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-T products were generated from autologous peripheral

7 TAA-Ts are a promising new treatment approach for patien

8 TAA-Ts safely induced disease stabilization, prolonged t

9 TAAs consist of three identical subunits that together f

10 TAAs form fibrous, adhesive structures on the bacterial

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

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

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

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

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

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

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

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

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

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

21 ial amino acids (EAA) and total amino acids (TAA) slightly decreased, ratio of EAA to TAA increased,

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

23 le acidity (TA), total antioxidant activity (TAA) and ascorbic acid (AA) decreased during cold storag

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

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

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

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

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

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

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

31 we investigated the safety of administering TAA-Ts that target Wilms tumor gene 1, preferentially ex

32 month progression-free survival of 73% after TAA-T infusion compared with a 38% 6-month progression-f

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

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

35 hain reaction was observed in patients after TAA-T infusion.

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

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

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

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

40 utions by hydrophobic tetra-n-alkylammonium (TAA(+)) cations-an effect not exerted by fully hydrated

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

42 Triangular, tris(4-aminophenyl)amine (TAA), and square, 1,3,6,8-tetrakis(p-formylphenyl)pyrene

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

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

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

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

47 TPC (8.90-14.72 mg GAE/g) and TAA (11.37-12.74 mumol TE/g) decreased significantly wit

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

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

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

51 -antigens such as MiHA in MiHApos donors and TAAs are present in peripheral blood of healthy individu

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

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

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

55 us complication of thoracic aortic aneurysm (TAA).

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

57 Data on thoracic aortic aneurysms (TAA), type B aortic dissections (TBAD), and traumatic ao

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

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

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

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

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

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

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

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

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

67 effects, inducing tumor-associated antigen (TAA) cross-priming with antitumor CD8+ T cell elicitatio

68 oma that is of low tumor-associated antigen (TAA) expression often respond poorly to PD-1/PD-L1 block

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

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

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

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

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

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

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

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

77 targeting several tumor-associated antigens (TAA).

78 ions by targeting tumor-associated antigens (TAA).

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

80 Tumor-associated antigens (TAAs) are monomorphic self-antigens that are proposed as

81 cells) targeting tumour-associated antigens (TAAs) can lead to on-target-off-tumour toxicity and to r

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

83 Tumour-associated antigens (TAAs) comprise a large set of non-mutated cellular antig

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

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

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

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

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

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

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

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

92 As TAAs are highly expressed in placental tissues we hypoth

93 expressed cellular antigens that function as TAAs(3,4).

94 range of endogenous tumour antigens, such as TAAs and neoantigens, for treating B cell malignancies.

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

96 D among patients with genetically associated TAA.

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

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

99 any cellular antigens previously shown to be TAAs, their presentation on major histocompatibility com

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

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

102 Tumor-associated antigen cytotoxic T cells (TAA-Ts) represent a new, potentially effective and nonto

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

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

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

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

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

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

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

110 use these structures to reconstruct complete TAA fibers.

111 Beyond this concentration, TAA showed an additive effect.

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

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

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

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

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

117 ent hierarchy was observed between different TAA.

118 owed better protein efficiency ratio and EAA/TAA (total) %, indicating the presence of good quality p

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

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

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

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

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

124 al dominant fashion and is known as familial TAA.

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

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

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

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

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

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

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

132 9518 TEVAR for TAA (n = 4436), TBAD (n = 3976) and TAI (n = 1106) were

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

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

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

136 measures could further reduce mortality from TAA and AD.

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

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

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

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

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

142 hat can be achieved because of heterogeneous TAA expression.

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

144 nd biochemical changes observed during human TAA development.

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

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

147 was increased approximately 20-fold in human TAAs.

148 and detailed annotation of newly identified TAAs.

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

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

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

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

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

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

155 ce the antitumor immune response by inducing TAA expression.

156 hs (range, 4.1 to 19.9 months) after initial TAA-Ts.

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

158 US to 72% in the UK (p < 0.001).Mean intact TAA (iTAA) diameter varied from 59 (US) to 69 mm (Nancy,

159 duce large panels of CARs against many known TAAs.

160 ion of individuals with genetically mediated TAA.

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

162 cells provokes T cell responses to multiple TAAs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 the nonradiative decay rates in the case of TAA-PTM radicals that have high CT energies are defined

182 aortic elastic lamellae is characteristic of TAA.

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

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

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

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

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

188 patic fibrosis induced by extended dosing of TAA.

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

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

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

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

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

194 more than two decades(1), yet the origins of TAA-specific T cells remain unclear.

195 ted against HLA*02:01-restricted peptides of TAA WT1-RMF, RHAMM-ILS, proteinase-3-VLQ, PRAME-VLD, and

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

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

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

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

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

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

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

203 ht into the immunological pathogenic role of TAAs.

204 e tumour cells may be an important source of TAAs for T cell priming(2), several recent studies sugge

205 This synergy was dependent on TAA cross presentation to cytolytic CD8+ T cells and on

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

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

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

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

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

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

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

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

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

215 e to stimulation with polyclonal antigens or TAA.

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

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

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

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

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

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

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

223 elow established thresholds for prophylactic TAA repair.

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

225 vator Vestigial-like 1 (VGLL1) as a putative TAA demonstrating overexpression in multiple tumor types

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

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

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

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

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

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

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

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

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

239 udies also implicate fibrillin-1 in sporadic TAA.

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

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

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

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

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

245 ar dynamics simulation results indicate that TAA(+) cations not only drive enhanced coordination of a

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

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

248 To expand the TAA landscape of pancreatic ductal adenocarcinoma (PDAC)

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

250 e gap law dependence that is observed in the TAA-PTM radicals that have low CT energies.

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

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

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

254 ignant samples) naturally overexpressing the TAA.

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

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

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

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

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

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

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

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

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

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

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

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

267 g to TAA expression in normal tissues and to TAA expression loss in tumour cells.

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

269 ds (TAA) slightly decreased, ratio of EAA to TAA increased, while the calculated protein efficiency r

270 -tumour toxicity and to resistance, owing to TAA expression in normal tissues and to TAA expression l

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

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

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

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

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

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

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

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

279 emitters based on substituted triarylamine (TAA) donors and a radical-carrying perchlorotriphenylmet

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

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

282 proaches to redirect T cells against various TAAs.

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

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

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

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

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

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

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

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

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

292 ar and histological features consistent with TAA disease.

293 metalloproteinase abundance, consistent with TAA formation.

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

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

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

297 TEVAR procedures per pathology varied, with TAA repair constituting from 40% of TEVARs in the US to

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