ライフサイエンスコーパス: arteritis

1 e in the initial diagnosis of GCA giant cell arteritis .

2 lopathy affecting large arteries (giant cell arteritis).

3 condition or in association with giant cell arteritis.

4 cute inflammatory illness marked by coronary arteritis.

5 tion, a response resembling clinical intimal arteritis.

6 and monocytes from patients with giant cell arteritis.

7 tes in patients with panarteritic giant cell arteritis.

8 ic cells (DC) in the development of coronary arteritis.

9 and regulate the patterning of the emerging arteritis.

10 ells are required for LCCWE-induced coronary arteritis.

11 s in the pathological mechanisms of coronary arteritis.

12 ings relevant to the diagnosis of giant-cell arteritis.

13 diagnosis of challenging cases of giant-cell arteritis.

14 erning diagnosis and treatment of giant-cell arteritis.

15 dulating inflammation in atherosclerosis and arteritis.

16 r-alpha is present in arteries in giant cell arteritis.

17 ents with large-vessel disease in giant cell arteritis.

18 lesion described as endotheliitis or intimal arteritis.

19 ar signaling in this mouse model of coronary arteritis.

20 chymal invasion and abscesses, and meningeal arteritis.

21 vation and granuloma formation in giant cell arteritis.

22 rom latent infection or induction of chronic arteritis.

23 the underlying pathomechanisms of giant cell arteritis.

24 d-free remission in patients with giant-cell arteritis.

25 s disease, multiple sclerosis and giant-cell arteritis.

26 , is the cause of gamma HV68-induced elastic arteritis.

27 during follow-up, with 1 caused by temporal arteritis.

28 ils and monocytes that precipitates coronary arteritis.

29 individuals and in patients with giant cell arteritis.

30 olvement in elderly patients with giant cell arteritis.

31 re also diagnosed with giant cell (temporal) arteritis.

32 A agonists may provide effective therapy for arteritis.

33 weanling mice exhibited milder large-vessel arteritis.

34 e age-related vasculitic syndrome giant cell arteritis.

35 s and tocilizumab) in patients with Takayasu arteritis.

36 omes are affected by the severity of intimal arteritis.

37 ains important in the management of Takayasu arteritis.

38 proach, prognosis, and treatment of brucella arteritis.

39 ring was studied in patients with giant-cell arteritis.

40 attractive for arterial lesions of Takayasu arteritis.

41 nd lumen pathologies resulting from Takayasu arteritis.

42 revascularization in patients with Takayasu arteritis.

43 es of its main branches, indicating Takayasu arteritis.

44 red the gold standard in imaging of Takayasu arteritis.

45 s disease and the first GWAS of equine viral arteritis.

46 cs and outcomes of 49 patients with Takayasu arteritis (80% female; median age, 42 years [20-55 years

47 Giant cell arteritis, a chronic autoimmune disease of the aorta and

48 s, such as Takayasu arteritis and giant cell arteritis, affect vital arteries and cause clinical comp

49 l and gene expression analyses of giant cell arteritis-affected temporal arteries revealed abundant e

50 me of whose phenotypes included large-vessel arteritis and cranial neuropathy.

51 equired for IL-1beta maturation) in coronary arteritis and evaluated the efficacy of IL-1 receptor an

52 r levels of chimerism, moderate CR including arteritis and fibrosis in the Peyer's patches and mesent

53 Large vessel vasculitides, such as Takayasu arteritis and giant cell arteritis, affect vital arterie

54 ecrotizing vasculitis, including necrotizing arteritis and hemorrhagic pulmonary capillaritis.

55 nd other recent investigations of giant cell arteritis and idiopathic intracranial hypertension is cl

56 A small number of patients with Takayasu arteritis and IgG4-related aortitis have also been succe

57 be the mainstay of treatment for giant cell arteritis and its complications.

58 ecessary to regulate MCMV-associated elastic arteritis and latency in vivo and reactivation of a herp

59 fection, limiting chronic diseases including arteritis and pulmonary fibrosis.

60 ge vessel inflammatory disorders (giant cell arteritis and Takayasu arteritis) are the most common fo

61 nflamed arteries of patients with giant cell arteritis and Takayasu arteritis, and serum levels of th

62 ssel vasculitides, including both giant cell arteritis and Takayasu arteritis, and the aortitis of Co

63 ulitis, Wegener's granulomatosis, giant cell arteritis and Takayasu's arteritis in the US amounted to

64 y available tests: pentraxin-3 in giant cell arteritis and Takayasu's arteritis; von Willebrand facto

65 ce are protected from LCCWE-induced coronary arteritis and that this protection is mediated through t

66 An unusual case of giant cell arteritis and the most significant symptoms and diagnost

67 cessful monitoring of patients with Takayasu arteritis and to plan possible interventional treatment.

68 countered are giant cell arteritis (temporal arteritis) and vasculitis secondary to infections.

69 2 of 203 (1.0%) for treatment of giant cell arteritis, and 1 of 193 (0.5%) for the pathophysiologic

70 nt, acute angle-closure glaucoma, giant cell arteritis, and central retinal artery occlusion.

71 ZV) vasculopathy produces stroke, giant cell arteritis, and granulomatous aortitis, and it develops a

72 ulomatosis, polyarteritis nodosa, giant-cell arteritis, and hypersensitivity vasculitis on the basis

73 teritis, in 1 of 1 cases of nongranulomatous arteritis, and in 5 of 18 control aortas (28%) obtained

74 is, the nongranulomatous variant of temporal arteritis, and Kawasaki's disease.

75 vasculitides (Takayasu arteritis, giant cell arteritis, and polyarteritis nodosa) to atherosclerosis,

76 ients with giant cell arteritis and Takayasu arteritis, and serum levels of this cytokine mirror dise

77 uding both giant cell arteritis and Takayasu arteritis, and the aortitis of Cogan syndrome and relaps

78 ndents (5.1%; 95% CI, 2.2%-8.0%), giant cell arteritis; and 10 of 218 respondents (4.6%; 95% CI, 1.8%

79 is, polymyalgia rheumatica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjogren's syndrom

80 in helping make the diagnosis of giant cell arteritis are discussed.

81 ima where pathological changes in giant cell arteritis are most pronounced.

82 Subsets of giant cell arteritis are probably caused by variations in the patho

83 ntracerebral VZV vasculopathy and giant cell arteritis are strongly associated with productive VZV in

84 The long-term effects of the acute coronary arteritis are unknown.

85 disorders (giant cell arteritis and Takayasu arteritis) are the most common form of systemic vasculit

86 the category of acute rejection with intimal arteritis (ARV) is relevant to short- and long-term clin

87 Giant cell arteritis has supplanted temporal arteritis as the preferred term for chronic granulomatou

88 e, our data demonstrate that in the coronary arteritis associated with KD, TGF-beta suppresses elasti

89 Intimal arteritis (Banff v-lesion) was an independent histologic

90 be effective for the treatment of Takayasu's arteritis, but their role in the treatment of other form

91 or RAO in cardiac surgery include giant cell arteritis, carotid stenosis, stroke, hypercoagulable sta

92 Granulomatous arteritis characterizes the pathology of giant cell arte

93 lammatory vascular disease, such as Takayasu arteritis, chemotherapy- or radiation-induced vascular i

94 c rejection grade, endotheliitis, transplant arteritis, coagulation necrosis, acute pancreatitis, pre

95 Giant-cell arteritis commonly relapses when glucocorticoids are tap

96 Giant cell arteritis continues to be a common cause of visual loss.

97 rtic involvement in patients with giant cell arteritis correlates with the significant detection of V

98 In temporal arteries affected by giant cell arteritis, DCs are highly enriched and activated and hav

99 multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophageal, stomach, pancreas, lung

100 ystemic granulomatous vasculitis, giant cell arteritis, diverse connective tissue disorders; viral, s

101 ustry as the causative agent of equine viral arteritis (EVA), a respiratory, systemic, and reproducti

102 T cells in vasculitic lesions of giant cell arteritis express several markers that identify them as

103 with such unusual manifestations of temporal arteritis facilitates early diagnosis and treatment, the

104 ontrol group, with significant reductions of arteritis, fibrosis, and cellular infiltration, includin

105 e provides a clinical overview of giant cell arteritis, focusing on diagnosis, treatment, and practic

106 thologic studies proposing an acute coronary arteritis followed by healing fail to account for the co

107 Giant-cell arteritis frequently poses diagnostic and therapeutic ch

108 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK) are major

109 her an association exists between giant cell arteritis (GCA) and the presence of varicella-zoster vir

110 Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are related inflammatory disorders occur

111 Giant cell arteritis (GCA) causes autoimmune inflammation of the ao

112 ticle aims to provide a review of giant cell arteritis (GCA) clinical features, differential diagnosi

113 Granuloma formation in giant cell arteritis (GCA) emphasizes the role of adaptive immunity

114 Giant cell arteritis (GCA) is a granulomatous and occlusive vasculi

115 Giant-cell arteritis (GCA) is a large-vessel vasculitis characteriz

116 Giant cell arteritis (GCA) is a systemic vasculitis preferentially

117 Giant cell arteritis (GCA) is a vasculitic syndrome that preferenti

118 Giant cell arteritis (GCA) is an immune-mediated disease of unknown

119 Giant cell arteritis (GCA) is an inflammatory vasculopathy in which

120 Glucocorticoid (GC) therapy for giant cell arteritis (GCA) is effective but requires prolonged admi

121 Arterial wall damage in giant cell arteritis (GCA) is mediated by several different macroph

122 Giant cell arteritis (GCA) is the most common form of systemic vasc

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

124 Giant cell arteritis (GCA) is the most common systemic vasculitis i

125 Giant cell arteritis (GCA) is the most common type of primary vascu

126 that extracranial involvement of giant cell arteritis (GCA) may be more extensive than previously ap

127 a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated vasculitis.

128 ge arteries is well-documented in giant-cell arteritis (GCA), but the risk for cardiovascular events

129 In giant cell arteritis (GCA), inflammatory lesions typically produce

130 n rheumatology care and age, sex, giant cell arteritis (GCA), PMR relapses, corticosteroid complicati

131 Giant cell arteritis (GCA), the most common form of systemic vascul

132 In giant cell arteritis (GCA), vasculitic damage of the aorta and its

133 psies taken from individuals with giant cell arteritis (GCA).

134 ve low-dose methotrexate (MTX) in giant cell arteritis (GCA).

135 scular accidents often complicate giant cell arteritis (GCA).

136 of polymyalgia rheumatica and/or giant cell arteritis (GCA).

137 bilateral AION were suggestive of giant cell arteritis (GCA).

138 ammation, pituitary apoplexy, and giant cell arteritis (GCA).

139 ies, ranging from the vasculitides (Takayasu arteritis, giant cell arteritis, and polyarteritis nodos

140 avian or axillary vessels; aortic giant-cell arteritis; giant-cell arteritis presenting as an intense

141 is characterizes the pathology of giant cell arteritis, granulomatous aortitis, and intracerebral var

142 The outlook in Takayasu arteritis has improved over the last decade, reflecting

143 Giant cell arteritis has supplanted temporal arteritis as the prefe

144 ), performed for the diagnosis of giant cell arteritis, has a low reported rate of complications.

145 , and some patients with refractory Takayasu arteritis have responded to the immunomodulator leflunom

146 Studies in giant cell arteritis have shown that differences in the immunomodul

147 viruses in temporal arteries with giant cell arteritis have yielded contradictory results.

148 ted during the 1984 outbreak of equine viral arteritis in central Kentucky subsequently became long-t

149 the diagnostic procedure of choice to detect arteritis in cranial vessels.

150 We conclude that (i) the induction of arteritis in gammaHV68-infected IFN-gammaR-deficient mic

151 the preferred term for chronic granulomatous arteritis in older adults.

152 iption of a premortum diagnosis of pulmonary arteritis in PAN in which the patient had a response to

153 lmonary capillaritis and splenic necrotizing arteritis in some.

154 Mild arteritis in the 150 day allografts of both strain combi

155 matosis, giant cell arteritis and Takayasu's arteritis in the US amounted to $150 million per year.

156 tion of LCCWE produced severe focal coronary arteritis in TLR4(-/-) and C57BL/6 control mice but not

157 s with pathologically verified granulomatous arteritis, in 1 of 1 cases of nongranulomatous arteritis

158 nd postoperative immunosuppression to render arteritis inactive.

159 f some of these conditions, such as Takayasu arteritis, includes a very long period of low level symp

160 urvival, parenchymal rejection, or occlusive arteritis, indicating that these processes are IFN-gamma

161 lammation of the arterial wall in giant cell arteritis induces a series of structural changes, includ

162 Giant cell arteritis is a granulomatous vasculitis of the aorta and

163 Visual loss caused by giant cell arteritis is a medical emergency that requires prompt re

164 Giant cell arteritis is a systemic condition with a strong predilec

165 ar lesions support the model that giant cell arteritis is a T-cell-driven disease.

166 Giant-cell arteritis is an immune-mediated disease characterized by

167 Takayasu arteritis is an inflammatory disease of large-diameter a

168 Giant cell arteritis is associated with a markedly increased risk o

169 Giant-cell arteritis is associated with increased risks for MI, CVA

170 We show here that LCCWE-induced coronary arteritis is dependent on intact TLR2 and MyD88 signalin

171 ysm formation in association with giant cell arteritis is discussed, along with the implications of r

172 general, the clinical outcome of giant-cell arteritis is excellent, and efforts must now concentrate

173 Although survival in giant cell arteritis is generally good, subsets of patients with an

174 In other vascular territories, giant-cell arteritis is most commonly diagnosed by vascular imaging

175 uced remission of newly diagnosed giant cell arteritis is of no benefit and may be harmful.

176 ussed here, and scalp necrosis in giant-cell arteritis is reviewed.

177 mes of 79 consecutive patients with Takayasu arteritis (median age, 39 years; interquartile range [IQ

178 ary arteries: acute self-limited necrotizing arteritis (NA), subacute/chronic (SA/C) vasculitis, and

179 results than in patients with GCA giant cell arteritis -negative results ( TAB temporal artery biopsy

180 Large-vessel involvement in giant cell arteritis occurs in over a quarter of patients with this

181 Takayasu arteritis occurs mainly in young women and, if left untr

182 ssociated with increased RAO were giant cell arteritis (odds ratio [OR], 7.73; CI, 2.78-21.52; P < 0.

183 were more likely to have had rejection with arteritis, odds ratio (OR): 4.83 (1.47-15.87), p = 0.009

184 -documented classic PAN was found to have an arteritis of medium-sized muscular pulmonary arteries.

185 ) Systemic vasculitis disorders (necrotizing arteritis of the polyarteritis type, hypersensitivity va

186 Fungal arteritis of the Y graft used to revascularize the whole

187 were associated with allograft loss, whereas arteritis (OR=0.5, 95% CI=0.2-1.2, P=0.11) and glomeruli

188 scription in temporal arteries of giant cell arteritis patients with and without up-regulated neoangi

189 sfer experiments, CCR6(+) T cells produce an arteritis pattern with media-invasive T cells damaging v

190 aled discrete, superficial, white retinitis; arteritis; phlebitis; and retinal hemorrhages with or wi

191 antly higher in patients with GCA giant cell arteritis -positive results than in patients with GCA gi

192 els; aortic giant-cell arteritis; giant-cell arteritis presenting as an intense systemic inflammatory

193 red for the cellular activation and coronary arteritis produced by LCCWE.

194 As in giant cell arteritis, recent evidence supports the role of aspirin

195 t virus replication is necessary for chronic arteritis, since antiviral therapy of mice with establis

196 and radiographic manifestations of Takayasu arteritis (TA) in a cohort from the US, evaluate the res

197 nflammation is a typical feature of Takayasu arteritis (TA), and tumor necrosis factor (TNF) is impor

198 ng been the standard for diagnosing temporal arteritis (TA), but in practice this test is less than 1

199 the wide variation in the course of Takayasu arteritis (TA), predicting outcome is challenging.

200 ust be able to confidently diagnose temporal arteritis (TA), since failure to make a correct diagnosi

201 in the assessment of patients with Takayasu arteritis (TA).

202 roximately 50% of all patients with Takayasu arteritis (TA).

203 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK) are major forms of large-vessel vasculit

204 Takayasu's arteritis (TAK) is a large-vessel vasculitis with a chro

205 elp accurately diagnose and monitor Takayasu arteritis (TAK).

206 Most frequently encountered are giant cell arteritis (temporal arteritis) and vasculitis secondary

207 regulation of neoangiogenesis in giant cell arteritis, temporal arteries were examined for the exten

208 ei (LCCWE) into mice causes a focal coronary arteritis that histopathologically mimics the coronary l

209 tract (LCCWE), mice develop a focal coronary arteritis that histopathologically resembles Kawasaki di

210 Giant cell vasculitis is an arteritis that predominantly affects medium- and large-s

211 Intimal arteritis (the presence of v-lesions) in kidney transpla

212 a for a positive biopsy result in giant cell arteritis, the imaging characteristics of primary angiit

213 Temporal arteritis, the most common form of systemic vasculitis i

214 imilar to the lesions observed in Takayasu's arteritis, the nongranulomatous variant of temporal arte

215 ve highlighted etiologies such as giant cell arteritis, trauma, neuro-syphilis and demyelination seco

216 ymyalgia rheumatica, 228,000 have giant cell arteritis, up to 3.0 million have had self-reported gout

217 AMR: T cell-mediated rejection with intimal arteritis (v) lesion (TCMRV; n = 78), total antibody-med

218 The Banff scores of intimal arteritis (v1, v2 and v3) represented low, moderate, and

219 apted virulent Bucyrus (VB) strain of equine arteritis virus (EAV) established persistent infection i

220 Equine arteritis virus (EAV) has a global impact on the equine

221 eptibility of CD3(+) T lymphocytes to equine arteritis virus (EAV) infection and establishment of per

222 f the virulent Bucyrus (VB) strain of equine arteritis virus (EAV) to produce the modified live virus

223 is the critical natural reservoir of equine arteritis virus (EAV), as venereal infection of mares fr

224 jor envelope proteins (G(L) and M) of equine arteritis virus (EAV), both individually and in heterodi

225 nalysis of CD3+ T cells infected with equine arteritis virus (EAV).

226 and possible cell entry receptor for equine arteritis virus (EAV).

227 so bind to the LDV-C 3'(-)NCR RNA and equine arteritis virus 3'(-)NCR RNA.

228 e determined the crystal structure of equine arteritis virus PLP2 in complex with ubiquitin (1.45 A).

229 s for processing of glycoprotein 3 of equine arteritis virus.

230 xin-3 in giant cell arteritis and Takayasu's arteritis; von Willebrand factor antigen in childhood ce

231 Giant cell arteritis was also identified in 5 patients.

232 Arteritis was associated with inclusion bodies and MCMV

233 Arteritis was associated with subsequent antibody-mediat

234 Acute KD coronary arteritis was characterized by transmural infiltration o

235 GCA giant cell arteritis was diagnosed or excluded clinically in all pa

236 Arteritis was observed only in the medium to large size

237 Arteritis was observed only in the medium to large size

238 , a significantly milder rejection with less arteritis was seen in the allografts of the recipient ma

239 s casei wall extract (LCWE) induces coronary arteritis, we show that LCWE increased TGF-beta signalin

240 ematosus (SLE), systemic sclerosis, Takayasu arteritis, Wegener granulomatosis, Behcet syndrome, and

241 tery specimens from patients with giant cell arteritis were analyzed bu two-color immunohistochemistr

242 ghty-eight percent of patients with Takayasu arteritis were inadequately controlled with or were into

243 patients suspected of having GCA giant cell arteritis were included in a prospective three-universit

244 ant role in the pathogenesis of equine viral arteritis when horses are infected with the virulent str

245 one of the RAG1(-/-) mice developed coronary arteritis, whereas 70% of WT and 100% of B cell(null) mi

246 the temporal arteries, mimicking giant cell arteritis, while, to our knowledge, the association betw

247 atments in refractory patients with Takayasu arteritis with an acceptable safety profile.

248 pes can be distinguished: cranial giant-cell arteritis with ischemic complications in the eye, the fa

249 An occlusive CD45+ arteritis with medial necrosis occurred with IL-10 defic

250 tral nervous system; large-vessel giant-cell arteritis with occlusions in the subclavian or axillary

251 t advances in medical management of Takayasu arteritis, with a special focus on the rationale and evi

252 Heterozygotes do not die from arteritis within a year of birth but do develop small le

253 ihood of stroke or visual loss in giant-cell arteritis without increasing bleeding complications.