ライフサイエンスコーパス: TAA

1 TAA administration for 8 weeks induced extensive hepatic

2 TAA and AD mortality (1994-2010) using International Cla

3 TAA and AD mortality trends show substantial heterogenei

4 TAA mortality has increased in Hungary, Romania, Japan,

5 TAA was significantly more common (than abdominal aortic

6 TAA- and PTX-treated animals were evaluated following CB

7 TAAs consist of three identical subunits that together f

8 TAAs form fibrous, adhesive structures on the bacterial

9 .07) and ruptured (28% versus 46%; P<0.0001) TAA.

10 on (53.4% TEVAR vs. 53.3% OPEN, P < 0.0001), TAA (55.8% TEVAR vs. 59.7% OPEN, P = 0.84), dissection (

11 halan (mel) using 3-thiophene acetic acid (3-TAA) as functional monomer was fabricated by electropoly

12 QCM) electrode by electropolymerization of 3-TAA in presence of mel template by cyclic voltammetry (C

13 se mutation animal model of CHM harbouring a TAA nonsense mutation, and (2) a primary human fibroblas

14 irst report of a specific export factor of a TAA, suggesting that at least in some cases TAA autotran

15 escribed the full fiber structure of SadA, a TAA of unknown function in Salmonella and other enteroba

16 mination of ascorbic acid (AA) and total AA (TAA) contents (as the sum of AA and dehydroascorbic acid

17 icular administered triamcinolone acetonide (TAA) is one of the drug treatments employed to ameliorat

18 tioxidant properties of trans-aconitic acid (TAA) alone or in the presence of usual antioxidants were

19 Thioesters and thioacetic acid (TAA) have been invoked as key reagents for the origin of

20 overexpression lines are dependent on active TAA genes.

21 c content (TPC), total antioxidant activity (TAA) (using DPPH and ORAC-values) and individual phenoli

22 determination of total antioxidant activity (TAA) based on ABTS assay was developed and validated on

23 on patterns were observed among 7 additional TAA-specific TCRs isolated from allogeneic versus autolo

24 ers of the Trimeric Autotransporter Adhesin (TAA) family play a crucial role in the adhesion of Gram-

25 (NadA), a trimeric autotransporter adhesin (TAA) that acts in adhesion to and invasion of host epith

26 of UpaG, a trimeric autotransporter adhesin (TAA).

27 Trimeric autotransporter adhesins (TAAs) are important virulence factors of many Gram-negat

28 Trimeric autotransporter adhesins (TAAs) are modular, highly repetitive surface proteins th

29 mice were treated with anakinra 3 days after TAA induction.

30 ed TAA, MFS augments risk for AoD even after TAA grafting.

31 Three weeks after TAA induction, aortas were harvested and tissue was coll

32 Three weeks after TAA induction, aortic luminal area increased by 38 +/- 1

33 hat CD8(+) TILs will be tumor-associated Ag (TAA) specific, it is unknown whether CD8(+) T cells with

34 that cross-react with tumor-associated Ags (TAA).

35 c T cells by generating universal allogeneic TAA-specific T cells from one donor that might be admini

36 epitopes of MAGE-A1 and NY-ESO-1 to analyze TAA-specific CD8(+) T-cell responses in a large cohort o

37 tterns of injury and fibrosis in the CDE and TAA model and to indisputably identify the fibrosis patt

38 foundation for future work using the CDE and TAA regimens to model a variety of human chronic liver d

39 ant regulatory associations between DEMs and TAA-induced liver carcinogenesis at an earlier stage tha

40 om WT mice treated with CCl(4), ethanol, and TAA released 2- to 3-fold higher levels of adenosine tha

41 Last, chronic CCl(4) injection and TAA treatment caused more liver fibrosis to WT than to O

42 Retention of pathogen- and TAA-specific immunity after alloanergization demonstrate

43 The TPC and TAA in MAE extracts were higher than the other three ext

44 Our genetic data show that YUC and TAA work in the same pathway and that YUC is downstream

45 in mortality from thoracic aortic aneurysm (TAA) and aortic dissection (AD) with the aim of identify

46 tin content during thoracic aortic aneurysm (TAA) development in a murine model.

47 re associated with thoracic aortic aneurysm (TAA) in Marfan syndrome.

48 Thoracic aortic aneurysm (TAA) is a common progressive disorder involving gradual

49 us complication of thoracic aortic aneurysm (TAA).

50 hy (GA) underlies thoracic aortic aneurysms (TAA) in younger adults.

51 red, degenerative thoracic aortic aneurysms (TAA), 2701 (24%) descending aortic dissections, 1033 (9%

52 s with descending thoracic aortic aneurysms (TAAs) after open and endovascular repair (TEVAR).

53 Thoracic aortic aneurysms (TAAs) are common, but experimental TAA models are limite

54 Thoracic aortic aneurysms (TAAs) develop secondary to abnormal aortic extracellular

55 icated that the detection level of each anti-TAA autoantibody in a given serum sample was strongly de

56 improve sensitivity and specificity for anti-TAA autoantibody detection.

57 f cancer, detection of only one type of anti-TAA autoantibody is not sufficient to give a reliable an

58 w here a mounting body of evidence that anti-TAA mAbs are capable of profoundly synergizing with T ce

59 stem to detect the eventual presence of anti-TAAs autoantibodies.

60 he GTF2b protein, a tumor-associate antigen (TAA) related to colorectal cancer.

61 such that only one tumor-associated antigen (TAA) can be targeted, limiting the efficacy that can be

62 The use of tumor-associated antigen (TAA) mRNA for therapeutic purposes is under active inves

63 Survivin is a tumor-associated antigen (TAA) that inhibits apoptosis and is widely overexpressed

64 t specificity to a tumor associated antigen (TAA) thereby conferring antitumor activity in vivo.

65 The presence of tumor-associated antigen (TAA)-specific CD8(+) T cell populations within SKILs (cr

66 LAG3 was higher on tumor-associated antigen (TAA)-specific CD8(+) TIL, compared with other CD8(+) TIL

67 n herpes virus and tumor-associated antigen (TAA)-specific immunity was measured with HLA-class I-res

68 t cancer antigens [tumor-associated antigen (TAA)].

69 Vaccines based on tumor-associated antigens (TAA) have limited therapeutic efficacy due to their weak

70 C-I/II-restricted tumor-associated antigens (TAA) of tyrosinase and gp100, depending on their HLA-DR4

71 vaccines based on tumor-associated antigens (TAA) represent an attractive approach for the treatment

72 ive at presenting tumor-associated antigens (TAA) to the immune system in a manner that is sufficient

73 targeting several tumor-associated antigens (TAA).

74 CTL responses to tumor-associated antigens (TAA).

75 luding well-known tumor-associated antigens (TAAs) and potential new biomarkers of breast cancer, wer

76 ptors recognizing tumor-associated antigens (TAAs) can now be engineered to be expressed on a wide ar

77 es (mAbs) against tumor-associated antigens (TAAs) is that their mechanism of action is dominated by

78 immunity against tumor-associated antigens (TAAs) may exert selective antileukemic activity reprievi

79 iple epitopes and tumor-associated antigens (TAAs) may provide effective immunotherapy in patients wi

80 taining universal tumor associated antigens (TAAs) present an attractive treatment modality for cance

81 ific antigens and tumor-associated antigens (TAAs) that can activate antitumor immune responses.

82 directed against tumor-associated antigens (TAAs) were shown to be relevant tumor markers.

83 TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS (TAA) family of amino transferases converts tryptophan to

84 ty and efficacy of total-ankle arthroplasty (TAA).

85 iant peptide vaccines were less effective as TAA expression increases, data presented in this article

86 We hypothesized that as TAA expression increases, the AH1 cross-reactivity of va

87 As TAAs are highly expressed in placental tissues we hypoth

88 Among patients with genetically associated TAA, MFS augments risk for AoD even after TAA grafting.

89 D among patients with genetically associated TAA.

90 reatment of WT mice with anakinra attenuated TAA formation (control: 99.2+/-15.5% versus anakinra: 68

91 class I and II-restricted epitopes augments TAA-specific CD8(+) T-cell responses, contributing to im

92 double electron transfer step involving both TAA(+) units rather than sequential single electron tran

93 TAA, suggesting that at least in some cases TAA autotransport is assisted by additional periplasmic

94 After chronic TAA administration, DPPIV(-) F344 rats exhibited progres

95 g lymphocyte (SKIL) cultures and circulating TAA-specific CD8(+) T cells.

96 we show that the transcription of both CKRC1/TAA and CKRC2/YUC8 can be induced by CK and that the phy

97 tandardized core laboratory tests classified TAA etiology and measured aortic size.

98 In conclusion, coactivating TAA-specific CD4(+) T-helper cells with DCs pulsed with

99 a thermophila--that reassign the stop codons TAA and TAG to glutamine, for the presence of tandem sto

100 equencies of the three classical stop codons TAA, TAG, and TGA were analyzed, and a publicly availabl

101 We compared TAA-specific and virus-specific CD8(+) T cells in the sa

102 use these structures to reconstruct complete TAA fibers.

103 Beyond this concentration, TAA showed an additive effect.

104 macological inhibition of IL-1beta decreased TAA formation and progression, indicating that IL-1beta

105 4-1BBL was also used as a vehicle to deliver TAAs in vivo to dendritic cells (DCs) constitutively exp

106 simplest thiolated acetic acid derivatives, TAA and methylthioacetate (MTA) were explored here.

107 Descending TAAs were induced in Yorkshire pigs (20-25 kg; n=7) thro

108 In 3 of 13 patients tested, we detected TAA-specific CD4(+)CD25(+)FoxP3(-) T cells with high pro

109 accinated with MHC-I-loaded DCs, we detected TAA-specific CD8(+) T cells with maintained IFN-gamma pr

110 ent hierarchy was observed between different TAA.

111 d clear immunodominance patterns within each TAA, but no consistent hierarchy was observed between di

112 vestigate the effects of elevated endogenous TAA expression on variant peptide-induced responses, we

113 miRNAs (DEMs) were identified in the entire TAA-treatment course.

114 After antigen-specific expansion, TAA-specific CD8(+) T cells were detectable by tetramer

115 neurysms (TAAs) are common, but experimental TAA models are limited and the role of interleukin-1beta

116 al dominant fashion and is known as familial TAA.

117 osomal loci, and further mapping of familial TAA genes has highlighted disease-causing mutations in a

118 Combining five TAAs (p53, Hsp60, Hsp70, Her2-Fc, NY-ESO-1) on two diffe

119 r T-cell receptor stimulation) covering five TAAs and the universal helper pan-DR epitope, formulated

120 ents represent a new potential biomarker for TAA and acute aortic dissection.

121 t suitable early and sensitive biomarker for TAA-induced hepatocarcinogenesis due to its consistent e

122 ied to be early and sensitive biomarkers for TAA-induced hepatocarcinogenicity.

123 he use of a powerful new adjuvant system for TAA-based cancer vaccines.

124 that IL-1beta may be a potential target for TAA treatment.

125 Folate signaling appears to be unique for TAA at 1 week (Folh1, Cubn), whereas aryl-hydrocarbon re

126 n developing thymocytes with specificity for TAAs expressed in the thymus could pose a risk for neopl

127 identify a novel immunological strategy for TAAs to boost the pathogenicity of A. pleuropneumoniae.

128 oducing CD8(+) T cells specific for all four TAA in the periphery as well as in liver and tumor tissu

129 measures could further reduce mortality from TAA and AD.

130 erol, and body mass index and mortality from TAA.

131 uce the expansion of T cells with functional TAA recognition.

132 Current (third generation) TAA prostheses feature cementless design and ligament pr

133 peptide-induced responses, we used the GP70 TAA model.

134 The greatest TAA was measured for SM followed by SUM, RM, WM and WUM.

135 dominal aortic aneurysm), and 1091 (86%) had TAA.

136 hat can be achieved because of heterogeneous TAA expression.

137 However, TAA-based subunit vaccines require potent adjuvants for

138 nd biochemical changes observed during human TAA development.

139 gens and a codon-optimized form of the human TAA survivin (coSVN), an oncoprotein that is overexpress

140 IL-1beta protein was measured in human TAAs and control aortas, and IL-1beta protein was increa

141 was increased approximately 20-fold in human TAAs.

142 und protein 10 (Grb10) as a newly identified TAA.

143 and detailed annotation of newly identified TAAs.

144 If TAA-specific CD4(+) T-cell responses were detected in SK

145 Depletion of Treg from cultures improved TAA-specific CD8(+) T-cell proliferation but did not res

146 Treatment with INT-747 in TAA and BDL reactivated the FXR downstream signaling pat

147 suggested that hydrogen atom abstraction in TAA by DPPH was located on -CH2- methylene bridge becaus

148 alloproteinases 3, 8, 9, and 12 increased in TAA tissue homogenates, whereas tissue inhibitors of met

149 red phenotype may play a significant role in TAA development through the enhancement of extracellular

150 d with an increased eNOS activity, which, in TAA, related to down-regulation of Rho-kinase and in BDL

151 During the course of tissue injury, TAA also induced cholangiocarcinomas.

152 However, patients with intact TAA selected for TEVAR had significantly worse survival

153 duce large panels of CARs against many known TAAs.

154 ion of individuals with genetically mediated TAA.

155 h protein and mRNA expression of melanocytic TAA in 15 melanoma lines (irrespective of initial Ag-exp

156 Microhomology (TAA and AGCT) at the breakpoints indicated that microhom

157 Neither TAA nor dissection was associated with fibrillin-2 or fi

158 Next, TAAs were induced in mice deficient of IL-1beta (IL-1bet

159 Nonsydromic TAA can occur as a genetically triggered, familial disor

160 l and predictors of outcomes in nonsyndromic TAA (NS-TAA) are incompletely defined compared to Marfan

161 Following CBDL, but not TAA exposure, rats developed HPS that was temporally cor

162 s show similar overall topology with a novel TAA fold predominantly composed of trimeric coiled-coils

163 Clinical outcomes for MFS and NS-TAA are similar but worse than BAV.

164 r NS-TAA, 8.7% for MFS, and 3.5% for BAV (NS-TAA and MFS vs. BAV p <0.05).

165 s (age 36.9 +/- 13.6 years, 26.8% female; NS-TAA, n = 311; MFS, n = 221; BAV, n = 228).

166 ith aortic dissection was more common for NS-TAA than MFS or BAV.

167 Calculated 10-year mortality was 7.8% for NS-TAA, 8.7% for MFS, and 3.5% for BAV (NS-TAA and MFS vs.

168 Management of NS-TAA, including surgical intervention, should be similar

169 edictors of outcomes in nonsyndromic TAA (NS-TAA) are incompletely defined compared to Marfan syndrom

170 MFS patients were younger than NS-TAA and BAV.

171 nd clinical outcomes for individuals with NS-TAA, MFS, and BAV.

172 Naturally occurring TAA-specific CD8(+) T-cell responses are present in pati

173 (LLO) and amino acid fragments 311 to 660 of TAA Mage-b (LM-LLO-Mage-b(311-660)) and the control stra

174 Especially, the addition of TAA at a concentration below 32mM to a solution containi

175 Conversely, oral administration of TAA caused both higher elastin accumulation and higher f

176 gs suggest that intranodal administration of TAA mRNA together with mRNA encoding immunomodulating mo

177 aortic elastic lamellae is characteristic of TAA.

178 ration of antioxidant for a concentration of TAA equal to 22.3mM.

179 we evaluated whether intranodal delivery of TAA mRNA together with TriMix, a mix of mRNA encoding CD

180 tic tests are available for the detection of TAA disease.

181 cal tissues, to evaluate the distribution of TAA in human cartilage after in vitro incubation.

182 However, the penetration and distribution of TAA into the avascular cartilage is not well understood.

183 patic fibrosis induced by extended dosing of TAA.

184 e same pathway and that YUC is downstream of TAA.

185 This boost and loss of TAA-specific immunity suggests that virtually every dono

186 Reduced ion mobilities of TAA cations (C2-C8) were calculated at 14% relative humi

187 ect of humidity on reduced ion mobilities of TAA cations is discussed.

188 s for the first time a large animal model of TAA that recapitulates the hallmarks of human disease an

189 equired to help unlock the full potential of TAA-specific CD8(+) T-cell responses.

190 restriction by selecting for the presence of TAA-specific CD8(+) T cells specifically recognizing tum

191 ion and maturation of DCs, hence, priming of TAA-specific T cells.

192 ic behavior and thermochemical properties of TAA and analogous esters have been preliminarily explore

193 nsive sequence divergence, the structures of TAA domains are highly constrained, due to the tight int

194 le the frequency of use of TAG, like that of TAA, was inversely proportional to the GC content of the

195 The patterns of use of TAA, TGA and TAG as real stop codons were less biased an

196 However, poor immunogenicity of TAAs requires potent adjuvants for therapeutic efficacy.

197 to host cells, but the immunopathogenesis of TAAs remains unknown.

198 To develop an experimental model of TAAs, 8- to 10-week-old male C57Bl/6 mice (wild type [WT

199 ht into the immunological pathogenic role of TAAs.

200 les PD-1, TIM3, and LAG3 are up-regulated on TAA-specific T cells isolated from human HCC tissues, co

201 beneficiaries discharged to home after open TAA repair (n = 12 679) and VHR (n = 52 807) between 200

202 y reduced the risk of readmission among open TAA patients who experienced perioperative complications

203 with a PCP after high-risk surgery (eg, open TAA repair), especially among patients with complication

204 red in 4649 patients (36.6%) undergoing open TAA repair and 4528 patients (8.6%) undergoing VHR durin

205 erall, 2619 patients (20.6%) undergoing open TAA repair and 4927 patients (9.3%) undergoing VHR were

206 adjusted regional analyses, undergoing open TAA repair in regions with high compared with low primar

207 ce, induction of liver injury with CCl(4) or TAA increased levels of autophagy.

208 Hepatic fibrosis was induced by CCl(4) or TAA treatment in CD73 knockout (CD73KO and C57BL/6 backg

209 T mice after treatment with either CCl(4) or TAA.

210 alitative and quantitative analysis of AA or TAA in pharmaceutical preparations or fruit beverages.

211 e to stimulation with polyclonal antigens or TAA.

212 Four patients [2 OR-AAA, 2 OR-TAA(A)] developed fatal postoperative intestinal ischemi

213 acic or thoracoabdominal aneurysm repair [OR-TAA(A)], 25 patients undergoing conventional open abdomi

214 gnificantly higher in patients undergoing OR-TAA(A) (P < 0.001).

215 vels increased in all patients undergoing OR-TAA(A) and OR-AAA reaching peak levels shortly after sur

216 only found in enterobacteria, whereas other TAAs are not typically associated with lipoproteins.

217 0.0001), and for the individual pathologies: TAA (182/3529 [5%] TEVAR vs. 451/3718 [12%] OPEN, P < 0.

218 In the perfused TAA and BDL cirrhotic liver, INT-747 improved endothelia

219 markers was observed at 8- and 16-week post-TAA-induction, whereas immunoreactivity for smooth-muscl

220 ous time points (2, 4, 8, and 16 weeks) post-TAA induction (0.5 M CaCl2, 15 minutes).

221 y, incidence, and pattern after prophylactic TAA surgery are poorly understood.

222 elow established thresholds for prophylactic TAA repair.

223 hat fulfilled size criteria for prophylactic TAA surgery at a subsequent AoD site.

224 immune responses against clinically relevant TAAs in 114 blood donors and 44 women during their first

225 sed in tumors, mimicking clinically relevant TAAs.

226 status, rather than exclusively representing TAA-specific T cells, and that PD-1 expression on CD8(+)

227 who underwent repair of intact and ruptured TAA, identified from a combination of procedural and dia

228 mode using tetraalkylammonium bromide salts (TAA), benzylamines (mono-, di-, and tri-), and illicit d

229 alanine (PolyAla), tetraalkylammonium salts (TAA), and hexakis(fluoroalkoxy)phosphazines (HFAP), in b

230 ype III secretion system to deliver selected TAA in the cytosol of professional antigen-presenting ce

231 tion with survivin (SVN) as a bona fide self TAA was effective in eradicating weakly immunogenic 3LL

232 irus 16 E7 oncoprotein or survivin as a self-TAA had potent therapeutic efficacy against TC-1 cervica

233 ed from tumor-associated self-antigens (self-TAA) are attractive targets for T-cell-based immunothera

234 sfected with full-length transcripts of self-TAA and HLA-A2 to allow presentation of all naturally pr

235 een underestimated and that a wealth of self-TAA can be targeted by T cells when using nontolerized T

236 It is necessary to use a set of several TAAs for determining specific autoimmune profiles.

237 Virulent but silent, TAA cries out for a biomarker that can predict the onset

238 Finally, to investigate treatment of small TAAs, WT mice were treated with anakinra 3 days after TA

239 Anakinra treatment in WT mice with small TAAs reduced aortic dilation on day 14 (control treatmen

240 DNA fragments that included genes specifying TAA.

241 udies also implicate fibrillin-1 in sporadic TAA.

242 lace all 314 TAG stop codons with synonymous TAA codons in parallel across 32 Escherichia coli strain

243 Changes to synIII include TAG/TAA stop-codon replacements, deletion of subtelomeric re

244 Engineered receptors targeting TAAs have most commonly been expressed on mature T cells

245 e of thioacetals is that terephthalaldehyde (TAA) sleeves, which are too flexible in the case of acet

246 l alkyl amine, 1,3,5,7-tetraaminoadamantane (TAA), combined with 1,3,5-triformylbenzene (TFB) or trif

247 When the stop codons TGA, TAA, and TAG are found in the second and third reading f

248 are partially IPA-deficient, indicating that TAAs are responsible for converting tryptophan to IPA, w

249 converted to indole-3-pyruvate (IPA) by the TAA family of amino transferases and subsequently IAA is

250 putably identify the fibrosis pattern in the TAA model as driven from the pericentral vein region.

251 (-)CD28(-)CD45RA(+)) that were absent in the TAA responses.

252 sing genomic GC content the frequency of the TAA codon decreases and that of the TGA codon increases

253 of Lewis lung carcinoma, vaccination of the TAA survivin with SA-4-1BBL/MPL yielded superior efficac

254 ve added to RM had negligible effects on the TAA of milk.

255 BALB/c mice display T cell tolerance to the TAA GP70(423-431) (AH1), expression of GP70 and suppress

256 ly important human herpes viruses and to the TAA WT1.

257 Both the YUCs and the TAAs have been shown to play essential roles in auxin bi

258 Thioacetamide (TAA) is a well-known hepatotoxicant and could be a liver

259 For thioacetamide (TAA)-induced hepatopathy rats, we observe that the propo

260 duct ligation (CBDL), but not thioacetamide (TAA)-induced nonbiliary cirrhosis, lung capillary densit

261 se) or oral administration of thioacetamide (TAA) for 1 year (mouse).

262 induced by administration of thioacetamide (TAA) in the drinking water for 21 wk or by repeated intr

263 ody (1D11), in a rat model of thioacetamide (TAA)-induced hepatic fibrosis.

264 injury by CCl(4) injection or thioacetamide (TAA) treatment elevated OPN expression.

265 duced in mice using CCl(4) or thioacetamide (TAA); liver tissues and stellate cells were analyzed.

266 with PBS, CCl(4), ethanol, or thioacetamide (TAA); their livers were harvested, and slices were incub

267 For this, thioacetamide (TAA)-intoxicated and bile-duct-ligated (BDL) rats were u

268 upplemented (CDE) diet versus thioacetamide (TAA) supplementation.

269 anted into DPPIV(-) rats with thioacetamide (TAA)-induced fibrosis/cirrhosis; rats were sacrificed 1,

270 Killing of tumor cells occurs through TAA-specific CTL-mediated cytolysis.

271 or virus-specific TILs, in sharp contrast to TAA-specific TILs in the same tumors.

272 Relative risk for AoD in relation to TAA etiology, incidence, and pattern after prophylactic

273 Relative to TAA without dissection, acute or subacute dissection (OR

274 rovides evidence that mortality secondary to TAA and mortality secondary to AD are both in decline.

275 he abiotic chemistry of compounds similar to TAA and the origins of metabolism.

276 to deliver activation stimuli in addition to TAAs to dendritic cells (DC).

277 g CD4(+) and/or CD8(+) T cells responding to TAAs compared with CMV or influenza Ags.

278 of strategies that aim to enhance the total TAA-specific CD8(+) T-cell response by therapeutic boost

279 The TPC, TAA and IPA of peel extracts using MAE was compared with

280 sensitizers and two peripheral triarylamine (TAA) donors was investigated by transient IR and UV-vis

281 ntramolecular electron transfer from the two TAA units (tau = 65 ps), followed by intermolecular prot

282 Unfortunately, TAA is not easily ionized by regular electrospray ioniza

283 proaches to redirect T cells against various TAAs.

284 and CD8(+) T cells and CTLs against various TAAs.

285 Therefore, combining various TAAs on different surfaces could improve sensitivity and

286 nificantly elevated at the end of the 8 week TAA treatment.

287 f all parameters in the CDE regimen, whereas TAA-treated mice had pericentral patterns of progressive

288 Genetic analyses of families affected with TAA have identified several chromosomal loci, and furthe

289 r microfibril fragments, are associated with TAA and dissection.

290 smoking prevalence were not associated with TAA or AD mortality trends.

291 detected in SKIL cultures, it coincided with TAA-specific CD8(+) T-cell responses.

292 Associations of fragment concentrations with TAA (versus abdominal aortic aneurysm) or with dissectio

293 ar and histological features consistent with TAA disease.

294 metalloproteinase abundance, consistent with TAA formation.

295 ighly expressed genes predominantly end with TAA, ensuring termination with either of the two release

296 Of those with TAA, 300 patients (27%) had chronic dissection and 109 (

297 e livers of Sprague-Dawley rats treated with TAA at three doses (4.5, 15 and 45 mg/kg) and four time

298 application of periadventitial elastase (WT TAA) or saline (WT control; n=30 per group).

299 8% and IL-1R knockout=62.6+/-17.2% versus WT TAA=104.7+/-23.8%; P<0.001for both).

300 WT TAAs demonstrated elastin fragmentation, smooth muscle c