ライフサイエンスコーパス: GCA

1 GCA and PMR in individuals from northwestern Spain are a

2 GCA can also involve large arteries, especially the subc

3 GCA giant cell arteritis was diagnosed or excluded clini

4 GCA is not a single entity but includes several variants

5 GCA was mostly associated with class II genes (HLA-DRB1/

6 GCA, first described by Horton et al., is a systemic imm

7 ded 272 cases of gastric adenocarcinoma (142 GCA, 103 GNCA, and 27 unspecified) and 524 controls who

8 We identified 204 GCA cases and 407 controls.

9 Of 214 GCA patients to whom the IRQ was sent, 145 (68%) respond

10 All 4 GCA-positive TAs contained viral antigen in skip areas,

11 er virus (VZV) antigen was found in all of 4 GCA-positive temporal arteries (TAs) but was not present

12 lin fixation, VZV DNA was detected in 2 of 4 GCA-positive, VZV antigen-positive TAs.

13 At the index date, 45 GCA patients (22%) and 125 non-GCA patients (31%) had ha

14 Of 45 GCA-negative participants whose TAs contained VZV antige

15 t rapidly in the presence of the sequence 5'-GCA-3'.

16 a-zoster virus antigen was found in 45 of 70 GCA-negative TAs (64%), compared with 11 of 49 normal TA

17 rlier study revealed VZV antigen in 68 of 93 GCA-positive TAs (73%), compared with 11 of 49 normal TA

18 In rare instances, a GCA lesion may result in tooth-root exposure.

19 This article presents a case of a GCA treated with a combined regenerative approach and re

20 vealed histologic features consistent with a GCA.

21 Guanylyl cyclase subtype A (GCA) is the main receptor that mediates the effects of a

22 ral correlates of general cognitive ability (GCA) in development could be extended to the rest of the

23 rivation of main (general combining ability (GCA)) and interaction (specific combining ability (SCA))

24 inal trait value, general combining ability (GCA), specific combining ability (SCA) and mid-parental

25 the hydrophilic bile acid, glycocholic acid (GCA), and either the antioxidants, alpha tocopherol, ebs

26 ), taurocholic acid (TCA), glycocholic acid (GCA), and tauroursodeoxycholic acid (TUDCA) all activate

27 odeoxycholic acid (TUDCA), glycocholic acid (GCA), glycodeoxycholic acid (GDCA), and S1P-induced acti

28 the conjugated bile acid, glycocholic acid (GCA).

29 a (ESCC) and gastric cardia adenocarcinomas (GCA) in common population.

30 estinal deconjugation of orally administered GCA.

31 n, and biliary secretion of the administered GCA.

32 The gingival cyst of the adult (GCA) is an uncommon developmental cyst of odontogenic or

33 vered adenovirus expressing O-GlcNAcase (Adv-GCA) into the myocardium of STZ-induced diabetic mice.

34 ly improved in diabetic hearts receiving Adv-GCA (P<0.05).

35 isolated from diabetic hearts receiving Adv-GCA exhibited improved calcium transients with a signifi

36 2-fold in the diabetic hearts receiving Adv-GCA.

37 ment in fat-soluble vitamin absorption after GCA treatment.

38 ere more pronounced in the first month after GCA diagnosis (combined HR, 4.92 [CI, 2.59 to 9.34]; HR

39 SIRT1 messenger RNA was down-regulated after GCA treatment, potentially through induction of microRNA

40 The ganglion cell analysis (GCA) algorithm was used to detect the macular GCIPL and

41 (RR = 2.43; 95% CI, 1.82-3.41; P < .001) and GCA-positive TAs (RR = 2.03; 95% CI, 1.52-2.86; P < .001

42 salts, GCDA binds exclusively to site 1 and GCA to site 2.

43 of OSCC (HR: 1.08, 95% CI: 1.01 to 1.16) and GCA (HR: 1.09, 95% CI: 1.00 to 1.20).

44 -matched healthy arteries, PMR arteries, and GCA arteries were coimplanted into SCID mice.

45 ificantly associated with decreased ESCC and GCA risk especially for the subjects with under-weight o

46 t the emulsification mechanisms for KLTA and GCA were different.

47 % and relapses by 36% to 54% in both PMR and GCA.

48 two types of gums, KLTA (Acacia senegal) and GCA (Acacia seyal), both in their native/untreated forms

49 Graft coronary arteriopathy (GCA) after heart transplantation is a major factor limit

50 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK) are major forms of l

51 ciation exists between giant cell arteritis (GCA) and the presence of varicella-zoster virus (VZV), b

52 a rheumatica (PMR) and giant cell arteritis (GCA) are related inflammatory disorders occurring in per

53 Giant cell arteritis (GCA) causes autoimmune inflammation of the aorta and its

54 to provide a review of giant cell arteritis (GCA) clinical features, differential diagnosis, treatmen

55 Granuloma formation in giant cell arteritis (GCA) emphasizes the role of adaptive immunity and highli

56 Giant cell arteritis (GCA) is a granulomatous and occlusive vasculitis that ca

57 Giant-cell arteritis (GCA) is a large-vessel vasculitis characterized by immun

58 Giant cell arteritis (GCA) is a systemic vasculitis preferentially affecting l

59 Giant cell arteritis (GCA) is an immune-mediated disease of unknown etiology.

60 icoid (GC) therapy for giant cell arteritis (GCA) is effective but requires prolonged administration,

61 rterial wall damage in giant cell arteritis (GCA) is mediated by several different macrophage effecto

62 Giant cell arteritis (GCA) is the most common form of systemic vasculitis that

63 Giant cell arteritis (GCA) is the most common form of vasculitis in individual

64 Giant cell arteritis (GCA) is the most common systemic vasculitis in elderly i

65 Giant cell arteritis (GCA) is the most common type of primary vasculitis.

66 cranial involvement of giant cell arteritis (GCA) may be more extensive than previously appreciated a

67 le genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated vasculitis.

68 is well-documented in giant-cell arteritis (GCA), but the risk for cardiovascular events is not well

69 In giant cell arteritis (GCA), inflammatory lesions typically produce interferon-

70 ogy care and age, sex, giant cell arteritis (GCA), PMR relapses, corticosteroid complications, comorb

71 Giant cell arteritis (GCA), the most common form of systemic vasculitis in adu

72 In giant cell arteritis (GCA), vasculitic damage of the aorta and its branches is

73 ituitary apoplexy, and giant cell arteritis (GCA).

74 methotrexate (MTX) in giant cell arteritis (GCA).

75 dents often complicate giant cell arteritis (GCA).

76 from individuals with giant cell arteritis (GCA).

77 ION were suggestive of giant cell arteritis (GCA).

78 ditionally, PLG and P4HA2 were identified as GCA risk genes at the genome-wide level of significance

79 The other assessed GCA status according to a standard protocol.

80 cortical atrophy scale for frontal atrophy (GCA-F).

81 -four case patients with subclavian/axillary GCA diagnosed by angiography and 74 control patients wit

82 idence of strong genetic differences between GCA and TAK in the HLA.

83 kely to be present in the adventitia of both GCA-negative TAs (RR = 2.43; 95% CI, 1.82-3.41; P < .001

84 We explored the domains of QOL affected by GCA in audiotaped focus groups.

85 xcessive O-GlcNAc modification is reduced by GCA expression, mitochondrial function improves; the act

86 ogy antigens and the risk of gastric cardia (GCA) and gastric noncardia (GNCA) adenocarcinomas in nor

87 VZV may cause GCA.

88 se in vivo role of these proteins in causing GCA has not been clarified.

89 these patients had histologically confirmed GCA (group 1), and 28 patients had negative results of a

90 ed in patients with histologically confirmed GCA.

91 ed in patients with histologically confirmed GCA.

92 tensities, bicaudate index, global cortical (GCA) and medial temporal lobe atrophy scores and single

93 e-vessel GCA from those with classic cranial GCA.

94 ne (BCA) and gamma-glutamyl-ss-cyanoalanine (GCA).

95 logy criteria should not be used to diagnose GCA and all patients suspected of having GCA should unde

96 lled trials in patients with newly diagnosed GCA was performed.

97 Each GCA patient was matched for age, sex, and length of medi

98 When I-BABP is presented with either GCA or GCDA alone, the ligands bind to both sites.

99 dentified, formalin-fixed, paraffin-embedded GCA-negative, GCA-positive, and normal TAs (50 sections/

100 However, a temporal artery biopsy excluded GCA, showing segmental stenosis of the lumen caused by a

101 Smoldering disease activity may expose GCA patients to the risk of progressive vascular disease

102 tive results of a temporal artery biopsy for GCA (group 2).

103 t in the vascular lesions characteristic for GCA, a subset of macrophages has the potential to suppor

104 merican College of Rheumatology criteria for GCA.

105 g/day or equivalent, and 40 to 60 mg/day for GCA, followed by individualized tapering regimens in bot

106 dditive and additive-by-additive effects for GCA and dominance-related effects for SCA and MPH, and a

107 The overall magnitude of the effects for GCA on the X tends to be lower than that on the autosome

108 ol/L, whereas they were >10 times higher for GCA.

109 nt and proposed other putative risk loci for GCA involved in Th1, Th17, and Treg cell function.

110 pecimens that were positive and negative for GCA showed a significant difference (P = 0.010).

111 and 29 specimens histologically negative for GCA.

112 ormed on seven of the specimens positive for GCA and five negative specimens.

113 temporal artery biopsy samples positive for GCA compared with the negative specimens.

114 formed on five of the specimens positive for GCA.

115 magnitude of the variation is not random for GCA.

116 We test whether genes significant for GCA are randomly distributed across chromosomes and use

117 there is a paucity of genes significant for GCA on the X relative to the autosomes.

118 ic background influencing susceptibility for GCA, we performed a genome-wide association screening in

119 The dynamics of the dissociation of ANP from GCA were investigated in cultured Chinese hamster ovary

120 ex vivo-generated dendritic cells (DC) from GCA patients were PD-L1(lo), whereas the majority of vas

121 additive-by-additive QTL were detected from GCA than from trait phenotype, and fewer QTL were from M

122 l function in patients with visual loss from GCA is poor.

123 ent with an adenovirus encoding O-GlcNAcase (GCA) resulted in improved calcium transients and SERCA2a

124 ch are reduced by expression of O-GlcNAcase (GCA).

125 tively, of CGamF, cholic acid (CA), glycoCA (GCA), tauroCA, and taurolithocholic acid-3-sulfate.

126 I-BABP binds two molecules of glycocholate (GCA) with low intrinsic affinity but an extraordinary hi

127 more pronounced in the case of glycocholate (GCA), the bile salt that binds with high positive cooper

128 site selectivity of I-BABP for glycocholic (GCA) and glycochenodeoxycholic (GCDA) acids using isotop

129 ed with reduced expression of hBD-1 (GGG>ACG>GCA; P < .001) and hBD-3 (GGG>GCA>ACG; P = .04) in skin

130 hBD-1 (GGG>ACG>GCA; P < .001) and hBD-3 (GGG>GCA>ACG; P = .04) in skin when measured 72 hours after w

131 We found a high-caries-experience haplotype (GCA), which increased DMFT scores two-fold, and a low- c

132 ed consent, 185 patients suspected of having GCA giant cell arteritis were included in a prospective

133 ose GCA and all patients suspected of having GCA should undergo a temporal artery biopsy.

134 d management of patients suspected of having GCA.

135 Due to male hemizygosity, GCA for X-linked phenotypes must be due to trans-acting

136 nitive impairment was associated with higher GCA score (OR = 6.2 per additional score; 95% confidence

137 In human GCA artery-severe combined immunodeficiency (SCID) mouse

138 In GCA, adjunctive treatment with MTX lowers the risk of re

139 In GCA, temporal artery biopsy may not be required in patie

140 In GCA, temporal artery biopsy remains the standard for def

141 id (ASA) had cytokine-repressing activity in GCA and could function as a steroid-sparing agent.

142 ies can aid in assessing disease activity in GCA.

143 hly "branched" nature of the carbohydrate in GCA gum was also thought to be responsible for the "spre

144 DCs are critical antigen-presenting cells in GCA.

145 Large-artery complication is common in GCA.

146 ed awareness of large-artery complication in GCA, particularly early-occurring aortic dissection, may

147 Thoracic aortic dissection in GCA is associated with markedly increased mortality.

148 GCs are therapeutically effective in GCA and the prednisone dosage was reduced to physiologic

149 producing Th17 cells have been implicated in GCA.

150 ell subsets promote vascular inflammation in GCA.

151 ecular mechanisms of arterial wall injury in GCA are not understood.

152 Lower extremity involvement in GCA and PMR may be associated with significant morbidity

153 cate potential involvement of neutrophils in GCA pathogenesis.

154 Thus, protein nitration in GCA is highly compartmentalized, reflecting the producti

155 fewer gynecologic malignancies were noted in GCA patients (OR 0.39 [95% CI 0.13-1.15], P = 0.09).

156 Assessment of QOL in GCA should include vision and other domains that are not

157 ncentrations of IL-6 and IL-17 quantified in GCA plasma at weeks 1 and 24 replicated this differentia

158 Nitrated tyrosine residues in GCA arteries were detected almost exclusively on endothe

159 Imaging studies in GCA and polymyalgia rheumatica (PMR) suggest that vascul

160 Thus, in GCA, a breakdown of the tissue-protective PD1/PD-L1 chec

161 n of TNF allele frequencies between isolated GCA and isolated PMR indicated that the main difference

162 In patients with isolated GCA, the primary association was with TNFa2, which was i

163 Treatment with 15 mg/kg GCA resulted in total duodenal bile acid concentrations

164 Localized GCA symptoms are the end-result of vascular insufficienc

165 ical change trajectories of higher and lower GCA groups were parallel through life, suggesting contin

166 , and temporal artery involvement, mimicking GCA.

167 ly transfected with wild-type (WT) or mutant GCA receptors.

168 nal benefit to patients with biopsy-negative GCA treated with corticosteroids, although the optimal a

169 malin-fixed, paraffin-embedded GCA-negative, GCA-positive, and normal TAs (50 sections/TA) collected

170 tients had other causes, including neoplasm, GCA, and brain stem infarction.

171 ndex date, 45 GCA patients (22%) and 125 non-GCA patients (31%) had had a previous cancer.

172 The non-GCA group consisted of 325 women (80%) and 82 men (20%).

173 This marker was confirmed as novel GCA risk factor using four additional cohorts (PGCA = 5.

174 .15 mum for sectoral GCIPL The Cirrus HD-OCT GCA algorithm can successfully segment macular GCIPL and

175 -analysis in comparison with the analysis of GCA and TAK separately.

176 Transcriptome analysis of GCA-affected temporal arteries revealed low expression o

177 The association of GCA with study outcomes is expressed with hazard ratios

178 ogy Project, we identified incident cases of GCA diagnosed between January 1, 1950 and December 31, 2

179 In the MTX group, there were fewer cases of GCA relapse heralded by symptoms of isolated polymyalgia

180 a role in the pathogenesis of some cases of GCA.

181 histopathological features characteristic of GCA, and 16 (36%) showed adventitial inflammation adjace

182 cluding loss of vision are characteristic of GCA.

183 t blindness, the most feared complication of GCA.

184 s on the systemic and vascular components of GCA are not understood.

185 Diagnoses of GCA, outcomes, and cardiovascular risk factors were iden

186 ced wall thickening support the diagnosis of GCA (specificity 78%-100% for ultrasound and 73%-97% for

187 ries is accurate in the initial diagnosis of GCA giant cell arteritis .

188 (H&E) staining to establish the diagnosis of GCA.

189 merican College of Rheumatology diagnosis of GCA.

190 solic factors with the cytoplasmic domain of GCA.

191 t association between histologic evidence of GCA and the presence of B19 DNA in TAB tissue (chi2 = 10

192 f VZV DNA or with the histologic evidence of GCA.

193 es tested that showed histologic evidence of GCA.

194 s warranted concerning the immunogenetics of GCA.

195 tive protein may be a more specific index of GCA compared with the ESR.

196 9 (MMP-9) is present in arterial lesions of GCA and may be involved in its pathogenesis.

197 mmatory cytokines in the vascular lesions of GCA.

198 an, Canada, also had no detectable levels of GCA and BCA.

199 highlights a novel clinical manifestation of GCA, with evidence for a neutrophil component and an esc

200 the systemic and vascular manifestations of GCA.

201 lmicus diagnosed 3 weeks before the onset of GCA symptoms.

202 The pathogenesis of GCA is T-cell dependent and antigen driven.

203 l reactivity occurred in the pathogenesis of GCA or during its clinical management with a canonical g

204 tia is an early event in the pathogenesis of GCA.

205 d tissues involved in the pathophysiology of GCA.

206 onsible for the emulsification properties of GCA gum, indicating that the emulsification mechanisms f

207 2- to 4-fold increase in remission rates of GCA in a randomized clinical trial (N = 30).

208 tios (HRs) for a first and second relapse of GCA were 0.65 (P = 0.04) and 0.49 (P = 0.02), respective

209 ion of GC therapy and permanent remission of GCA (median of 22 months), the total median dose of pred

210 hism was associated with a decreased risk of GCA (T vs. C: OR = 0.95; 95%CI = 0.91-0.98; P < 0.01).

211 sociated with significantly elevated risk of GCA.

212 emorgin C did not affect uptake/secretion of GCA by the liver but inhibited its fetal-maternal transf

213 corticosteroid treatment, clinical signs of GCA disappeared in all patients; however, 60% of the pat

214 Clinical subsets of GCA appear to result from variable cytokine expression.

215 s for whom there was a clinical suspicion of GCA.

216 d biopsies from 25 patients with symptoms of GCA as well as positive H&E pathology and 25 patients wi

217 n of variation in mRNA abundance in terms of GCA (general combining ability or additive variance).

218 the presence and mode of action (in terms of GCA and SCA) of undetected polygenes.

219 Initial treatment of GCA with IV GC pulses allowed for more rapid tapering of

220 a rheumatica (PMR), a subclinical variant of GCA, adventitial DCs were mature and produced the chemok

221 icoids as the most effective therapy for PMR/GCA.

222 Diagnosis of PMR/GCA is made by clinical features and elevated inflammato

223 Biopsy-positive GCA is associated with TA infection by varicella-zoster

224 Patients with biopsy-positive GCA underwent two consecutive temporal artery biopsies,

225 Twenty-seven patients with biopsy-proven GCA were enrolled in a randomized, double-blind, placebo

226 Twenty-five patients with biopsy-proven GCA were enrolled into a prospective treatment study.

227 patients with temporal artery biopsy-proven GCA without large vessel involvement matched for the dat

228 al arteries from patients with biopsy-proven GCA.

229 repancy to an effect of the mutations in P(R-GCA) on promoter clearance.

230 e level, while transcription directed by P(R-GCA) was the same as that directed by the wild-type prom

231 ional mutation at position -30 (yielding P(R-GCA)) suppresses this effect.

232 per se or ATP alone cannot account for rapid GCA receptor-ligand dissociation under physiological con

233 n therapies aimed at preventing HCMV-related GCA and improving the long-term result of cardiac transp

234 and membranes containing GCC, or the related GCA.

235 equences were determined to be GAC(5N)RTAAY, GCA(6N)CTGA, GTCA(6N)TGAY and CAC(5N)TGGC, respectively.

236 In patients with clinically suspected GCA, prevalence of VZV in their TAs is similar independe

237 ation-based case-control study indicate that GCA patients had significantly fewer malignancies prior

238 The GCA group included 163 women (80%) and 41 men (20%).

239 Among the GCA-negative group, herpes zoster antigen was not detect

240 Among the GCA-positive group, 3 patients had positive staining for

241 s both recognize the same bases (U73 and the GCA anticodon) of tRNA for aminoacylation, they have dif

242 nd activate T cells that originated from the GCA lesions.

243 was with TNFa2, which was independent of the GCA associations with HLA-DRB1*0401 and *0101.

244 gum was found to be superior to that of the GCA gum.

245 mbined regenerative approach and reviews the GCA literature with an emphasis on the clinical aspects

246 liac/femoral artery stenosis attributable to GCA.

247 initial remissions, serious morbidity due to GCA, cumulative CS dose, or treatment toxicity.

248 osed to GCDC, and to a much lesser extent to GCA.

249 of the resume codon was reverted from GGC to GCA.

250 have identified aspects of QOL important to GCA patients.

251 dentified wherein area related positively to GCA in development.

252 ning the ESE, and mutation of GAA repeats to GCA within the ESE inhibited both exon 3 recognition in

253 lass I and II molecules to susceptibility to GCA.

254 ng disease activity in untreated and treated GCA patients.

255 file of untreated and glucocorticoid-treated GCA was examined in peripheral blood and temporal artery

256 culitides enrolled patients with unequivocal GCA.

257 ion distinguished patients with large-vessel GCA from those with classic cranial GCA.

258 l presentation of patients with large-vessel GCA, whereas symptoms related to impaired cranial blood

259 egative in 42% of patients with large-vessel GCA.

260 ists in the diabetic heart, and that in vivo GCA overexpression reduces overall cellular O-GlcNAcylat

261 ted in bile in the conjugated form, of which GCA represented 59.6 +/- 9.3% of the total biliary bile

262 s must be due to trans-acting factors, while GCA for autosomal phenotypes may be due to cis- or trans

263 idents of Olmsted County, Minnesota, in whom GCA was diagnosed between January 1, 1950, and December

264 idents of Olmsted County, Minnesota, in whom GCA was diagnosed between January 1, 1950, and December

265 other case of root exposure associated with GCA and no previous report of regenerative therapy.

266 ndicated that the strongest association with GCA was provided by the TNFa2 allele, although DRB1*0401

267 B explained most of the HLA association with GCA, consistent with previously reported associations of

268 of the ternary complex of human I-BABP with GCA and GCDA, we introduced single-residue mutations at

269 nd 25 patients with symptoms compatible with GCA but negative H&E pathology.

270 biopsies would not have been diagnosed with GCA using American College of Rheumatology criteria alon

271 criteria and would have been diagnosed with GCA.

272 microsatellite associations were found with GCA and PMR.

273 c and/or abdominal aorta) and the group with GCA without large-artery complication.

274 ith control myocytes, whereas infection with GCA adenovirus resulted in improved myocytes enhancer fa

275 of site selectivity in its interactions with GCA and glycochenodeoxycholate (GCDA), the two major bil

276 infecting high glucose-treated myocytes with GCA adenovirus reduced the degree of specificity protein

277 Among 3408 patients with GCA (73% female; mean age, 73 years), the incidence rate

278 ompared with that in all other patients with GCA (P < 0.001).

279 Survival of patients with GCA and large-artery stenosis was not different from tha

280 proach was used to compare 136 patients with GCA and/or PMR with 147 ethnically matched controls.

281 itis -positive results than in patients with GCA giant cell arteritis -negative results ( TAB tempora

282 s were significantly higher in patients with GCA giant cell arteritis -positive results than in patie

283 data derived from a sample of patients with GCA suggest that the G allele of MMP-9 polymorphism rs22

284 retrospective chart review for patients with GCA was conducted.

285 ortality in the whole group of patients with GCA with large-artery complication was similar to that i

286 ication was similar to that in patients with GCA without large-artery complication.

287 was not different from that of patients with GCA without large-artery complication.

288 tment with corticosteroids for patients with GCA.

289 the risk of ischemic events in patients with GCA.

290 uces ischemic complications in patients with GCA.

291 tment, and visual prognosis of patients with GCA.

292 main the standard treatment in patients with GCA.

293 nes and monocytes derived from patients with GCA.

294 ive dose and toxicity of CS in patients with GCA.

295 increased more than 17-fold in patients with GCA.

296 identified 125 Olmsted County residents with GCA diagnosed between 1950 and 1991 and obtained followu

297 cohort, comprising 1,651 case subjects with GCA and 15,306 unrelated control subjects from six diffe

298 erred, women, older patients, and those with GCA, PMR relapses, and corticosteroid complications had

299 h third cranial nerve palsies and those with GCA, the incidence of other causes for isolated fourth a

300 gth of medical history to 2 subjects without GCA from the same population.