in the RA group (8.8%; 95% CI, 6.5-11.0) compared with the SVG

256 2.1-5.0), and 4.4% (95% CI, 2.8-6.0) in the RA group and 3.4% (95% CI, 2.0-4.8), 4.0% (95% CI, 2.5-5

257 t compounds were effective in inhibiting the RA overexpressed hCA IX and XII, with KI values in the l

258 mia cells for several days and release their RA payloads within a few minutes upon exposure to blue/U

259 The mechanism of this RA is not well understood.

260 ro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RARbeta.

261 evated (P < 0.05) in OA patients compared to RA patients.

262 A genetic predisposition to RA, such as HLA-DR4 positivity, indicates that dendritic

263 tores high-risk neuroblastoma sensitivity to RA.

264 Susceptibility to RA teratogenesis is further potentiated in embryos with

265 sion of the disease from arthralgia or UA to RA.

266 Eight thousand six hundred twenty-two RA cases (3069 radial and 5553 femoral) were included in

267 Open globe injuries repaired under RA-MAC had significantly shorter wound length (p<0.001),

268 rly clinical outcomes in patients undergoing RA using radial or femoral access.

269 arge real-world study of patients undergoing RA, radial access was associated with equivalent 30-day

270 patients in England and Wales who underwent RA between January 1, 2005, and March 31, 2014.

271 l growth restriction occurred in pups in UPI/RA, but not in UPI/OIR.

272 Upon RA treatment, WHHERE and Ehmt2 become enriched at RA tar

273 Upon RA-mediated differentiation, Oct1-deficient cells induce

274 Restoration of PML nuclear bodies upon RA- and/or arsenic-initiated PML/RARA degradation is ess

275 affected by androgen signaling in HVC versus RA.

276 affected by androgen signaling in HVC versus RA.

277 ure and incapacitance tests using an in vivo RA model.

278 When RA receptor-alpha signaling was conditionally blocked in

279 ted PML/RARA degradation is essential, while RA-triggered transcriptional activation is dispensable f

280 alysis was needed in 6 patients (0.15%) with RA and 14 patients (0.34%) with FA (p = 0.0814).

281 AKI occurred in 634 patients (15.4%) with RA and 712 patients (17.4%) with FA (odds ratio [OR]: 0.

282 e is to identify metabolites associated with RA and its cofounders using a new untargeted metabolomic

283 Fifty subjects per group with RA, PsA, OA or IBD and 50 healthy controls were included

284 uishable among controls and individuals with RA, spondyloarthropathy, and CPPD.

285 -T was significantly higher in patients with RA (19.3 +/- 4.8) than in HC group (16.9 +/- 5.8), espec

286 iodontitis was noted in 98% of patients with RA and 82% of the HC group (P <0.01).

287 schemic and nonischemic HF) in patients with RA and to assess the impact of RA disease factors.

288 Patients with RA are at increased risk of HF that cannot be explained

289 diac baroreflex sensitivity in patients with RA compared to matched controls.

290 In the cohort of patients with RA of any duration, the HRs were between 1.71 and 1.88 f

291 oncentrations in aCCP-positive patients with RA was found, importance of periodontal pathogenic bacte

292 ynovial fluid (SF) and sera in patients with RA was measured using ELISA.

293 BAL fluid from 40% of patients with RA was positive for a pathogenic microbe.

294 METHOD: Sixty patients with RA, 30 patients with nonrefractory asthma (NRA), and 20

295 nfection was present in 40% of patients with RA, which likely contributed to neutrophilic inflammatio

296 s aberrant in CD1c(+) DCs from patients with RA, with upregulation of miR-34a and lower levels of AXL

297 mucosal and joint immunity in patients with RA.

298 isolated from the synovium of patients with RA.

299 ed to periodontal condition in patients with RA.

300 associations among anti-CCP- adults without RA and potential mechanisms.