ライフサイエンスコーパス: vasculopathy

1 tified 18 patients (43 +/- 15 y, 12 moyamoya vasculopathy).

2 y also play a role in the development of SCD vasculopathy.

3 ctivity attenuates development of transplant vasculopathy.

4 nce of phosphorylated SMAD2/3, and degree of vasculopathy.

5 en in the presence of only mild angiographic vasculopathy.

6 ft ventricular assist devices and transplant vasculopathy.

7 n C57BL/6 recipients and developed allograft vasculopathy.

8 ronal features without clinically detectable vasculopathy.

9 ficking, alloimmunity, and cardiac allograft vasculopathy.

10 polyarteritis nodosa (cPAN) and early-onset vasculopathy.

11 ases, such as atherosclerosis and transplant vasculopathy.

12 stenosis, vein graft stenosis, and allograft vasculopathy.

13 degree of peritoneal fibrosis, but not with vasculopathy.

14 of skin and organ fibrosis and obliterative vasculopathy.

15 tly of the breakdown of the BRB and onset of vasculopathy.

16 helial reactivity and induction of pulmonary vasculopathy.

17 actin expression and inflammatory pulmonary vasculopathy.

18 play a hitherto unsuspected role in diabetic vasculopathy.

19 large antibody loads, and chronic allograft vasculopathy.

20 lgia, myelitis, meningoencephalitis, and VZV vasculopathy.

21 ivation and development of cardiac allograft vasculopathy.

22 to halt the progression of cardiac allograft vasculopathy.

23 ing from thrombocytopenia, coagulopathy, and vasculopathy.

24 therapy for idiopathic polypoidal choroidal vasculopathy.

25 wall can detect and grade coronary allograft vasculopathy.

26 dy-mediated rejection, and chronic allograft vasculopathy.

27 was found in deaths due to cardiac allograft vasculopathy.

28 isease, such as atherosclerosis and diabetic vasculopathy.

29 ntly accompanied by hearing loss and retinal vasculopathy.

30 ts with macula-involved polypoidal choroidal vasculopathy.

31 pecies (ROS) is a common finding in diabetic vasculopathy.

32 inadequate for detecting the early stages of vasculopathy.

33 agic presentation) with polypoidal choroidal vasculopathy.

34 signalling are not essential for the lethal vasculopathy.

35 nt recipients is the development of coronary vasculopathy.

36 hotoreceptor injury but had no effect on the vasculopathy.

37 d be used therapeutically to reverse choroid vasculopathy.

38 n important determinant of cardiac allograft vasculopathy.

39 n, followed by downstream endothelin-induced vasculopathy.

40 nsity of inflammation implicated in diabetic vasculopathy.

41 helial dysfunction, platelet activation, and vasculopathy.

42 ts showed association with chronic allograft vasculopathy.

43 bout the role of CD16 in promoting allograft vasculopathy.

44 fibrosis of the skin and internal organs and vasculopathy.

45 ly correlate with the severity of arteriolar vasculopathy.

46 ecific Fli1-knockout mice recapitulating SSc vasculopathy.

47 d intracerebral varicella zoster virus (VZV) vasculopathy.

48 icator of graft rejection or coronary artery vasculopathy.

49 flow velocities (>/= 200 cm/s) but no severe vasculopathy.

50 regression of polyps in polypoidal choroidal vasculopathy.

51 ercept in management of polypoidal choroidal vasculopathy.

52 sociated with widespread tissue fibrosis and vasculopathy.

53 o mechanisms of chronic allograft injury and vasculopathy.

54 ence of acute rejection or chronic allograft vasculopathy.

55 r risk, and reduce the incidence of coronary vasculopathy.

56 r, could attenuate development of transplant vasculopathy.

57 avitreal aflibercept in polypoidal choroidal vasculopathy.

58 rts an ischemic pathogenesis of this retinal vasculopathy.

59 er general anesthesia for a range of retinal vasculopathies.

60 ensin II (Ang-II), are commonly increased in vasculopathies.

61 ities in a variety of vascular disorders and vasculopathies.

62 ole in the development of fibroproliferative vasculopathies.

63 ute to the pathogenesis of TGF-beta-mediated vasculopathies.

64 important event in atherosclerosis and other vasculopathies.

65 tions are known collectively as the TGF-beta vasculopathies.

66 a group called the smooth muscle contraction vasculopathies.

67 The commonest etiology was HIV-associated vasculopathy (24 [38%]), followed by opportunistic infec

68 t of patients has an associated inflammatory vasculopathy affecting large arteries (giant cell arteri

69 r risk of acute rejection, cardiac allograft vasculopathy after heart transplantation, and potentiall

70 myocardial infarction and cardiac allograft vasculopathy after heart transplantation.

71 ive paracrine factors is a strategy to treat vasculopathies and to promote tissue regeneration.

72 us (HIV) infection are at risk for premature vasculopathy and cardiovascular disease (CVD).

73 two patients with autosomal dominant retinal vasculopathy and cerebral leukoencephalopathy (previousl

74 es, brain regions from patients with retinal vasculopathy and cerebral leukoencephalopathy that harbo

75 responsible for the progression of allograft vasculopathy and chronic rejection.Recent work has sugge

76 d by healing fail to account for the complex vasculopathy and clinical course.

77 l patients with NAION for systemic survey of vasculopathy and control of modifiable risk factors to p

78 essive condition characterized with cerebral vasculopathy and early onset of stroke in 14 individuals

79 Because intracerebral VZV vasculopathy and giant cell arteritis are strongly assoc

80 as tested using a murine model of transplant vasculopathy and human cells.

81 Proliferative vasculopathy and hydranencephaly-hydrocephaly syndrome (

82 c sclerosis (SSc) is manifested by fibrosis, vasculopathy and immune dysregulation.

83 logical examination of the skin showed graft vasculopathy and occasional C4d deposits in cutaneous ca

84 d deep vessels, leading, as in SOT, to graft vasculopathy and often to graft loss.

85 HIV-associated vasculopathy and opportunistic infections are common cau

86 nal vascular associations leading to retinal vasculopathy and paracentral acute middle maculopathy in

87 pathological vascular remodeling during VZV vasculopathy and persistent inflammation in infected lun

88 rk for understanding the pathogenesis of NF1 vasculopathy and potential therapeutic and diagnostic in

89 lcineurin antagonists reduces posttransplant vasculopathy and prolongs survival following cardiac tra

90 r aneurysm formation in a novel model of NF1 vasculopathy and provide a potential therapeutic target.

91 in humans with SCD and in mice to markers of vasculopathy and pulmonary hypertension.

92 Coronary artery vasculopathy and survival were not significantly impacte

93 de accelerated arterial disease in allograft vasculopathy and systemic autoimmune diseases and involv

94 Abs and complement, including posttransplant vasculopathy and systemic lupus erythematosus.

95 e of effective viral clearance occurs in VZV vasculopathy and VZV infection of the lung is a step tow

96 contrast, chronic rejections, as defined by vasculopathy and/or fibrosis and atrophy of skin and oth

97 promote vasomotor dysfunction, proliferative vasculopathy, and a multitude of clinical complications

98 sis (SSc) is characterized by calcification, vasculopathy, and endothelial wall damage, all of which

99 ssue disorder characterized by autoimmunity, vasculopathy, and extensive cutaneous and visceral fibro

100 d a marked reduction in dermal inflammation, vasculopathy, and fibrosis compared with that seen in th

101 the pathological processes of inflammation, vasculopathy, and fibrosis in human diseases and their a

102 ical features of SSc including autoimmunity, vasculopathy, and fibrosis, and provide a unified diseas

103 ith denervated hearts and coronary allograft vasculopathy, and future study aimed at improving the ma

104 time until graft failure, cardiac allograft vasculopathy, and hospitalization for rejection.

105 ed by fibrosis of the skin and inner organs, vasculopathy, and immunological abnormalities.

106 play a significant role in cardiac allograft vasculopathy, and in animal models, ERAs improve pulmona

107 I]) levels in SCD will limit vaso-occlusion, vasculopathy, and inflammation, we used 2 strategies to

108 early-onset systemic inflammation, cutaneous vasculopathy, and pulmonary inflammation.

109 -year AMR/CMR (>/= grade 2), coronary artery vasculopathy, and survival.

110 te macular neuroretinopathy (AMN) or retinal vasculopathy, and that may indicate an underlying pathog

111 -cell-depleted donors developed only minimal vasculopathy, and the alloantibody responses were weaker

112 nifestations of SSc, including inflammation, vasculopathy, and tissue fibrosis, with bleomycin-treate

113 verse events, the mechanisms of drug-induced vasculopathy are not well understood.

114 ification of patients with cardiac allograft vasculopathy are problematic.

115 ssure reductions in the setting of an active vasculopathy as a potential underlying mechanism.

116 nction reported in cbs(-/-) mice may reflect vasculopathy as well as neuropathy.

117 direct insight on the central nervous system vasculopathies associated with excessive hemolysis.

118 nopathy prior to loss of eyesight, pulmonary vasculopathy associated with pulmonary hypertension, and

119 lihood of death, graft failure, or allograft vasculopathy at 5 years after transplant (hazard ratio,

120 hat vanin-1/pantetheinase controls fibrosis, vasculopathy, autoimmunity, and oxidative stress in SSc.

121 ncy in mice enables suppression of allograft vasculopathy (AV) after aorta transplantation, a DSA-med

122 DADA2 is not only limited to cPAN and vasculopathy but also includes immunodeficiency that aff

123 show that H+LTx attenuates cardiac allograft vasculopathy by decreasing the rate of plaque volume and

124 e etiology of PAH, and may contribute to PAH vasculopathy by enabling inflammatory mediator flux acro

125 inib mesylate enhanced rat cardiac allograft vasculopathy, cardiac fibrosis, and late allograft loss

126 chanisms, including opportunistic infection, vasculopathy, cardioembolism, and coagulopathy.

127 diated rejection (AMR) and cardiac allograft vasculopathy (CAV) after human heart transplantation (HT

128 Chronic allograft vasculopathy (CAV) contributes to heart transplant failu

129 Cardiac allograft vasculopathy (CAV) has a high prevalence among patients

130 Cardiac allograft vasculopathy (CAV) has an incidence of 43% at 8 years af

131 raphy (CCTA) for detecting cardiac allograft vasculopathy (CAV) in comparison with conventional coron

132 Chronic allograft vasculopathy (CAV) in murine heart allografts can be eli

133 Cardiac allograft vasculopathy (CAV) is a major limitation in long-term gr

134 Cardiac allograft vasculopathy (CAV) is the main cause of graft failure an

135 Because cardiac allograft vasculopathy (CAV) is the major cause of late mortality

136 Cardiac allograft vasculopathy (CAV) is the preeminent cause of late cardi

137 Cardiac allograft vasculopathy (CAV) is the principal cause of long-term g

138 Although cardiac allograft vasculopathy (CAV) is typically characterized by diffuse

139 y established, its role in cardiac allograft vasculopathy (CAV) is unclear.

140 Chronic allograft vasculopathy (CAV) limits the lifespan of pediatric hear

141 Cardiac allograft vasculopathy (CAV) remains a leading cause of mortality

142 Cardiac allograft vasculopathy (CAV) remains the Achilles' heel of long-te

143 Cardiac allograft vasculopathy (CAV) remains the leading cause of morbidit

144 ived cardiac transplants, coronary allograft vasculopathy (CAV) remains the most prevalent cause of l

145 onance (CMR) for detecting cardiac allograft vasculopathy (CAV) using contemporary invasive epicardia

146 appearance and prevalence of coronary artery vasculopathy (CAV) was established by appropriate histol

147 Cardiac allograft vasculopathy (CAV) was graduated in accordance with the

148 tural killer (NK) cells in cardiac allograft vasculopathy (CAV) was suggested by our earlier observat

149 antation and indicators of chronic allograft vasculopathy (CAV) were quantified.

150 E for recipient mortality, cardiac allograft vasculopathy (CAV), and primary graft failure (PGF).

151 cells experienced the same chronic allograft vasculopathy (CAV), which is a pathognomonic feature of

152 prevent the development of cardiac allograft vasculopathy (CAV).

153 nt angiographic grading of cardiac allograft vasculopathy (CAV); however, no data exist on the utilit

154 Pulmonary arterial hypertension (PAH) is a vasculopathy characterized by enhanced pulmonary artery

155 rterial hypertension (PAH) is an obstructive vasculopathy characterized by excessive pulmonary artery

156 Importance: Vasculopathy characterized by functional and structural

157 terial hypertension (PAH) is a proliferative vasculopathy characterized by high circulating CD34(+)CD

158 l/fl) recipients developed severe transplant vasculopathy (chronic rejection).

159 the native heart in allografts with chronic vasculopathy compared to isograft controls on day 28 (P

160 afts, with reduced cellular infiltration and vasculopathy compared with wild type cardiac grafts.

161 Historically, polypoidal choroidal vasculopathy complexes are less responsive to anti-vascu

162 s of (1) a nitric oxide deficiency state and vasculopathy consequent to intravascular hemolysis, (2)

163 agnosis (OR=200; P=0.04), and severe chronic vasculopathy (cv>/=2) on index biopsy (OR=50; P=0.06).

164 giopathy (lobar structures) and hypertensive vasculopathy (deep brain structures).

165 support, in a model of alloantibody-mediated vasculopathy, depletion of NK cells from a C57BL/6 recip

166 HIV-associated vasculopathy describes various cerebrovascular changes,

167 raft survival and to delay cardiac allograft vasculopathy development and antidonor alloAb production

168 ses the IVW findings of various intracranial vasculopathies, differentiating characteristics and indi

169 nts developed severe intimal hyperplasia and vasculopathy early post-transplant.

170 histologic signs of severe chronic allograft vasculopathy eventually led to amputation of the graft.

171 g-term recipients showed increased degree of vasculopathy, fibrosis and perivascular C3d depositions

172 xposure on the ln-scale) of fetal thrombotic vasculopathy (FTV) both with increasing PM2.5 [adjusted

173 A novel MRA vasculopathy grading scale demonstrated frequent severe

174 The novel SWiTCH vasculopathy grading scale warrants validation testing a

175 d macular degeneration, polypoidal choroidal vasculopathy has differing clinical manifestations and t

176 In addition to his severe cutaneous vasculopathy, he experienced recurrent fevers, interstit

177 transfusions, and have no MRA-defined severe vasculopathy, hydroxycarbamide treatment can substitute

178 agents for SSc and other fibroproliferative vasculopathies in which EndoMT plays a pathogenetic role

179 vitreal aflibercept for polypoidal choroidal vasculopathy in 21 eyes was conducted.

180 and better prevention of coronary allograft vasculopathy in children.

181 f CNI-induced nephrotoxicity and endothelial vasculopathy in chronic allograft rejection.

182 mechanism that leads to BK channelopathy and vasculopathy in diabetes.

183 oonotic viruses that show various degrees of vasculopathy in humans.

184 also exist in patients with STING-associated vasculopathy in infancy (SAVI).

185 imb and scalp defects might also be due to a vasculopathy in NOTCH1-related AOS.

186 rcts in either treatment group, but worsened vasculopathy in one participant who received standard tr

187 tion of retinal telangiectasia or Coats-like vasculopathy in patients with CRB1 mutations that are th

188 ograft vascular rejection and in progressive vasculopathy in patients with systemic sclerosis.

189 s of subependymal cysts and lenticulostriate vasculopathy in postnatal imaging.

190 xidation, may be central to the evolution of vasculopathy in SCD and may suggest therapeutic modaliti

191 Endothelin-1 promotes vasculopathy in systemic sclerosis after macitentan, an

192 edoid rash, hepatosplenomegaly, and systemic vasculopathy in three unrelated patients.

193 vel mechanism contributes to protection from vasculopathy in transplanted organs treated with exogeno

194 f KLF15 exhibited an aggressive inflammatory vasculopathy in two distinct models of vascular disease:

195 (s) of RR6-induced attenuation of transplant vasculopathy in vivo.

196 Liver injury leads to a vasculopathy in which post-translational modifications o

197 SCD-related vasculopathies include, but are not limited to, moyamoya

198 ortuosity were associated with extracoronary vasculopathy including fibromuscular dysplasia (P<0.05 f

199 ve stress is a promising target for diabetic vasculopathies, including atherosclerosis.

200 es of SCAD are associated with extracoronary vasculopathy, including fibromuscular dysplasia.

201 ical complications of pulmonary and systemic vasculopathy, including pulmonary hypertension, leg ulce

202 trate lasting gene expression changes in the vasculopathies initiated by previous exposure to high gl

203 velop systemic inflammation characterized by vasculopathy, interstitial lung disease, ulcerative skin

204 ications that may extend beyond BAS to other vasculopathies involving vascular remodeling.

205 ccurate and timely diagnosis of intracranial vasculopathies is important due to significant risk of m

206 with the hypothesis that HIV-related retinal vasculopathy is a contributing factor to vision dysfunct

207 This review evaluates evidence that SCD vasculopathy is a harbinger for organ dysfunction and re

208 Cardiac allograft vasculopathy is a key prognostic determinant after heart

209 Development of transplant vasculopathy is a major cause of graft loss and mortalit

210 Cardiac allograft vasculopathy is a multifactorial process in which the im

211 Polypoidal choroidal vasculopathy is a variant of choroidal neovascularizatio

212 Coronary allograft vasculopathy is the leading cause of late death after he

213 Cardiac allograft vasculopathy is the major cause of late allograft loss a

214 To exclude vasculopathy, it is important to measure the integrity o

215 dings would support the concept of pulmonary vasculopathy leading to altered ventilation perfusion ma

216 ucing T cells and enhanced cardiac allograft vasculopathy lesion formation.

217 Cardiac allograft vasculopathy lesions contain alloreactive T cells that s

218 Furthermore, subtypes of HIV-associated vasculopathy may manifest as a result of an immune recon

219 0.21-0.65; P=0.0005), incidence of coronary vasculopathy (odds ratio, 0.33; 95% confidence interval,

220 SAMHD1 remains unclear, but the inflammatory vasculopathies of the brain found in the patients with S

221 aldosterone may contribute to the pulmonary vasculopathy of hypoxia.

222 ardi-Goutieres syndrome and STING-associated vasculopathy of infancy (SAVI).

223 The vasculopathy of Kawasaki disease appears to be distinct

224 ications of heart transplantation (HTx), the vasculopathy of the allograft (CAV), a phenomenon of chr

225 The molecular pathways involved in the vasculopathy of the antiphospholipid syndrome are unknow

226 mic lesions with calcifications; glomeruloid vasculopathy of the central nervous system and retinal v

227 arterial hypertension (PAH), a proliferative vasculopathy of the pulmonary circulation, but the origi

228 hree features of SSc, including fibrosis and vasculopathy of the skin and lung, B-cell activation and

229 e, which suggests that strokes are caused by vasculopathy of the small and medium-size cerebral arter

230 Progression of organ-specific vasculopathy often precedes organ dysfunction and may pr

231 the application and findings of the various vasculopathies on IVW can help guide diagnostic and ther

232 nts had Stanford grade IV coronary allograft vasculopathy on intravascular ultrasound, 3 of whom had

233 base was searched for patients with moyamoya vasculopathy or atherosclerotic cerebrovascular disease

234 rom early-onset recurrent stroke to systemic vasculopathy or vasculitis.

235 termediate-term mortality, cardiac allograft vasculopathy, or primary graft failure rates in hearts a

236 differences between primary cause of death, vasculopathy, or rejection.

237 tal abruption, infarction, hypoxia, decidual vasculopathy, or thrombosis of fetal vessels (n = 240 ca

238 unologic and graft survival as well as graft vasculopathy outcomes after VCA.

239 loss even in children with mild angiographic vasculopathy (p < 0.0001).

240 matching groups in the frequency of coronary vasculopathy (P=0.19) or rejection in the first post-tra

241 of risk, the pathogenesis of HIV-associated vasculopathy (particularly of arterial endothelial damag

242 d in 7 cases, including polypoidal choroidal vasculopathy (PCV) and macular fibrosis or atrophy.

243 Patients with polypoidal choroidal vasculopathy (PCV) had a worse final outcome.

244 Polypoidal choroidal vasculopathy (PCV), a subtype of 'wet' age-related macul

245 scularization (CNV) and polypoidal choroidal vasculopathy (PCV).

246 predict retreatment in polypoidal choroidal vasculopathy (PCV).

247 of the pathogenesis of polypoidal choroidal vasculopathy (PCV).

248 Eyes with polypoidal choroidal vasculopathy previously treated with ranibizumab and bev

249 iated with pulmonary hypertension, and renal vasculopathy prior to the onset of chronic renal disease

250 Varicella-zoster virus (VZV) vasculopathy produces stroke, giant cell arteritis, and

251 ssant attenuates long-term cardiac allograft vasculopathy progression and may improve long-term allog

252 inhibitor use, attenuating cardiac allograft vasculopathy progression and reducing cytomegalovirus in

253 e long-term attenuation of cardiac allograft vasculopathy progression and the effects on cardiac-rela

254 ment of a progressive proliferative systemic vasculopathy, pulmonary hypertension (PH), and left vent

255 DA2 results in variable autoinflammation and vasculopathy (recurrent fevers, livedo reticularis, poly

256 y were all followed up for a severe cerebral vasculopathy related to sickle cell disease.

257 ate, previously documented cardiac allograft vasculopathy), relative perfusion defects, mean myocardi

258 ronic rejection leading to cardiac allograft vasculopathy, remains a major cause of graft loss.

259 We hypothesized that cardiomyopathy and vasculopathy resulting from acute hyperglycemia are depe

260 intermediate/posterior/panuveitis, systemic vasculopathy, retinal vascular disease, or active inflam

261 recurrence of strokes secondary to cerebral vasculopathy seems to always be associated with poor out

262 -treated grafts had higher cardiac allograft vasculopathy severity scores during treatment relative t

263 ion fraction, cerebral blood flow, degree of vasculopathy, severity of anaemia, and presence of prior

264 These findings suggest that vasculopathy should be a focus of frequent monitoring in

265 therapeutic targets to prevent DENV-induced vasculopathy, suggesting MC-stabilizing drugs should be

266 erstanding of the levamisole-agranulocytosis vasculopathy syndrome.

267 tion (AMR) resulting in transplant allograft vasculopathy (TAV) is the major obstacle for long-term s

268 significant/fatal graft rejection, coronary vasculopathy, terminal cancer, and overall survival.

269 r-Degos disease) is a rare thrombo-occlusive vasculopathy that can affect multiple organ systems.

270 me disease groupings, for example, pulmonary vasculopathies, there may be several appropriate classif

271 l retinal function before the development of vasculopathy, thereby resulting in visual deficits.

272 l of autoantibody-mediated cardiac allograft vasculopathy to clarify the alloimmune responses mediate

273 content did not correlate with quantitative vasculopathy traits.

274 Transplant vasculopathy (TV) is a major cause for late graft loss a

275 The pathogenesis of transplant vasculopathy (TV) is a multifactorial process.

276 Transplant vasculopathy (TV) represents a major obstacle to long-te

277 try in human arteries affected by transplant vasculopathy (TV), a vascular condition that is a leadin

278 Similarly, cardiac allograft vasculopathy up to 5 years and primary graft failure up

279 ft from the development of cardiac allograft vasculopathy using coronary three-dimensional (3D) volum

280 cluding neointimal proliferation, transplant vasculopathy, vessel wall fibrosis, progressive luminal

281 Cerebral vasculopathy was a major hallmark of the condition with

282 rejection or development of coronary artery vasculopathy was not seen.

283 istent with the debilitating effects of such vasculopathy, we also observe increased retinal apoptosi

284 atous proliferation and polypoidal choroidal vasculopathy were excluded.

285 sponses and blocked development of allograft vasculopathy, whereas class II specific Tregs were ineff

286 rus-infected arteries from patients with VZV vasculopathy, while downregulation of MHC-I prevents vir

287 ial new insights into the nature of diabetic vasculopathy will be discussed.

288 dence of active rejection or coronary artery vasculopathy with 35 age-matched normal controls.

289 Retinal vasculopathy with cerebral leukodystrophy (RVCL) is a ra

290 ogressive disease characterized by pulmonary vasculopathy with elevation of pulmonary artery pressure

291 ne deaminase, can cause polyarteritis nodosa vasculopathy with highly varied clinical expression.

292 k-fib mouse strain, a constitutive pulmonary vasculopathy with medial thickening, a perivascular prol

293 sickle cell disease (SCD) leads to a chronic vasculopathy with multiple organ involvement.

294 ed stimulator of interferon genes-associated vasculopathy with onset in infancy (SAVI) caused by gain

295 lator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) develop system

296 STING-associated vasculopathy with onset in infancy (SAVI) is an autoinfl

297 e I interferonopathy called STING-associated vasculopathy with onset in infancy (SAVI).

298 outieres syndrome (AGS) and STING-associated vasculopathy with onset of infancy (SAVI).

299 IIDeltak-fib model, which develops pulmonary vasculopathy with pulmonary hypertension that is exacerb

300 aled a predominantly small-vessel thrombotic vasculopathy with varying degrees of vasculitis.