ライフサイエンスコーパス: CAV

1 CAV constitutes a significant complication that limits t

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

3 CAV is the most important determinant of cardiac allogra

4 CAV limits long-term survival after heart transplantatio

5 CAV progression and adverse clinical events were studied

6 CAV progression was assessed by measuring the Delta chan

7 CAV shares genomic organization, genomic orientation, an

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

9 CAV was diagnosed through intravascular ultrasound perfo

10 CAV was diagnosed using 2010 International Society for H

11 CAV was investigated using intravascular ultrasound.

12 CAV was present in 17 (46.0%) reference coronary angiogr

13 CAV, including epicardial and microvascular components,

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

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

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

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

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

19 of ALK-1, and it is mediated by caveolin-1 (CAV-1) and dynamin-2 (DNM2) but not clathrin heavy chain

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

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

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

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

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

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

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

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

28 heart transplant recipients, we identified 4 CAV trajectories and their respective independent predic

29 The 4 CAV trajectories manifested consistently in the US indep

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

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

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

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

34 hat could protect cardiac allografts against CAV.

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

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

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

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

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

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

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

42 ing lipid rafts throughout the epidermis and CAV-1-containing rafts only in the upper epidermis.

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

44 ation was observed between CMV infection and CAV, except for patients who experienced a breakthrough

45 ation was observed between CMV infection and CAV, except for patients who experienced a breakthrough

46 otal and free testosterone plasma levels and CAV grading.

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

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

49 ction was diagnosed in 96 (37%) patients and CAV in 149 (57%) patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 we address the mechanism by which DSA causes CAV.

65 , 76 (32%) patients were diagnosed with CAV (CAV group).

66 Caveolins (CAVs) are structural proteins of caveolae that function

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

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

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

70 ation improves the sensitivity for detecting CAV without reducing specificity.

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

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

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

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

75 llograft recipients who are prone to develop CAV.

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

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

78 to detect HTx patients at risk of developing CAV.

79 oup of patients with high risk of developing CAV.

80 cells play critical roles in the development CAV.

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

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

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

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

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

86 n alone is not reliable enough for excluding CAV.

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

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

89 RNAs may serve as noninvasive biomarkers for CAV.

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

91 Consecutive patients undergoing CCTA for CAV surveillance were identified.

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

93 09; P=0.03) are independent risk factors for CAV.

94 >=34 were associated with a high hazard for CAV (HR = 1.8 [95% CI 1.10-4.53, P = 0.03] and 2.5 [95%

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

96 Optimal diagnostic cut-offs for CAV, with coronary angiography as gold standard, were de

97 The main outcome was a prediction for CAV trajectory.

98 lasma levels were independent predictors for CAV.

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

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

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

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

103 ne was 70.6% sensitive and 100% specific for CAV.

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

105 h B cells and antibodies were protected from CAV.

106 ejection poses a far greater risk for future CAV than rejection on protocol biopsy in pediatric HT re

107 tion is more strongly associated with future CAV than rejection diagnosed on protocol biopsy.

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

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

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

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

112 We identified CAV trajectories by using unsupervised latent class mixe

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

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

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

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

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

118 tribution of immune and nonimmune factors in CAV development.

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

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

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

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

123 stability may also play an important role in CAV.

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

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

126 lso showed decreased severity of DSA-induced CAV.

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

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

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

130 ver time (23.1%), and (4) patients with mild CAV at 1 year and accelerated progression (13.0%).

131 V progression (7.6%), (3) patients with mild CAV at 1 year and mild progression over time (23.1%), an

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

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

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

135 /-0.60 vs. 2.81+/-0.78 s) with respect to No-CAV patients.

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

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

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

139 0 matched recipients with CAV and 10 with no-CAV were initially screened with a protein array.

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

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

142 Analysis of CAV centers with scanning confocal microscopy indicates

143 r conversion to SRL have less attenuation of CAV progression and higher mortality risk.

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

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

146 rteries, which is the main characteristic of CAV.

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

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

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

150 >=34 was at highest risk for development of CAV (HR = 5.2, 95% CI 2.27-15.17, P = 0.001).

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

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

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

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

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

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

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

158 r HTx are associated with the development of CAV.

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

160 77%, and 98%, respectively, for diagnosis of CAV with any degree of stenosis, but for CAV with 50% or

161 ority of heart transplants shows evidence of CAV.

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

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

164 t have contributed to the lower incidence of CAV.

165 Knockdown of CAV-1 reduces BMP-9-mediated internalization of ALK-1, B

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

167 Loss of CAV protein expression is associated with impaired contr

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

169 primary endpoint was first manifestation of CAV diagnosed by coronary angiography.

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

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

172 development of clinical prediction models of CAV.

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

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

175 nse may contribute to the pathophysiology of CAV through a mechanism that needs to be identified.

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

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

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

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

180 gression analysis, independent predictors of CAV were: number of rejection episodes (cause-specific h

181 gression analysis, independent predictors of CAV were: number of rejection episodes (CSHR (95% CI): 1

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

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

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

185 ntify the different evolutionary profiles of CAV and to determine the respective contribution of immu

186 We identified 4 distinct profiles of CAV trajectories over 10 years.

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

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

189 Little is known about the prototypes of CAV trajectories at the population level.

190 n protocol biopsy were not at higher risk of CAV (hazard ratio [HR] 1.09, 95% confidence interval [CI

191 jection was associated with a higher risk of CAV (HR 4.27, 95% CI: 2.42-7.51) if it was clinical reje

192 on was significantly associated with risk of CAV (HR 4.84, 95% CI: 2.99-7.83).

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

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

195 icant effect of CMV infection on the risk of CAV was seen only among HTx recipients with CMV breakthr

196 icant effect of CMV infection on the risk of CAV was seen only among HTx recipients with CMV breakthr

197 = .01) with proteinuria but similar risk of CAV-related events (P = .61).

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

199 ylation and gene expression and silencing of CAV-1 and DNM2 diminishes LDL-mediated ALK-1 internaliza

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

201 e influence of testosterone plasma levels on CAV development.

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

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

204 628-5p value above 1.336 was able to predict CAV with a sensitivity of 72% and a specificity of 83%.

205 Preventing CAV should therefore become the focus of medical managem

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

207 al function as well as significantly reduced CAV than patients randomized to standard CNI treatment.

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

209 [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

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

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

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

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

214 99% vs. 97%, p = 0.06) to detect significant CAV with 64-slice compared with 16-slice CCTA.

215 ts without CAV at 1 year and late-onset slow CAV progression (7.6%), (3) patients with mild CAV at 1

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 The CAV group patients had lower exercise capacity (5.2 +/-

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 the independent predictive variables of the CAV trajectories and their association with mortality.

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

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

227 ndition throughout this period despite their CAV.

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

229 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 =

230 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,

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

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

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

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

235 Time to CAV diagnosis was assessed using a Cox model with occurr

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

237 Coronary allograft vasculopathy (CAV) assessed by coronary intravascular ultrasound was p

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

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

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

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

242 Cardiac allograft vasculopathy (CAV) is a major contributor of heart transplant recipien

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

244 Cardiac allograft vasculopathy (CAV) is an increasingly important complication after car

245 Cardiac allograft vasculopathy (CAV) is associated with intragraft B cell infiltrates.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 nfection and cardiac allograft vasculopathy (CAV) were conducted on patients transplanted in the pre

261 nfection and cardiac allograft vasculopathy (CAV) were conducted on patients transplanted in the prev

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

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

264 tenuation of cardiac allograft vasculopathy (CAV), improvement in glomerular filtration rate (GFR), a

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

269 ssociated with coronary artery vasculopathy (CAV) in pediatric heart transplant (HT) recipients.

270 an control cell surface levels of ALK-1, via CAV-1, to regulate both BMP-9 signaling and LDL transcyt

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

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

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

274 ide new insight into the mechanisms by which CAV gene expression is repressed in hypertrophied BSM in

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

276 l expansion in human cardiac allografts with CAV.

277 B-3 serum concentrations are associated with CAV.

278 pted the interaction and colocalization with CAV-1.

279 onths, 76 (32%) patients were diagnosed with CAV (CAV group).

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

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

282 8%) red foxes had inapparent infections with CAV-1, as detected by a nested PCR, in a range of sample

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

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

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

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

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

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

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

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

291 < .001) volumes were higher in patients with CAV, whereas calcified plaque was not (median 0.0 vs 0.0

292 Both ratios were higher in HTx patients with CAV.

293 ume is significantly higher in patients with CAV.

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

295 ell infiltrates using 4 graft specimens with CAV.

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 sion over time (56.3%), (2) patients without CAV at 1 year and late-onset slow CAV progression (7.6%)

300 s were characterized by (1) patients without CAV at 1 year and nonprogression over time (56.3%), (2)

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