ライフサイエンスコーパス: RA

1 RA activity was assessed using the 28-joint Disease Acti

2 RA features sporadic 'flares' or inflammatory episodes-m

3 RA has been considered as an anti-cancer agent, whereas

4 RA is also required to generate pancreatic progenitors f

5 RA is an inflammatory joint disease and, compared with t

6 RA patients (n = 52, F:M = 40:12), patients with Behcet'

7 RA patients displaying RF-IgA levels >75 IU/mL exhibited

8 RA strain and strain rate using CMR-FT had fair and good

9 RA-regulated epigenetic marks were identified near RA ta

10 RAs(3) where R = Ca, Sr, thus, offers a unique opportuni

11 us 7.5%), SGLT-2i (10.3% versus 8.1%), GLP-1 RA (3.4% versus 2.4%), and insulin (13.8% versus 9.4%).

12 min-based background therapy, specific GLP-1 RAs and SGLT-2 inhibitors have a favorable effect on cer

13 ncet DBS samples were collected from n = 100 RA patients with active disease at baseline and 6 weeks

14 dy assessed dietary intake from 32 AN and 21 RA healthy middle-aged volunteers before screening colon

15 With P = 0.18 (T1D) and P = 0.26 (RA) imprinting variances were not significant.

16 ethylation in CD4(+) T and/or B cells at 37% RA loci.

17 e compounds including b-AP15, VLX1570, RA-9, RA-190, EF24, HO-3867, and MCB-613.

18 n in alveolar ECs to generate retinoic acid (RA) and supports the synthesis of RA from type II alveol

19 Inhibition of CYP450-mediated retinoic acid (RA) metabolism by RA metabolism blocking agents increase

20 Retinoic acid (RA) signaling is essential for multiple developmental pr

21 Retinoic acid (RA) signaling was identified as a regulator of SMC to SE

22 nduces tumor cells to produce retinoic acid (RA), which polarizes intratumoral monocyte differentiati

23 1 silences transiently active retinoic acid (RA)-induced enhancers and their target genes.

24 d gene expression data from a retinoic acid (RA)-induced mouse embryonic stem cells (mESCs) different

25 a rate-limiting enzyme in the retinoic acid (RA)-producing pathway.

26 26b1)-mediated degradation of retinoic acid (RA).

27 basil, the concentration of rosmarinic acid (RA) increased after application of 100 mg/L of ChL.

28 clinical remission as compared to the active RA (p value < 0.0001).

29 ore >3.2, indicative of moderate/very active RA.

30 (CRC) (~91:100,000), whereas rural African (RA) people have the lowest risk (<5:100,000).

31 Synthetic RAR agonist RA-568 was more potent than RA in rescuing RA/RAR activi

32 tions argue that these reintroduced alleles (RAs) are more likely to be tolerated by modern humans th

33 )Ga(0.07)In(0.53)As quaternary random alloy (RA).

34 Furthermore, an RA-responsive gene signature in human monocytes correlat

35 cocultured with PN-stimulated mDCs showed an RA-dependent 4-fold increase in production of IL-5 and e

36 ation of each of these radionuclide analogs (RAs) was shown to be dependent upon their chemical speci

37 me, closed-loop system to record and analyze RA from multiple intracardiac leads, and deliver dynamic

38 edictor of mortality in Ebstein anomaly, and RA dysfunction and hypertension are hemodynamic biomarke

39 RALDH2 induction by PN in APCs and RA-promoted T(H)2 differentiation could be an important

40 -) lungs are caused by both RA-dependent and RA-independent mechanisms.

41 n between the presence of these features and RA was examined by using logistic regression.

42 reas OA was characterized by fibroblasts and RA of lymphocytes.

43 ected in gingival crevicular fluid (GCF) and RA parameters.

44 itis at metatarsophalangeal (MTP) joints and RA.

45 er arthritis activity in both K/BxN mice and RA patients.

46 te the association between periodontitis and RA, and monitoring the bacterial composition of GCF migh

47 regulator of SMC to SEM cell transition, and RA signaling was dysregulated in symptomatic human ather

48 fast overall transport times of all aqueous RAs investigated.

49 nch vocal robust nucleus of the arcopallium (RA) shares numerous markers (e.g. SNCA, PVALB) with the

50 er name), robust nucleus of the arcopallium (RA), Area X, lateral magnocellular nucleus of the anteri

51 of complete spatial summation (Ricco's area, RA) in eyes with and without non-pathological, axial myo

52 the long-term patency of the radial artery (RA) with that of the right internal thoracic artery (RIT

53 for the management of rheumatoid arthritis (RA) and other chronic conditions, but the safety of long

54 clinical management of rheumatoid arthritis (RA) and other chronic inflammatory diseases.

55 s for the treatment of rheumatoid arthritis (RA) and other forms of inflammatory arthritis, low-dose

56 ory diseases including rheumatoid arthritis (RA) and spondyloarthritis (SpA).

57 non-resistant malaria, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).

58 Patients with rheumatoid arthritis (RA) are at high risk of developing cardiovascular diseas

59 drug-free remission in rheumatoid arthritis (RA) are unknown.

60 natures to distinguish rheumatoid arthritis (RA) from non-inflammatory arthralgia (NIA), self-limitin

61 Rheumatoid arthritis (RA) is a chronic immune-mediated disease that primarily

62 Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease linked

63 Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by j

64 Rheumatoid arthritis (RA) is a debilitating and painful inflammatory autoimmun

65 imary manifestation of rheumatoid arthritis (RA) is articular disease; however, extra-articular disea

66 Rheumatoid arthritis (RA) is characterised by painful, stiff and swollen joint

67 Rheumatoid arthritis (RA) is closely associated with shared epitope (SE)-codin

68 in the pathogenesis of rheumatoid arthritis (RA) owing to their ability to generate citrullinated pro

69 oled synovial fluid of rheumatoid arthritis (RA) patients.

70 Many patients with rheumatoid arthritis (RA) report symptom relief from certain foods.

71 Rheumatoid arthritis (RA) risk has a large genetic component (~60%) that is st

72 immunopathogenesis of rheumatoid arthritis (RA) spans decades, beginning with the production of auto

73 main cell types of the rheumatoid arthritis (RA) synovium, possess phenotypic and molecular character

74 s and 35 patients with rheumatoid arthritis (RA) were included.

75 Rheumatoid arthritis (RA), a chronic inflammatory disease affecting primarily

76 s in the management of rheumatoid arthritis (RA), a substantial minority of patients are exposed to m

77 ltiple sclerosis (MS), rheumatoid arthritis (RA), and others are increasingly recognized as disease e

78 to improve outcomes in rheumatoid arthritis (RA), but current diagnostic tools have limited sensitivi

79 nds is associated with rheumatoid arthritis (RA), it is unknown whether tenosynovitis of the forefoot

80 th osteolysis, such as rheumatoid arthritis (RA), often leading to disability in patients.

81 oints of patients with rheumatoid arthritis (RA), together with compelling data from in vitro and exp

82 in the pathogenesis of rheumatoid arthritis (RA), we evaluated the role of PON1 in murine inflammator

83 ved in-vitro assay for Rheumatoid arthritis (RA), which yielded 5 promising genes, one of which is un

84 tracellular trap (NET) rheumatoid arthritis (RA)-rmAbs derived from CD19(+) B cells within RA human s

85 e 1 diabetes (T1D) and rheumatoid arthritis (RA).

86 rily used for treating rheumatoid arthritis (RA).

87 in the pathogenesis of rheumatoid arthritis (RA).

88 sification accuracy of rheumatoid arthritis (RA).

89 sera of patients with rheumatoid arthritis (RA).

90 mmune diseases such as rheumatoid arthritis (RA).

91 for the development of rheumatoid arthritis (RA).

92 in many patients with rheumatoid arthritis (RA).

93 ory conditions such as rheumatoid arthritis (RA); however, it has only been during the twenty-first c

94 lerosis (MS, n = 147), rheumatoid arthritis (RA, n = 229), Crohn's disease (n = 148), or ulcerative c

95 the treatment of ROS-driven diseases such as RA.

96 sual acuity (BSCVA), refractive astigmatism (RA), endothelial cell density, immunologic rejection, he

97 Impaired right atrial (RA) reservoir strain and elevated estimated RA pressure

98 Currently available RA metabolism blocking agents (i.e., liarozole and talar

99 a subset of the known shared markers between RA and human laryngeal motor cortex (e.g. SLIT1, RTN4R,

100 tive correlation also being observed between RA and measures of co-localised peripheral ocular length

101 STE and also assess the relationship between RA and LA strain.

102 strong association has been reported between RA and periodontal disease, and Porphyromonas gingivalis

103 ved in Cyp26b1(-/-) lungs are caused by both RA-dependent and RA-independent mechanisms.

104 50-mediated retinoic acid (RA) metabolism by RA metabolism blocking agents increases endogenous retin

105 ing our approach; plus, many other candidate RA target genes were found.

106 ignaling pathways may be necessary to combat RA persistence.

107 luated the ability of this system to control RA and reduce arrhythmia susceptibility, in vivo.

108 Considering the challenges to control RA, this study provides robust data supporting that inhi

109 research has been carried out on how to cure RA, and the term 'cure' still requires definition for th

110 ose limits are delta(RA)/(12)(1/2) and delta(RA)/(3)(1/2), with delta(RA) being defined as the differ

111 of a range of values, whose limits are delta(RA)/(12)(1/2) and delta(RA)/(3)(1/2), with delta(RA) bei

112 (12)(1/2) and delta(RA)/(3)(1/2), with delta(RA) being defined as the difference between the maximum

113 at are among the key markers for determining RA's pathophysiology.

114 In evolving IA patients, 219/294 developed RA; the risk-score included naive and/or Treg and predic

115 , and particularly PDZK1IP1 may discriminate RA patients.

116 t in the inflammatory arthritis groups (i.e. RA and UA) and confirmed by qRT-PCR.

117 mporal expression patterns of genes encoding RA-synthesizing and -degrading enzymes, such as cytochro

118 (RA) reservoir strain and elevated estimated RA pressure were associated with worse baseline MELD-XI

119 ificant for T1D (P = 1.60 x 10(-24)) and for RA (P = 0.02).

120 ficant therapeutic effects a mouse model for RA.

121 inhibitor DX314 has enhanced selectivity for RA-metabolizing enzyme CYP26B1 and may offer an improved

122 The specificity for RA was 63 of 284 (78%; 95% CI: 72%, 82%) compared with o

123 isted NIR-II PMI provides a new strategy for RA theranostics, therapeutic monitoring and the beyond.

124 refore be a potential treatment strategy for RA.

125 hy controls and may have practical value for RA diagnosis.

126 al blood (PB) Foxp3+ Treg was collected from RA patients for determination of Treg inhibitory activit

127 Hence, RA/RAR in CD cells is a convergence point of regulation

128 in the T-cell group, 73% and 70% in the IL2-RA group, and 70% and 68% in the NI group (P = 0.001 and

129 were 68% in the T-cell group, 74% in the IL2-RA group, and 71% in the NI group (P = 0.0006).

130 In RA B cell hybrid clone RA015/11.88 and RA056/11.23.2, NE

131 BDNF expression was virtually absent in RA neurons of SD birds, increasing to barely detectable

132 espective pathogenic roles of SE and ACPA in RA nor the mechanisms underlying their coassociation are

133 ro-PEG-folate to image arthritis activity in RA with favourable imaging characteristics of rapid clea

134 hances the effect of most biologic agents in RA.

135 in K/BxN mice with chronic arthritis, and in RA patients and healthy controls.

136 he differences between remission and cure in RA are first defined, followed by a discussion of the un

137 ers) that prevent the achievement of cure in RA by triggering sustained immune activation and effecto

138 the obstacles to the achievement of cure in RA.

139 tion, there was no significant difference in RA between the groups and no relationship with periphera

140 study signals for coronary artery disease in RA signaling target gene loci and correlation between co

141 ovel therapeutic target for joint disease in RA with potential for vascular benefit, which warrants f

142 have shown to be individually efficacious in RA (in vitro, in vivo, and/or in humans) and provide a s

143 upports a pathogenic role for PAD enzymes in RA as both promoters and targets of the autoimmune respo

144 cellular matrix and joint lubricants, FLS in RA produce pathogenic mediators such as cytokines and pr

145 etic properties of [18F]fluoro-PEG-folate in RA patients.

146 n 16 of 32 AN participants, but not found in RA participants.

147 The next frontier in RA is the development of curative interventions, for exa

148 B (TrkB) for BDNF, prevented the increase in RA neuron firing rate in LD+T birds.

149 Treatment with TNF inhibitors in RA patients reverses the expression changes of the netwo

150 hritis and systemic inflammation not only in RA, but possibly also in other inflammatory conditions.

151 and food components on clinical outcomes in RA, but insufficient evidence exists to provide specific

152 h as destructive peripheral polysynovitis in RA versus axial and peripheral osteoproliferative inflam

153 reduced endothelial-dependent relaxation in RA.

154 act of anti-TNF therapy on Th17 responses in RA is not well understood.

155 ons as biomarkers of DMARD responsiveness in RA.

156 ight important mechanisms of genetic risk in RA and the wider context of immune dysregulation.

157 trexate therapy remains the gold standard in RA therapy.

158 e, has been a regularly achievable target in RA.

159 e role of newly identified bacterial taxa in RA warrants further investigations.

160 omising genes, one of which is unexplored in RA.

161 R-wave triggered pacing can induce RA, the magnitude of which can be modulated by varying t

162 ts inactive isomer inhibits IL-1beta-induced RA-FLS activation and proliferation.

163 (RDHs); and oxidation of retinaldehyde into RA by aldehyde dehydrogenases family 1, subfamily A (ALD

164 nt weighting and regression adjustment (IPTW-RA).

165 In IPTW-RA survival analysis, an average FHS user had a 44% lowe

166 monstrate that RDH10 and ALDH1a3 are the key RA-synthesis enzymes involved in vestibular development.

167 Females had larger RA reservoir strain (39 +/- 15% vs. 32 +/- 13%, p = 0.04

168 For spectacle corrected measurements, RA was significantly larger in the myopic group, with a

169 hich is necessary for increased ROS-mediated RA pathogenesis.

170 with notable decreases in T effector memory RA(+) cells.

171 ulated epigenetic marks were identified near RA target genes already known to be required for body ax

172 xpressing endothelium and identifies a novel RA modulator in lung development.

173 concentrations increased the accumulation of RA and anthocyanins, while the level of total phenolic c

174 The dramatic change in the activity of RA neurons during the breeding season provides a clear e

175 Exogenous administration of RA during late gestation partially mimics these defects;

176 was developed in respect to loaded amount of RA, composition of the loading solution, washing solvent

177 ated proteins - the hallmark autoantigens of RA.

178 ns of these findings in the wider context of RA pathogenesis.

179 During the course of RA, the synovium transforms into a hyperplastic invasive

180 Thus, degradation of RA during embryogenesis is required for formation of hig

181 R-A as a potential biomarker in diagnosis of RA, and targeting SR-A might be a therapeutic strategy.

182 study, we demonstrate that the disruption of RA signaling within the NEUROG3-expressing endocrine pro

183 differentiation by limiting the duration of RA signalling.

184 In kidneys, the beneficial effect of RA has been reported in multiple disease models, such as

185 In addition, the therapeutic evaluation of RA mice by NIR-II PMI is shown to be consistent with cli

186 il the contrasting aspects, a Janus face, of RA signaling that may guide its therapeutic use.

187 rioration of these functions, and failure of RA signaling is perhaps associated with normal cognitive

188 er, these data demonstrate the importance of RA signaling in endocrine specification and identify con

189 Genetic inhibition of RA production in tumor cells or pharmacologic inhibition

190 n tumor cells or pharmacologic inhibition of RA signaling within TME increases stimulatory monocyte-d

191 Levels of RA in tissues are regulated by spatiotemporal expression

192 tinal image size (RIS) on the measurement of RA, refractive error was separately corrected with (i) t

193 In a rat model of RA, the most promising derivative (5c) showed major anti

194 erosive pathway in an experimental model of RA.

195 im of our study was to compare all phases of RA strain using CMR-FT and STE and also assess the relat

196 This leads to production of RA, which acts on T(H) cells to induce IL-5 and gut-homi

197 A typifying property of RA CD4 T cells is the shunting of glucose away from glyc

198 Thus, SHM in the IgVH and/or VL regions of RA synovial B cells is necessary for the immunoreactivit

199 n be used to effectively predict the risk of RA and identify cases in early stages to prevent or alte

200 However, the role of RA signaling during endocrine specification has not been

201 can exacerbate the incidence and severity of RA.

202 Our data suggest that suppression of RA directly reduces arrhythmia susceptibility and reinfo

203 noic acid (RA) and supports the synthesis of RA from type II alveolar ECs to suppress excessive activ

204 Controlled synthesis of RA is essential for regulating synaptic plasticity in re

205 The synthesis of RA requires two enzymatic reactions: oxidation of retino

206 d TCZ-PNPs, for PA-imaging-guided therapy of RA.

207 Early recognition and treatment of RA is essential for achieving effective therapeutic outc

208 lly the first-line drug for the treatment of RA, psoriatic arthritis and other forms of inflammatory

209 design of new regimens for the treatment of RA.

210 with promising outcomes for the treatment of RA.

211 Our current understanding of RA risk has suggested cell-type-specific contexts for ca

212 the existence of maternal genetic effects on RA was indicated, contributing up to 16.00% (+/- 3.00%)

213 anssynaptic trophic effect exerted by HVC on RA.

214 bacterial composition of GCF might inform on RA activity.

215 r validate these independent effects for one RA in vitro.

216 o their possible treatment with vitamin A or RA.

217 ation and immobilization of most particulate RAs.

218 ent of novel strategies to treat and prevent RA.

219 that DX314, but not all-trans-RA or previous RA metabolism blocking agents, appears to protect epider

220 Furthermore, prolonged RA exposure phenocopies LSD1 inhibition, suggesting that

221 rated measure of fluctuations-the reactivity RA of a given entity.

222 iabetes mellitus) were randomized to receive RA or SV graft.

223 eavy albuminuria was associated with reduced RA/RAR activity in CD cells.

224 we designate as non-inflammatory refractory RA (NIRRA).

225 ignate as persistent inflammatory refractory RA (PIRRA); and those with supposed refractory RA who ha

226 roaches towards the definition of refractory RA and the application of single-cell and integrated omi

227 nologies to the identification of refractory RA endotypes are also discussed.

228 This Review of refractory RA focuses on two types of patients: those for whom mult

229 (PIRRA); and those with supposed refractory RA who have continued disease activity that is predomina

230 rapeutic approach in the anti-TNF refractory RA.

231 reat', 'treatment-resistant' or 'refractory' RA.

232 t RA-568 was more potent than RA in rescuing RA/RAR activity repressed by albumin, high glucose, angi

233 Systemic administration of alphaASGR1-RSPO2-RA in mice specifically upregulated Wnt target genes and

234 lting bi-specific molecule (alphaASGR1-RSPO2-RA) enhanced Wnt signaling effectively in vitro, and its

235 nti-NET/cit-H2B immunoreactivity of selected RA-rmAbs was abrogated in the VH and VL GL counterpart.

236 e diagnosis for early stage and seronegative RA.

237 tment and PA monitoring using TCZ-PNPs shows RA is significantly suppressed.

238 The results suggest RA changes with axial elongation in myopia to compensate

239 ore, 16S rRNA gene sequencing showed that TA@RAs could increase the diversity of the saliva-derived b

240 model were applied and demonstrated that TA@RAs could prevent secondary dental caries effectively.

241 eutral medium was used and confirmed that TA@RAs could respond to the critical pH value of de-/remine

242 etic RAR agonist RA-568 was more potent than RA in rescuing RA/RAR activity repressed by albumin, hig

243 sceptibility and reinforces the concept that RA plays a critical role in the pathophysiology of arrhy

244 We further determine that RA-mediated regulation of endocrine cell differentiation

245 patient survival estimate was 72.6% for the RA group versus 65.2% for the SV group (hazard ratio for

246 he estimated 10-year patency was 85% for the RA versus 71% for the SV (hazard ratio for graft failure

247 r patient survival estimate was 90.9% in the RA arm versus 83.7% in the RITA arm (hazard ratio for mo

248 eminatus were significantly increased in the RA group, only Porphyromonas gingivalis displayed signif

249 In the RA versus SV comparison, the estimated 10-year patency w

250 The 10-year patency rate of the RA is significantly higher than that of the free RITA an

251 In addition, the inhibition of the RA pathway in hESC-derived pancreatic progenitors downst

252 In comparison with STE derived strain, the RA reservoir and conduit strain were not significantly d

253 Infusion of BDNF protein adjacent to the RA of SD birds caused an increase in the spontaneous neu

254 with gene regulatory activity and that these RAs were more tolerated than NDAs.

255 Thus, RAs and their distinct evolutionary histories must be co

256 ined ex vivo using intact rat aortic tissue (RA) after pharmacological activation of p38 MAPK and als

257 We also identify markers truly unique to RA and thus likely linked to modulation of vocal motor f

258 depleted for regulatory activity compared to RAs, while RAs have activity levels similar to non-intro

259 thromboembolic events among mothers nor Tpo-RA-related fetal or neonatal complications were observed

260 Median time of Tpo-RA exposure during pregnancy was 4.4 weeks (range, 1-39

261 safety and efficacy of off-label use of Tpo-RAs during pregnancy, a multicenter observational and re

262 ary findings, temporary off-label use of Tpo-RAs for severe and/or refractory ITP during pregnancy se

263 1-39 weeks); the indication for starting Tpo-RAs was preparation for delivery in 10 (58%) of 17 pregn

264 Response to Tpo-RAs was achieved in 77% of cases, mostly in combination

265 X314 can potentiate the effects of all-trans-RA in healthy and diseased reconstructed human epidermis

266 sults indicate that DX314 inhibits all-trans-RA metabolism with minimal off-target activity and shows

267 dly discovered that DX314, but not all-trans-RA or previous RA metabolism blocking agents, appears to

268 nism of JQ1 action, we subjected JQ1-treated RA-FLS to transcriptional profiling and determined BRD2

269 d closed regions of chromatin in JQ1-treated RA-FLS.

270 6(+) T) cells isolated from anti-TNF-treated RA patients classified as responders or nonresponders to

271 might be a therapeutic approach to treating RA.

272 In 120 untreated RA patients, the risk-score for predicting treatment-ind

273 face imprinted polymers were generated using RA as the template.

274 In RAPCO-SV (the SV versus RA arm of the RAPCO trial), 225 patients >=70 years of a

275 dienone compounds including b-AP15, VLX1570, RA-9, RA-190, EF24, HO-3867, and MCB-613.

276 dependent on SHM in the IgVH region whereas RA B cell hybrid clone RA015/11.91 required affinity mat

277 n and identify conserved mechanisms by which RA signaling directs pancreatic endocrine cell fate.

278 r regulatory activity compared to RAs, while RAs have activity levels similar to non-introgressed var

279 p = 0.000542) and PDZK1IP1 (p = 0.0206) with RA-specific gene expression profiles and elevated expres

280 ttranslational modifications associated with RA, such as citrullination and oxidation, reduced C4b de

281 synovitis of the forefoot is associated with RA.

282 and 20 age-similar non-myopic controls, with RA estimated using iterative two-phase regression analys

283 ptional analyses comparing Cyp26b1(-/-) with RA-treated lungs reveal overlapping, but distinct, respo

284 d serum samples from patients diagnosed with RA and in just 75 min.

285 morbidity and mortality in individuals with RA.

286 be a rare occurrence among individuals with RA.

287 tor-A (sSR-A) are increased in patients with RA and correlate positively with clinical and immunologi

288 nce for atherosclerotic CVD in patients with RA and provides a contemporary analysis of what is known

289 VD risk and risk management in patients with RA are discussed.

290 ndations for CVD prevention in patients with RA compared with the general population.

291 up can accurately discriminate patients with RA from healthy controls and may have practical value fo

292 d with the general population, patients with RA have approximately double the risk of atherosclerotic

293 Studies in patients with RA have yielded a disease-specific metabolic signature,

294 VD has been known for decades, patients with RA receive poorer primary and secondary CVD preventive c

295 d March 2016, newly presenting patients with RA, patients with other early arthritides, and healthy c

296 In patients with RA, the IFN signature is characterised by up-regulation

297 et reduces disease activity in patients with RA.

298 ed CVD preventive measures for patients with RA.

299 management and prevention for patients with RA.

300 A)-rmAbs derived from CD19(+) B cells within RA human synovial tissues frequently react against NETs.