ライフサイエンスコーパス: GCA

1 GCA can also involve large arteries, especially the subc

2 GCA giant cell arteritis was diagnosed or excluded clini

3 GCA is designed to quantify growth cone morphodynamics f

4 GCA was associated with 10 other AIDs and TA was associa

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 Age 20 GCA accounted for 40% of variance in the same measure in

9 Supporting that idea, age 20 GCA, but not education, was associated with late midlife

10 We identified 204 GCA cases and 407 controls.

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

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

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

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

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

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

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

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

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

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

21 or of metabolism caused by an expansion of a GCA-repeat tract in the 5' untranslated region of the ge

22 vealed histologic features consistent with a GCA.

23 BFA) and the quinoline compound Golgicide A (GCA) inhibited HSV-1 entry via beta-galactosidase report

24 tment with brefeldin A (BFA) or Golgicide A (GCA) significantly reduces the yield of infectious viral

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

26 er accounting for general cognitive ability (GCA) at an average age of 20 y, additional education, oc

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

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

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

30 ked the lsBSH crystal with glycocholic acid (GCA), a substrate, and obtained a 2.10 angstrom structur

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

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

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

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

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

36 estinal deconjugation of orally administered GCA.

37 n, and biliary secretion of the administered GCA.

38 on-namely, downstream effects of early adult GCA.

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

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

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

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

43 2-fold in the diabetic hearts receiving Adv-GCA.

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

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

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

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

48 (Carl Zeiss Meditec) Ganglion Cell Analysis (GCA) was extracted, and structure-function relationships

49 itations, we developed Growth Cone Analyzer (GCA).

50 (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

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

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

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

54 We show that both BFA and GCA, as well as interfering with the synthesis of GBF1,

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

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

57 % and relapses by 36% to 54% in both PMR and GCA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Giant cell arteritis (GCA) is the most common type of primary vasculitis in We

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

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

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

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

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

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

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

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

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

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

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

85 dents often complicate giant cell arteritis (GCA).

86 from individuals with giant cell arteritis (GCA).

87 Giant cell arteritis (GCA, also called temporal arteritis) is a rare and Takay

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

89 tocytes using a gametocyte conversion assay (GCA).

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

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

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

93 Management of both GCA and PMR is hampered by the lack of universally accep

94 Significant familial associations of both GCA and TA with such a number of other AIDs provide evid

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

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

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

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

99 VZV may cause GCA.

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

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

102 ed in patients with histologically confirmed GCA.

103 ed in patients with histologically confirmed GCA.

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

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

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

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

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

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

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

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

112 dy we describe familial risk for GCA and for GCA and TA with any other AID based on the Swedish hospi

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

114 merican College of Rheumatology criteria for GCA.

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

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

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

118 wed that family history is a risk factor for GCA.

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

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

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

122 and 29 specimens histologically negative for GCA.

123 magnitude of the variation is not random for GCA.

124 ion-wide study we describe familial risk for GCA and for GCA and TA with any other AID based on the S

125 The familial risk for GCA was 2.14, 2.40 for women and non-significant for men

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

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

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

129 ticoids are the cornerstone of treatment for GCA and PMR, which are interrelated diseases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 d management of patients suspected of having GCA.

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

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

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

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

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

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

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

152 ies can aid in assessing disease activity in GCA.

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

154 DCs are critical antigen-presenting cells in GCA.

155 Large-artery complication is common in GCA.

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

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

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

159 producing Th17 cells have been implicated in GCA.

160 ell subsets promote vascular inflammation in GCA.

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

162 cate potential involvement of neutrophils in GCA pathogenesis.

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

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

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

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

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

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

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

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

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

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

173 , and temporal artery involvement, mimicking GCA.

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

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

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

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

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

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

180 .15 mum for sectoral GCIPL The Cirrus HD-OCT GCA algorithm can successfully segment macular GCIPL and

181 We demonstrate the adaptability of GCA through the analysis of growth cone morphological va

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

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

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

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

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

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

188 cluding loss of vision are characteristic of GCA.

189 t blindness, the most feared complication of GCA.

190 Possible long-term complications of GCA include aneurysm and stenosis of vessels, even in pa

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

192 o a highly polar pocket, the sterane core of GCA is stabilized by aromatic and hydrophobic interactio

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

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

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

196 merican College of Rheumatology diagnosis of GCA.

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

198 solic factors with the cytoplasmic domain of GCA.

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

200 s warranted concerning the immunogenetics of GCA.

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

202 9 (MMP-9) is present in arterial lesions of GCA and may be involved in its pathogenesis.

203 mmatory cytokines in the vascular lesions of GCA.

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

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

206 the systemic and vascular manifestations of GCA.

207 While the glycine moiety of GCA is exposed into a highly polar pocket, the sterane c

208 The number of GCA patients in the offspring generation was 4695, compa

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

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

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

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

213 d tissues involved in the pathophysiology of GCA.

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

215 2- to 4-fold increase in remission rates of GCA in a randomized clinical trial (N = 30).

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

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

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

219 sociated with significantly elevated risk of GCA.

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

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

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

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

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

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

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

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

228 mbly, since in the presence of either BFA or GCA, the assembly of infectious mature triple-layered vi

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

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

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

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

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

234 al arteries from patients with biopsy-proven GCA.

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

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

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

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

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

240 and membranes containing GCC, or the related GCA.

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

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

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

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

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

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

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

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

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

250 the 24-2C grid fell close to or outside the GCA grid when corrected for ganglion cell displacement.

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

252 liac/femoral artery stenosis attributable to GCA.

253 ructure containing complex of lsBSH bound to GCA and cholic acid (CA), a product.

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

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

256 have identified aspects of QOL important to GCA patients.

257 dentified wherein area related positively to GCA in development.

258 lass I and II molecules to susceptibility to GCA.

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

260 culitides enrolled patients with unequivocal GCA.

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

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

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

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

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

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

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 hose parents or siblings were diagnosed with GCA, TA or any other AID.

272 criteria and would have been diagnosed with GCA.

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 ng and long-term management of patients with GCA and PMR, including the tapering of treatment.

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.