ライフサイエンスコーパス: CAV

1 CAV can develop as a consequence of non-MHC incompatibil

2 CAV constitutes a significant complication that limits t

3 CAV continues to limit the long-term survival of heart t

4 CAV is the most important determinant of cardiac allogra

5 CAV limits long-term survival after heart transplantatio

6 CAV shares genomic organization, genomic orientation, an

7 CAV was defined as an intimal thickening >/= 0.5 mm in t

8 CAV was diagnosed through intravascular ultrasound perfo

9 CAV was investigated using intravascular ultrasound.

10 CAV, including epicardial and microvascular components,

11 CAV-1 and DLC1 expression levels were correlated in two

12 CAV-1 was detected in the urine of three red foxes with

13 CAV-2 was not detected by PCR in any red foxes examined.

14 timal hyperplasia (61.6 vs 23.8%; P < 0.05), CAV-affected vessel number (55.3 vs 15.9%; P < 0.05), an

15 gether with the scaffold protein caveolin 1 (CAV-1), also acts as a negative regulator of TLR4 signal

16 Caveolin-1 (CAV-1) functions as a tumor suppressor in most contexts

17 sess the role of cholesterol and caveolin-1 (CAV-1) in the diffusion, expression, and functionality o

18 caveolar structural protein gene Caveolin-1 (CAV-1) were identified in two patients with non-BMPR2-as

19 Caveolin-1 (CAV-1), a structural protein of the cell membrane, is in

20 Canine adenovirus type 1 (CAV-1) causes infectious canine hepatitis (ICH), a frequ

21 Consistent with restoration of HO-1/CAV-1-negative regulation of TLR4 signaling, genetic or

22 ed the efficacy of canine adenovirus type 2 (CAV-2) vectors to transduce keratocyte in vivo in mice a

23 The role of canine adenovirus type 2 (CAV-2), primarily a respiratory pathogen, was also explo

24 response, is defective in CF MPhis through a CAV-1-dependent mechanism, exacerbating the CF MPhi resp

25 may be at an increased risk for accelerated CAV as detected by consecutive volumetric three-dimensio

26 ADMA levels and reduced risk of accelerated CAV.

27 fied and characterized a small 10-amino acid CAV subsequence (90-99) that accounted for the majority

28 xes were seropositive for canine adenovirus (CAV) by ELISA.

29 ty, H60 incompatible hearts develop advanced CAV.

30 hat could protect cardiac allografts against CAV.

31 investigate the effect of riboflavin against CAV at 60 days.

32 on (HTx), the vasculopathy of the allograft (CAV), a phenomenon of chronic rejection, is still a seri

33 These manipulations re-established HO-1 and CAV-1 cell surface localization in CF MPhis.

34 les were compared in CAV-positive (n=52) and CAV-free patients (n=51).

35 on in CD4+Th secreting IL-10 in both AMR and CAV.

36 Superior freedom from AR and CAV in the TAC-MMF group did not result in better long-t

37 We quantified FAs, CFV, and CAV in a breast milk sample collected before the infant'

38 s that the interplay between cholesterol and CAV-1 provides the molecular basis for modulating the fu

39 ny difference in rates of PGF at 90 days and CAV at 5 years between recipients of donor hearts with i

40 formation between the DLC1 START domain and CAV-1 contributes to DLC1 tumor suppression via a RhoGAP

41 d forward loop between HO-1/CO induction and CAV-1 expression.

42 otal and free testosterone plasma levels and CAV grading.

43 repair discriminate between CAV-negative and CAV-positive heart transplant recipients.

44 tion did not differ between CAV-negative and CAV-positive patients.

45 high discrimination between CAV-positive and CAV-negative patients (C-statistic 0.812; 95% confidence

46 icles discriminated between CAV-positive and CAV-negative patients.

47 t present antigen, both T cell responses and CAV were markedly reduced.

48 The development of any angiographic CAV was also more common in DSA II+ patients as compared

49 Patients with only mild angiographic CAV have significantly better outcomes than do patients

50 ng CCTA versus CCAG for the detection of any CAV (> luminal irregularities) and significant CAV (sten

51 Embase for all prospective trials assessing CAV using CCTA was performed using a standard approach f

52 Abs (p < 0.05; odds ratio [OR], associating CAV with anti-CM Ab = 13, 95% confidence interval [CI] 3

53 unique form of accelerated atherosclerosis, CAV remains the leading cause of late morbidity and mort

54 atory/antioxidant properties, will attenuate CAV.

55 nd CXCR3 blockade by TAK-779 would attenuate CAV in an experimental model.

56 optin toxicity in tumor cells and attenuates CAV replication, suggesting it may be a future target fo

57 C number and function did not differ between CAV-negative and CAV-positive patients.

58 and endothelial repair discriminate between CAV-negative and CAV-positive heart transplant recipient

59 thelial microparticles discriminated between CAV-positive and CAV-negative patients.

60 dictors provided high discrimination between CAV-positive and CAV-negative patients (C-statistic 0.81

61 EK 293 cells show an interdependence between CAV-1 and alphaC418W that could confer end plates rich i

62 To test the relationship between CAV and anti-CM autoimmunity in humans, we performed a c

63 groups, we analyzed the relationship between CAV and the effector-to-regulatory T cell ratio.

64 Both CAV-1 and FLOT-2 (flotillin-2), organizing proteins of c

65 Both CAV-1 and FLOT-2 knockdowns reduce TNF-mediated activati

66 rated from three different pairs of PV and C-CAV.

67 t PV neutralizing antibodies, contemporary C-CAV, like their ancestor(s), could be fertile ground for

68 of PV from a C-cluster coxsackie A virus (C-CAV) ancestor through mutation of the capsid that caused

69 from a pool of different human pathogens (C-CAVs).

70 we address the mechanism by which DSA causes CAV.

71 hus in the structural changes characterizing CAV.

72 Strategies to control CAV traditionally have focused on lymphocyte functions.

73 mimetic peptide, is effective in controlling CAV via induction of HO-1 in the graft and a direct effe

74 CXCR3 by TAK-779 is effective in controlling CAV.

75 MPhis in response to LPS is due to decreased CAV-1 expression, which is controlled by the cellular ox

76 s of OHT patients with confirmed high-degree CAV and a matched control group consisting of patients w

77 ity and specificity of 81% and 75% to detect CAV (intimal thickening >0.5 mm), whereas the PPV and NP

78 rably with invasive angiography in detecting CAV in heart transplant recipients and may be a preferab

79 L-6-deficient cardiac grafts did not develop CAV after transplantation into allogeneic Rag(-/-) mice.

80 Almost one-third of patients develop CAV by 5 years post-transplant and 1 in 8 deaths beyond

81 al tPA in subsequent biopsies rarely develop CAV or graft failure during the next 10 years and potent

82 llograft recipients who are prone to develop CAV.

83 Untreated animals developed CAV with luminal obliteration of 25.2+/-13.6% and 41.4+/

84 d an adoptive transfer of NK cells developed CAV, supporting the role of NK cells in CAV development.

85 entify patients at higher risk of developing CAV after HT.

86 oup of patients with high risk of developing CAV.

87 to detect HTx patients at risk of developing CAV.

88 cells play critical roles in the development CAV.

89 ial biomarker of CAV, clearly discriminating CAV and non-CAV patients (area under curve [AUC] = 0.955

90 production via the Cav-1 scaffolding domain (CAV; amino acids 82-101).

91 peptide containing this sequence pulls down CAV-1 (caveolin-1) and TNFR1 from cell lysates but fails

92 CAV but that their ability to mediate early CAV can be modulated by Tregs.

93 T cells, NK cells depletion alone eliminated CAV at 3 weeks.

94 pathway with CO-releasing molecules enhances CAV-1 expression in CF MPhis, suggesting a positive-feed

95 limus inhibited a progression of established CAV but did not reverse the luminal obliteration.

96 n alone is not reliable enough for excluding CAV.

97 e show that intracellular delivery of a F92A CAV(90-99) peptide can promote NO bioavailability in eNO

98 going routine coronarography angiography for CAV diagnosis (median 5 years since HT).

99 RNAs may serve as noninvasive biomarkers for CAV.

100 of CAV with any degree of stenosis, but for CAV with 50% or more stenosis, the corresponding values

101 All other traditional risk factors for CAV or immunosuppression were similar between the groups

102 09; P=0.03) are independent risk factors for CAV.

103 Surveillance methods for CAV have significant limitations, particularly for detec

104 lasma levels were independent predictors for CAV.

105 angiography has a Class I recommendation for CAV surveillance and annual or biannual surveillance ang

106 CCTA is currently not recommended for CAV screening due to the limited accuracy reported by ea

107 njured grafts may play a reciprocal role for CAV development in an IL-6-independent manner.

108 ter heart transplantation, and screening for CAV is performed on annual basis.

109 Additional sequence data were obtained from CAV-1 positive samples, revealing regional variations in

110 IFN-gamma(-/-) mice that are protected from CAV, T-bet(-/-) recipients develop markedly accelerated

111 h B cells and antibodies were protected from CAV.

112 h normal cardiac CT angiographic results had CAV on the basis of invasive angiographic images.

113 absent in 82 patients, five (6%) of whom had CAV with 50% or more stenosis.

114 data support the continued evaluation of HD CAV-2 vectors to treat diseases affecting corneal kerato

115 ing by the injection a helper-dependent (HD) CAV-2 vector (HD-RIGIE) harboring the human cDNA coding

116 CT, whereas trans FAs were related to higher CAV and CFV.

117 In CAV patients, plasma levels of miR-628-5p and miR-155 we

118 eting IFN-gamma and IL-5 in AMR and IL-17 in CAV, with reduction in CD4+Th secreting IL-10 in both AM

119 oped CAV, supporting the role of NK cells in CAV development.

120 sease; however, the impact of collaterals in CAV is unknown.

121 A/CD16 Fc-receptor profiles were compared in CAV-positive (n=52) and CAV-free patients (n=51).

122 and IGFBP-3 are differentially expressed in CAV compared with no-CAV patients (P=0.037 and P<0.0001,

123 Abnormal vascular fibroproliferation in CAV occurs as a result of coronary endothelial inflammat

124 tance of nitric oxide synthase inhibition in CAV pathogenesis.

125 n concentrations were significantly lower in CAV (0.46+/-0.37 mg/L) as compared with no-CAV patients

126 n concentrations were significantly lower in CAV patients (159.7+/-114 ng/mL) as compared with no-CAV

127 ardiovascular diseases; however, its role in CAV pathogenesis remains unknown.

128 stability may also play an important role in CAV.

129 ve samples, revealing regional variations in CAV-1 sequences.

130 anti-NK1.1 reduced significantly DSA-induced CAV, as judged morphometrically.

131 lso showed decreased severity of DSA-induced CAV.

132 Interestingly, cold ischemia-induced CAV posttransplantation was not seen in T/B/NK cell-defi

133 that cold ischemia of cardiac grafts induces CAV after transplantation into Rag1(-/-) mice.

134 sized that ADMA concentrations may influence CAV progression during the first postoperative year.

135 CAV[-]: 242 +/- 68 mug/mL, P=0.025) and KAT (CAV[+]: 768 +/- 206 mug/mL, CAV[-]: 196 +/- 72 mug/mL, P

136 We conclude that antibody mediates CAV through NK cells, by an Fc dependent manner.

137 =0.025) and KAT (CAV[+]: 768 +/- 206 mug/mL, CAV[-]: 196 +/- 72 mug/mL, P=0.001) with increased frequ

138 to-Abs to Col-V (CAV[+]: 835 +/- 142 mug/mL, CAV[-]: 242 +/- 68 mug/mL, P=0.025) and KAT (CAV[+]: 768

139 performed angiography for detecting moderate CAV (area under the curve, 0.89 [95% confidence interval

140 nted without increasing recipient mortality, CAV, or PGF.

141 assay in 44 randomly selected CAV and 50 no-CAV patients at two time points.

142 /-0.60 vs. 2.81+/-0.78 s) with respect to No-CAV patients.

143 n CAV (0.46+/-0.37 mg/L) as compared with no-CAV patients (1.03+/-0.73 mg/L; P=0.04).

144 ents (159.7+/-114 ng/mL) as compared with no-CAV patients (234.1+/-136 ng/mL; P=0.02).

145 erentially expressed in CAV compared with no-CAV patients (P=0.037 and P<0.0001, respectively).

146 0 matched recipients with CAV and 10 with no-CAV were initially screened with a protein array.

147 r of CAV, clearly discriminating CAV and non-CAV patients (area under curve [AUC] = 0.955; P = 0.001)

148 P3Treg and Tact-to-CD127Treg ratios than non-CAV patients, with P less than 0.01 and P less than 0.00

149 Analysis of CAV centers with scanning confocal microscopy indicates

150 miR-628-5p as a novel potential biomarker of CAV in patients after OHT.

151 CD127Treg ratio was a potential biomarker of CAV, clearly discriminating CAV and non-CAV patients (ar

152 Advanced changes of CAV were found at 56 days in transplants involving incom

153 rteries, which is the main characteristic of CAV.

154 Degree of CAV was assessed by using a 15-coronary segments model.

155 s of cardiac CT angiography for detection of CAV with any degree of stenosis and greater than or equa

156 y, specificity, and NPV for the detection of CAV.

157 FK778 prevents the development of CAV and inhibits a progression of established disease.

158 sses that are involved in the development of CAV are summarized.

159 bitors (ACEIs) may retard the development of CAV but have not been well studied after HT.

160 did not prevent or accelerate development of CAV but inhibited the effect of CD25 T cell depletion.

161 y of the ACEI ramipril on the development of CAV early after HT.

162 in peripheral blood with the development of CAV in HTx patients.

163 Development of CAV was significantly higher in patients with MS (59% vs

164 ensitization and AMR with the development of CAV, a major limiting factor affecting long-term graft s

165 ly I/R injury and reduces the development of CAV, most likely due to alloantigen-independent effects

166 e criteria of MS had a higher development of CAV: no criteria (4%); one criterion (4%); two criteria

167 77%, and 98%, respectively, for diagnosis of CAV with any degree of stenosis, but for CAV with 50% or

168 ority of heart transplants shows evidence of CAV.

169 unological and non-immunological features of CAV, investigators can thoroughly explore contributory m

170 We conclude that the GG genotype of CAV-1 is protective, associated with a decreased overall

171 Angiographic incidence of CAV was 5%, 15%, and 28% at 2, 5, and 10 years, respecti

172 t have contributed to the lower incidence of CAV.

173 s was highly and independently indicative of CAV (OR = 45, 95% CI 4.04-500.69).

174 Small interfering RNA-mediated knockdown of CAV-1 but not FLOT-2 strikingly reduces caveolae number.

175 ated in Bmpr2(+/-) PECs, and localization of CAV-1 to the plasma membrane is restored after treating

176 r a novel approach in clinical management of CAV.

177 a significant difference in manifestation of CAV between the groups after 10 years.

178 ells accelerated the onset and maturation of CAV at both 2 and 3 weeks (P<0.02 and P<0.001, respectiv

179 anti-CM immunity is a pathogenic mediator of CAV.

180 mic inflammation is an important mediator of CAV.

181 d a previously characterized murine model of CAV.

182 d a previously characterized murine model of CAV.

183 Cav-1 (Kd = 49 nM), and computer modeling of CAV(90-99) docking to eNOS provides a rationale for the

184 development of clinical prediction models of CAV.

185 important role in the early pathogenesis of CAV but that their ability to mediate early CAV can be m

186 The pathogenesis of CAV is not fully elucidated.

187 During the pathogenesis of CAV, cells from the innate and the adaptive immune syste

188 to understand the complex pathophysiology of CAV, improve surveillance techniques, and develop therap

189 the first three months for the prediction of CAV and graft failure due to CAV.

190 asive biomarkers available for prediction of CAV in transplanted patients.MicroRNAs (miRNAs) are high

191 ified as a baseline-independent predictor of CAV risk (odds ratio, 4.7; P=0.023).

192 ndent marker correlated with the presence of CAV at the time of coronary angiography by using multiva

193 to prior studies in which the prevention of CAV at 8 weeks required the codepletion of NK and CD4 T

194 However, prevention of CAV in this setting required the depletion of both NK an

195 independently associated with progression of CAV and predicts a higher incidence of CV events and CV

196 There was accelerated progression of CAV in the DSA II+ group demonstrated by accelerated pro

197 on and with higher subsequent progression of CAV.

198 s can significantly delay the progression of CAV; however, their optimal use remains to be establishe

199 patients with MS developed a higher risk of CAV 1 year after HTx.

200 Lp-PLA2 may be a useful marker for risk of CAV and a therapeutic target in posttransplant patients.

201 Early identification of patients at risk of CAV is essential to target invasive follow-up procedures

202 consisting of patients without any signs of CAV at least 5 years after OHT.

203 f FCGR3A/CD16 in the early stratification of CAV risk.

204 e influence of testosterone plasma levels on CAV development.

205 e influence of testosterone plasma levels on CAV development: indirectly increasing traditional risk

206 Specifically, carbon antisite-vacancy pairs (CAV centers) in 4H-SiC, which serve as single-photon emi

207 628-5p value above 1.336 was able to predict CAV with a sensitivity of 72% and a specificity of 83%.

208 of caveolae and caveolar structural proteins CAV-1 and Cavin-1 and that these defects are reversed af

209 immunosorbent assay in 44 randomly selected CAV and 50 no-CAV patients at two time points.

210 [95% CI: 0.42 to 0.77], p = 0.01) and severe CAV (area under the curve, 0.88 [95% CI: 0.78 to 0.98] v

211 ed 59 (12%) subjects with moderate-to-severe CAV.

212 Patients with severe CAV had raised serum von Willebrand factor and decreased

213 V (> luminal irregularities) and significant CAV (stenosis >/=50%), showed mean weighted sensitivitie

214 IMT) > 0.5 mm was used to define significant CAV.

215 99% vs. 97%, p = 0.06) to detect significant CAV with 64-slice compared with 16-slice CCTA.

216 act DSA regularly elicited markedly stenotic CAV in recipients over 28 days.

217 It is concluded that CAV-1 is endemic in free-ranging red foxes in the UK and

218 as suggested by our earlier observation that CAV arises even in the absence of detectable antidonor T

219 Although we have recently shown that CAV residue Phe-92 is responsible for eNOS inhibition, t

220 The CAV development was evaluated with morphometric analysis

221 oduction was substantially inhibited and the CAV severity score was markedly reduced.

222 -VV genotype was significantly higher in the CAV(+) group (odds ratio, 3.9; P=0.0317) than in the CAV

223 roup (odds ratio, 3.9; P=0.0317) than in the CAV(-) group.

224 investigated a genetic predisposition of the CAV-1 gene on survival, acute and chronic rejection, lym

225 In 503 of 568 patients, the CAV-1 (rs3807989) polymorphism was successfully determin

226 ndition throughout this period despite their CAV.

227 B cells contributed to CAV by supporting splenic lymphoid architecture, T cell

228 OR for one- and 10-year graft failure due to CAV = 1.81, p = 0.025, 95% CI = 1.08-3.03; and 1.31, p =

229 R] for one- and 10-year graft failure due to CAV = 38.70, p = 0.002, 95% CI = 4.00-374.77; and 3.99,

230 he exception of 10-year graft failure due to CAV in which the three-month model was more predictive.

231 e prediction of CAV and graft failure due to CAV.

232 t and 1 in 8 deaths beyond a year are due to CAV.

233 Variables related to CAV in a multivariate analysis were MS (odds ratio [OR]

234 ction fraction (LVEF) < or =45% secondary to CAV and CV death.

235 of free-ranging red foxes (Vulpes vulpes) to CAV-1 in the United Kingdom (UK) and to examine their ro

236 se low density membrane domains depends upon CAV-1 or FLOT-2.

237 AV also developed DSA and auto-Abs to Col-V (CAV[+]: 835 +/- 142 mug/mL, CAV[-]: 242 +/- 68 mug/mL, P

238 or attenuate cardiac allograft vasculopathy (CAV) (classic chronic rejection lesions found in transpl

239 on (AMR) and cardiac allograft vasculopathy (CAV) after human heart transplantation (HTx).

240 een Lp-PLA2, cardiac allograft vasculopathy (CAV) assessed by 3D intravascular ultrasound, and incide

241 Chronic allograft vasculopathy (CAV) contributes to heart transplant failure, yet its pa

242 Cardiac allograft vasculopathy (CAV) has a high prevalence among patients that have unde

243 Cardiac allograft vasculopathy (CAV) has an incidence of 43% at 8 years after heart tran

244 or detecting cardiac allograft vasculopathy (CAV) in comparison with conventional coronary angiograph

245 Chronic allograft vasculopathy (CAV) in murine heart allografts can be elicited by adopt

246 Cardiac allograft vasculopathy (CAV) is a major cause of death after heart transplantati

247 Cardiac allograft vasculopathy (CAV) is a major limitation in long-term graft survival a

248 Cardiac allograft vasculopathy (CAV) is the main cause of graft failure and death 1 year

249 Because cardiac allograft vasculopathy (CAV) is the major cause of late mortality after heart tr

250 Cardiac allograft vasculopathy (CAV) is the preeminent cause of late cardiac allograft f

251 Cardiac allograft vasculopathy (CAV) is the principal cause of long-term graft failure f

252 Although cardiac allograft vasculopathy (CAV) is typically characterized by diffuse coronary inti

253 its role in cardiac allograft vasculopathy (CAV) is unclear.

254 Chronic allograft vasculopathy (CAV) limits the lifespan of pediatric heart transplant r

255 nificance in cardiac allograft vasculopathy (CAV) progression.

256 Cardiac allograft vasculopathy (CAV) remains a leading cause of mortality after heart tr

257 Cardiac allograft vasculopathy (CAV) remains the Achilles' heel of long-term survival af

258 Cardiac allograft vasculopathy (CAV) remains the leading cause of morbidity and mortalit

259 ransplants, coronary allograft vasculopathy (CAV) remains the most prevalent cause of late allograft

260 or detecting cardiac allograft vasculopathy (CAV) using contemporary invasive epicardial artery and m

261 Cardiac allograft vasculopathy (CAV) was graduated in accordance with the new ISHLT clas

262 NK) cells in cardiac allograft vasculopathy (CAV) was suggested by our earlier observation that CAV a

263 ndicators of chronic allograft vasculopathy (CAV) were quantified.

264 t mortality, cardiac allograft vasculopathy (CAV), and primary graft failure (PGF).

265 ced the same chronic allograft vasculopathy (CAV), which is a pathognomonic feature of chronic reject

266 velopment of cardiac allograft vasculopathy (CAV).

267 velopment of cardiac allograft vasculopathy (CAV).

268 B6) model of chronic allograft vasculopathy (CAV).

269 ogression of chronic allograft vasculopathy (CAV).

270 tation, and coronary allograft vasculopathy (CAV).

271 c grading of cardiac allograft vasculopathy (CAV); however, no data exist on the utility of these gui

272 prevalence of coronary artery vasculopathy (CAV) was established by appropriate histologic methods.

273 d DNA viruses, such as chicken anemia virus (CAV) and porcine circovirus 2 (PCV2), as serious pathoge

274 Chicken anemia virus (CAV) is a single-stranded circular DNA virus that carrie

275 The chicken anemia virus (CAV) protein apoptin is known to induce tumor cell-speci

276 l-free virus (CFV) or cell-associated virus (CAV) in breast milk.

277 kg) was either started early or delayed when CAV was already present.

278 patients at least 2 years after HTx, 17 with CAV and 12 without CAV.

279 y of 72 heart transplant recipients: 40 with CAV and 32 without.

280 B-3 serum concentrations are associated with CAV.

281 pted the interaction and colocalization with CAV-1.

282 Patients diagnosed with CAV also developed DSA and auto-Abs to Col-V (CAV[+]: 83

283 kin (IL)-6 expression in cardiac grafts with CAV.

284 Infections with CAV (family Anelloviridae, genus Gyrovirus) and PCV2 (fa

285 8%) red foxes had inapparent infections with CAV-1, as detected by a nested PCR, in a range of sample

286 region of DLC1 required for interaction with CAV-1 to the DLC1 START domain.

287 dicts a favorable prognosis in patients with CAV and suggests that interventions aimed at promoting c

288 regulated in plasma samples of patients with CAV and therefore were selected for verification by quan

289 Sera from 65% of patients with CAV contained anti-CM Abs, whereas <10% contained Abs to

290 PBMCs from patients with CAV responded more frequently to, and to a broader array

291 In the cross-sectional study, patients with CAV showed statistically significant higher values of Th

292 specimens revealed that among patients with CAV, the presence of coronary collaterals correlated wit

293 ated with improved outcomes in patients with CAV, we performed a retrospective analysis of patients f

294 Both ratios were higher in HTx patients with CAV.

295 Serum samples of 10 matched recipients with CAV and 10 with no-CAV were initially screened with a pr

296 HTx subjects with CAV had significant lower total testosterone plasma leve

297 nce of a distinct eNOS binding domain within CAV.

298 years after HTx, 17 with CAV and 12 without CAV.

299 contrast, 13% of sera from patients without CAV contained anti-CM Abs (p < 0.05; odds ratio [OR], as

300 y of, CM-derived peptides than those without CAV (p = 0.01).