ライフサイエンスコーパス: occlusive

1 Occlusive agents, referred to as embolics, vary in mater

2 attenuate the severity of outcomes from vaso-occlusive and hemolytic crises.

3 s double-positive for HMGA1 and SM22alpha in occlusive and plexogenic lesions.

4 had acute ischaemic stroke with large artery occlusive anterior circulation stroke confirmed on CT an

5 We have shown that occlusive arterial lesions in patients with heterozygous

6 rmore, 3F8 prevented ferric chloride-induced occlusive arterial thrombogenesis in vivo.

7 n collagen fibers ex vivo and in 2 models of occlusive arterial thrombosis in vivo.

8 affecting integrin ligation, and suppresses occlusive arterial thrombosis without affecting bleeding

9 AP/SLAP2 knockout mice displayed accelerated occlusive arterial thrombus formation and a dramatically

10 in shortened tail bleeding times and faster occlusive arterial thrombus formation.

11 n time and prevented the stable formation of occlusive arteriolar thrombi.

12 subtypes (undetermined, cardioembolic, steno-occlusive arteriopathies), no statistically significant

13 ned, 16 of 89; cardioembolic, 6 of 40; steno-occlusive arteriopathies, 24 of 79; p = 0.08).

14 Such impairment is known to lead to occlusive artery disease, and may be an important risk f

15 ion is an attractive therapeutic strategy in occlusive atherosclerotic diseases.

16 ces, veins via paradoxical embolism, and non-occlusive atherosclerotic plaques in the aortic arch, ce

17 poE(-/-) or dKO) mice] spontaneously develop occlusive, atherosclerotic coronary artery disease (CAD)

18 ed collagen membrane with a traditional cell occlusive barrier membrane.

19 andomly divided into two groups, as follows: occlusive bovine collagen membranes (OM control group, 1

20 entially modifiable mediator or predictor of occlusive cardiovascular events in these patients.

21 nd in a model of ferric chloride induced non-occlusive carotid artery thrombosis.

22 ty were evaluated in rat models of mural and occlusive carotid artery thrombosis.

23 ellular and soluble participants in the vaso-occlusive cascade.

24 were included in multivariate analysis, and occlusive catheterization was identified as an independe

25 ressure and hypertrophy and pulmonary artery occlusive changes.

26 e influence of margination and shear rate on occlusive clot formation is not fully understood yet.

27 id crystalline droplets form phase-separated occlusive compartments around rod-shaped bacteria leadin

28 Current treatments to reduce vaso-occlusive complications include chronic hydroxyurea ther

29 s, but also impact on many of the other vaso-occlusive complications of SCD.

30 ociated with endurance exercise training and occlusive coronary artery disease.

31 el HypoE/SRBI(-/-) has been shown to develop occlusive coronary atherosclerosis followed by myocardia

32 particle number, the hazard ratios for major occlusive coronary event per 1-SD-higher level were 0.91

33 Major occlusive coronary events were equally strongly associat

34 ts at steady state and 6 during painful vaso-occlusive crises (pVOC).

35 Treatment of vaso-occlusive crises (VOC) or events in sickle cell disease

36 A unique feature of SCD is vaso-occlusive crises (VOCs) characterized by episodic, recur

37 perfusion (H/R) stress, mimicking acute vaso-occlusive crises (VOCs), increased bone turnover, osteoc

38 Vaso-occlusive crises are the main acute complication in sick

39 cold exposure are known to precipitate vaso-occlusive crises by still unclear mechanisms.

40 ulation and is characterized by painful vaso-occlusive crises in deep tissues.

41 stress, which have been associated with vaso-occlusive crises in SCD.

42 inking hemolysis- and infection-induced vaso-occlusive crises to TLR4 signaling.

43 mes included the incidences of malaria, vaso-occlusive crises, and serious adverse events.

44 sorder that is characterized by painful vaso-occlusive crises, for which there are few treatment opti

45 ity and blood rheology in precipitating vaso-occlusive crises.

46 chronic hemolytic anemia and iterative vaso-occlusive crises.

47 presentations of osteomyelitis (OM) and vaso-occlusive crisis (VOC) bone infarction in children with

48 Painful vaso-occlusive crisis (VOC) is the most common complication o

49 Vaso-occlusive crisis (VOC) is the primary cause of morbidity

50 HTRs induced acute vaso-occlusive crisis (VOC), resulting in shortened survival

51 hydroxyurea (HU) treatment or during a vaso-occlusive crisis and at steady-state.

52 d secondary endpoints-rates of clinical vaso-occlusive crisis and hemolytic events, blood transfusion

53 the protective effect of IVIG on acute vaso-occlusive crisis caused by neutrophil recruitment and ac

54 The rate of vaso-occlusive crisis events per person-year was 2.30 in the

55 and inflammation play a central role in vaso-occlusive crisis in sickle cell disease.

56 ts with sickle cell anemia, the rate of vaso-occlusive crisis was not significantly lower among those

57 The primary end point was the rate of vaso-occlusive crisis, a composite of painful crisis or acute

58 cell disease (SCD) is characterized by vaso-occlusive crisis.

59 ny infection, organ failure, or hepatic veno-occlusive disease (1-year cumulative incidence, 71% vs 8

60 24-3.33]; P = .002), and peripheral arterial occlusive disease (adjusted HR, 2.15 [95% CI, 1.26-3.66]

61 Hepatic veno-occlusive disease (HVOD), alias sinusoidal obstruction s

62 w L-Ficolin was associated with hepatic veno-occlusive disease (P = .0053, AUC = 0.80).

63 efore the procedure (P<0.01), and peripheral occlusive disease (P=0.04).

64 and their heterogeneity in peripheral artery occlusive disease (PAOD) still is limited.

65 Peripheral vascular occlusive disease (PVOD) is a common manifestation of at

66 Pulmonary veno-occlusive disease (PVOD) is an uncommon form of pulmonar

67 Pulmonary veno-occlusive disease (PVOD) is an uncommon form of pulmonar

68 terial hypertension (PAH) and pulmonary veno-occlusive disease (PVOD), respectively.

69 s, and it is therefore termed pulmonary veno-occlusive disease (PVOD).

70 12) and patients with primary pulmonary veno-occlusive disease (PVOD; n=17).

71 ic retinal disease (DRD), and retinal venous occlusive disease (RVO).

72 Rates of veno-occlusive disease (VOD) and thrombotic microangiopathy (

73 ction syndrome (SOS), previously called veno-occlusive disease (VOD) can be a difficult problem after

74 The incidence of hepatic veno-occlusive disease (VOD) was 5% for IV-BU and 1% with TBI

75 Hepatic veno-occlusive disease (VOD), also called sinusoidal obstruct

76 ide for the treatment of severe hepatic veno-occlusive disease (VOD), showing a 23% improvement in da

77 Rates of veno-occlusive disease and interstitial pneumonitis were high

78 treated with dasatinib, peripheral arterial occlusive disease and other arterial disorders in patien

79 ed deletion of Aplnr manifest pulmonary veno-occlusive disease and right heart failure, detectable at

80 ment of extracranial carotid atherosclerotic occlusive disease and the basis of these recommendations

81 , organ failure, infections, or hepatic veno-occlusive disease between groups.

82 o worsening pre-existing peripheral arterial occlusive disease in a patient who had received only ima

83 stemming from flow reversal,attributable to occlusive disease in the subclavian artery proximal to t

84 tion in native vessels included age, chronic occlusive disease intervention, rotational atherectomy u

85 nial internal carotid artery atherosclerotic occlusive disease is a common ischemic stroke mechanism.

86 Atherosclerotic vertebrobasilar (VB) occlusive disease is a significant etiology of posterior

87 Pulmonary veno-occlusive disease is caused by excessive cell proliferat

88 Severity of tissue injury in occlusive disease is dependent on the extent (number and

89 Veno-occlusive disease may also affect the lungs, and it is t

90 atation of proximal internal carotid artery, occlusive disease of terminal internal carotid artery, a

91 tion-related mortality; acute toxicity (veno-occlusive disease or acute graft versus-host disease [Gv

92 e hemodynamic impairment associated with the occlusive disease process does not fully account for the

93 randomized patients with peripheral arterial occlusive disease referred for 64-section multidetector

94 RG and APLNR in patients with pulmonary veno-occlusive disease undergoing lung transplantation were s

95 culation in patients with chronic aortoiliac occlusive disease undergoing subclavian transcatheter ao

96 melphalan group had Bearman grades 1-3 veno-occlusive disease versus 21 (9%) of 239 in the carboplat

97 essive primary immunodeficiency disease veno-occlusive disease with immunodeficiency syndrome (VODI),

98 clerosis, chronic lymphocytic leukemia, veno-occlusive disease with immunodeficiency, as well as Myco

99 t lower after treatment of femoral-popliteal occlusive disease with paclitaxel versus nonpaclitaxel d

100 dal obstruction syndrome (also known as veno-occlusive disease) in patients during study treatment or

101 capillary hemangiomatosis and pulmonary veno-occlusive disease, an autosomal recessively inherited di

102 ents suspected of having peripheral arterial occlusive disease, and diagnostic performance was simila

103 ipid syndrome is a rare cause of ocular vaso-occlusive disease, but is associated with significant sy

104 months of age as a result of pulmonary veno-occlusive disease, capillary hemorrhage, and pancytopeni

105 (NCF) in patients with severe carotid artery occlusive disease, depending on baseline brain perfusion

106 ructive syndrome, also known as hepatic veno-occlusive disease, is a potentially life-threatening com

107 result from an intrinsic cerebral arteriolar occlusive disease, little is known about how these proce

108 related macular degeneration, retinal venous occlusive disease, retinopathy of prematurity, and optic

109 act the detrimental consequences of vascular occlusive disease, such as stroke or myocardial infarcti

110 imal crossing, location, and stenotic versus occlusive disease.

111 patients with symptomatic atherosclerotic VB occlusive disease.

112 m that protects against ischemia in arterial occlusive disease.

113 17 patients (3%) had hepatic veno-occlusive disease.

114 rucial for the development of pulmonary veno-occlusive disease.

115 y less than 3 days to attenuate rebound vaso-occlusive disease.

116 dent Ca(2+) signaling that promotes vascular occlusive disease.

117 saminase and bilirubin without signs of veno-occlusive disease.

118 nction, and a high frequency of hepatic veno-occlusive disease.

119 , diabetic macular edema, and retinal venous occlusive disease.

120 ic and heritable PAH and with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis re

121 or heritable PAH and 16 with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis we

122 with a clinical diagnosis of pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis.

123 ne (EIF2AK4) are described in pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis.

124 Classical veno-occlusive disease/sinusoidal obstruction syndrome (VOD/S

125 and D lesions in superficial femoral artery occlusive disease; ISRCTN48164244).

126 Arterial occlusive diseases are major causes of morbidity and mor

127 s undergoing carotid intervention for severe occlusive diseases were prospectively recruited.

128 ent is common in older patients with carotid occlusive diseases.

129 in linking vascular inflammation and thrombo-occlusive diseases.

130 lenge in clinical treatment of acute thrombo-occlusive diseases.

131 th both asymptomatic and symptomatic carotid occlusive diseases.

132 rain represents a model for retinal vascular occlusive disorders and ischemic retinopathy.

133 smooth muscle cells (SMCs) is a hallmark of occlusive disorders such as atherosclerosis, postangiopl

134 Ocular arterial occlusive disorders were divided into central (CRAO) and

135 schemia differ among various ocular arterial occlusive disorders.

136 ive patients (728 eyes) with ocular arterial occlusive disorders.

137 esions in different types of ocular arterial occlusive disorders.

138 llateral flow index (CFI), the ratio of mean occlusive divided by mean nonocclusive arterial blood pr

139 care protocols, involving moisture-retentive occlusive dressing, or standard of care alone.

140 reduced hydration status and that the use of occlusive dressings that prevent water loss from wounds

141 protocol-driven use of skin antiseptics and occlusive dressings.

142 g platelets and myeloid leukocytes fostering occlusive DVT formation.

143 We study occlusive dynamics within a model microvascular network:

144 Here, using vaso-occlusive episodes (VOEs) of sickle cell disease as a va

145 hes to both prevention and treatment of vaso-occlusive episodes in SCD.

146 broad range of complications, including vaso-occlusive episodes, acute chest syndrome (ACS), pain, an

147 hydroxyurea to reduce the frequency of vaso-occlusive episodes, sickle cell disease (SCD) has contin

148 is is a key factor in the initiation of vaso-occlusive episodes, the hallmark of SCD.

149 in the patient with SCD) elimination of vaso-occlusive episodes.

150 ation of neutrophils that can stimulate vaso-occlusive episodes.

151 The efficacy endpoint for a confirmed occlusive event within 7 days was not significantly redu

152 deviation and alerts patients of a potential occlusive event.

153 ent reduced the median rate of clinical vaso-occlusive events (0 compared with 1.0 per year, P < 0.00

154 of 152 patients given imatinib had arterial occlusive events (p=0.052); arterial occlusive events we

155 studies showing a reduced incidence of vaso-occlusive events and reduced mortality.

156 ti XII has immediate benefits for acute vaso-occlusive events and survival in SCD mice exceeding thos

157 erlie complex disorders, such as the thrombo-occlusive events associated with myocardial infarction,

158 The question of the exact locations of occlusive events at the microcirculatory scale remains o

159 stained haemolytic anaemia and episodic vaso-occlusive events drive the development of end-organ comp

160 nilotinib, and venous and arterial vascular occlusive events during ponatinib.

161 Objective: To assess the risk of vascular occlusive events in patients with CML treated by new gen

162 l-cell adhesion and aggregation mediate vaso-occlusive events in patients with sickle cell disease (S

163 ther it has immediate benefits in acute vaso-occlusive events in SCD patients.

164 endothelial injury and facilitate acute vaso-occlusive events in transgenic SAD mice.

165 ight be benefit, although with more arterial occlusive events than with imatinib at the doses studied

166 ntration, reduce hemolysis, and prevent vaso-occlusive events that cause additional increases in pulm

167 Risk of vascular occlusive events was increased with dasatinib (OR, 3.86;

168 rterial occlusive events (p=0.052); arterial occlusive events were designated serious in ten (6%) of

169 There was no increase in vascular occlusive events with tranexamic acid, with no heterogen

170 ydroxyurea use reduced the incidence of vaso-occlusive events, infections, malaria, transfusions, and

171 s, type of intervention and data on vascular occlusive events, overall survival, and major molecular

172 xemplified by the risk of developing arterio-occlusive events, which is greatest for patients who hav

173 ted due to an important increase of vascular occlusive events.

174 , nilotinib, and ponatinib increase vascular occlusive events.

175 sease dominated by hemolytic anemia and vaso-occlusive events.

176 ombotic state, which may contribute to acute occlusive events.

177 sible role played by such aggregates in vaso-occlusive events.

178 , underlie devastating, and sometimes fatal, occlusive events.

179 nflammation, blood flow impairment, and vaso-occlusive events.

180 itant retinal vasculitis or retinal vascular occlusive events.

181 fy the effect of tranexamic acid on vascular occlusive events.

182 ll as direct observation, we show that these occlusive feedbacks are tuned throughout the trunk netwo

183 Our analysis shows that tuning of occlusive feedbacks increase the total dissipation withi

184 meter ratio, postprocedure compression time, occlusive hemostasis, and insufficient anticoagulation a

185 lial function, expressed as the time to peak occlusive hyperemia (Tmax), were examined.

186 ascular neoangiogenesis and results in lumen-occlusive intimal hyperplasia.

187 rtery; P < 0.001), and catheterization type (occlusive into the ophthalmic artery [OA] vs. nonocclusi

188 pothesis that SMC hyperplasia contributes to occlusive lesions in patients with ACTA2 missense mutati

189 a cerebrovascular disorder characterized by occlusive lesions of the circle of Willis.

190 novo superficial femoral artery stenotic or occlusive lesions were randomized to treatment with plai

191 s associated with angiographically minimally occlusive lesions.

192 Atherosclerosis, the build-up of occlusive, lipid-rich plaques in arterial walls, is a fo

193 Veno-occlusive liver disease of any grade occurred in 15 pati

194 Veno-occlusive liver disease was a major adverse event associ

195 tion associated with early onset of TAAD and occlusive moyamoya-like cerebrovascular disease.

196 onolayer in response to injury can result in occlusive neointima formation in diseases such as athero

197 nsion (PH) that generates robust and diffuse occlusive neointimal lesions across the pulmonary vascul

198 undergoing massive clonal expansion to form occlusive neointimal lesions.

199 pressing human alpha-Def-1 developed larger, occlusive, neutrophil-rich clots after partial inferior

200 that traverses the SER3 promoter and elicits occlusive nucleosome rearrangements.

201 erious adverse event in both groups was vaso-occlusive pain (11 events in five [8%] patients with hyd

202 ith hydroxyurea use, including rates of vaso-occlusive pain (98.3 vs. 44.6 events per 100 patient-yea

203 SCA) admitted to the hospital for acute vaso-occlusive pain (VOC).

204 onfidence interval [CI], 0.34 to 0.54), vaso-occlusive pain crises (incidence rate ratio, 0.43; 95% C

205 oppler velocity >200 cm/s (n = 2), >/=3 vaso-occlusive pain crises per year (n = 12), or >/=2 acute c

206 y chronic hemolytic anemia and episodic vaso-occlusive pain crises.

207 % confidence interval [CI], 0.06-0.91), vaso-occlusive pain episodes (11 studies, 1219 participants;

208 ties are often used during treatment of vaso-occlusive pain episodes (VOE), the major cause of morbid

209 acutely deficient in SCD patients with vaso-occlusive pain episodes (VOE).

210 associated with increased incidence of vaso-occlusive pain events, acute chest syndrome episodes, an

211 composite SCA-related clinical outcome (vaso-occlusive painful crisis, dactylitis, acute chest syndro

212 ascular cell injury, which underpins vasculo-occlusive pathologies such as atherogenesis and restenos

213 n, is characterized by inflammatory and vaso-occlusive pathologies.

214 ainguinal bypass procedures performed due to occlusive pathology in the Vascular Quality Initiative d

215 Furthermore, until the underlying occlusive pathophysiology of RVO can be addressed, our t

216 ination of antiangiogenic treatment and vaso-occlusive PDT.

217 The clinical consequences of occlusive peripheral arterial disease include intermitte

218 The clinical consequences of occlusive peripheral arterial disease include pain on wa

219 nsplantation of the EC clones caused arterio-occlusive PH in rats exposed to chronic hypoxia.

220 Distal occlusive pressure and toe oxygen saturation (Sao2) were

221 tio of simultaneously recorded mean coronary occlusive pressure divided by mean aortic pressure both

222 etween simultaneously recorded mean coronary occlusive pressure divided by mean aortic pressure, both

223 an arterial pressure, MPAP, pulmonary artery occlusive pressure, PVRI, and systemic vascular resistan

224 an arterial pressure, MPAP, pulmonary artery occlusive pressure, systemic vascular resistance index,

225 collateral flow index (CFIp, calculated as (occlusive pressure-central venous pressure)/(aortic pres

226 In the subgroup undergoing an occlusive procedure, placement of the catheter tip into

227 regate formation drive the inflammatory vaso-occlusive processes associated with sickle cell anemia (

228 HU) acute administration in diminishing vaso-occlusive processes in sickle cell disease (SCD) mice.(1

229 that clonally enriched primitive ECs promote occlusive pulmonary arteriopathy and severe PH.

230 g the progenitor marker CD117 promote severe occlusive pulmonary hypertension (PH).

231 h signaling in PAH, possibly contributing to occlusive pulmonary vascular remodeling triggered by EC

232 Post-occlusive reactive hyperaemia (PORH) in the skin microci

233 on and possible cellular contribution to the occlusive remodeling that characterizes advanced idiopat

234 The presence of an occlusive restenosis at the time of treatment was not as

235 ased restenosis rate, when compared with non-occlusive restenosis, at 1 year.

236 We report a case of hemorrhagic occlusive retinal vasculitis (HORV) after prophylactic i

237 tion, diagnosis, and outcomes of hemorrhagic occlusive retinal vasculitis (HORV).

238 Hemorrhagic occlusive retinal vasculitis is a rare, potentially deva

239 Considering the association of hemorrhagic occlusive retinal vasculitis with vancomycin and the com

240 risis, Purtscher's retinopathy, inflammatory occlusive retinal vasculitis, post-H1N1 vaccine, hyperte

241 elevated in the presence of high-grade (sub-occlusive) stenosis.

242 gnificant CAD was defined by the presence of occlusive/subocclusive stenoses or FFR measurements </=

243 acilitated by applying the allergen under an occlusive tape.

244 ng HDM on unmanipulated ear skin or under an occlusive tape.

245 on by LPS, and that platelets immobilized in occlusive thrombi are activated over time to produce IL-

246 mice had a delayed time to the formation of occlusive thrombi compared with wild-type (WT) in a FeCl

247 microscopy, and a failure to generate stable occlusive thrombi following FeCl3 injury of carotid arte

248 Basing this relation on measurements from occlusive thrombi formed in our flow chamber experiments

249 Occlusive thrombi formed under high flow shear rates dev

250 tran inhibited thrombin and the formation of occlusive thrombi in AD; preserved cognition, cerebral p

251 as able to correct bleeding in vivo and form occlusive thrombi in mesenteric vessels after FeCl(3) tr

252 sion and activity and promoted generation of occlusive thrombi in wild-type mice, whereas SIRT1 activ

253 These results suggest that stability of occlusive thrombi involves additional and as-yet-unident

254 we demonstrated that the inner structure of occlusive thrombi is heterogeneous and primarily determi

255 Normal, alpha2AP(+/+) mice developed large, occlusive thrombi within 5 hours after ligation; thrombi

256 at NAC might cleave the VWF multimers inside occlusive thrombi, thereby leading to their dissolution

257 fically disaggregating the external layer of occlusive thrombi, which is constituted of platelet aggr

258 FeCl(3) treatment resulted in intra-arterial occlusive thrombogenesis within 10 min in wild-type (WT)

259 ntages over fII(WT) animals: protection from occlusive thrombosis after arterial injury and markedly

260 F interactions restores vessel patency after occlusive thrombosis by specifically disaggregating the

261 3 exhibited significantly prolonged times to occlusive thrombosis compared to WT mice indicating a pr

262 eceptors in conferring in vivo resistance to occlusive thrombosis in this model.

263 (mural thrombosis model) or embolic stroke (occlusive thrombosis model) followed by recombinant tiss

264 rothrombocytopenia but also protects against occlusive thrombosis or cerebral infarction,providing ne

265 vs one [2%] of 42) such as reduced caliber, occlusive thrombosis, and lack of visibility; focal nodu

266 n-occlusive thrombosis; and grade 3, central occlusive thrombosis.

267 pendently of their ability to participate in occlusive thrombosis.

268 ivo neoangiogenesis, plaque development, and occlusive thrombosis.

269 pheral thrombosis; grade 2, intermediate non-occlusive thrombosis; and grade 3, central occlusive thr

270 Dase-1 were resistant to the formation of an occlusive thrombus after FeCl(3)-induced carotid artery

271 as a key determinant of the formation of an occlusive thrombus after vascular injury.

272 d FUT7 (Fut(-/-) mice) had a shorter time to occlusive thrombus formation in the injured carotid arte

273 The time to occlusive thrombus formation lengthened in these mice an

274 ed in KC-Tie2 and control mice; mean time to occlusive thrombus formation was shortened by 64% (P=0.0

275 anisms driving platelet cross-linking during occlusive thrombus formation.

276 to promote effective hemostasis and prevent occlusive thrombus formation.

277 Key components of STEMI include formation of occlusive thrombus, mediation and ultimately amplificati

278 e that this contributes to development of an occlusive thrombus.

279 le brachial index results, the prevalence of occlusive tibial and pedal arch disease is very high.

280 ns in BPMR2 signaling and is involved in the occlusive vas cular remodeling of PAH, findings that may

281 (ie, 10% absolute benefit) with pre-existing occlusive vascular disease (secondary prevention) and in

282 ute to development of TAAD and proliferative occlusive vascular disease.

283 horacic aortic aneurysms and dissections and occlusive vascular diseases, including early onset coron

284 ttractive strategy for treating debilitating occlusive vascular diseases, yet clinical trials have th

285 formation and neointimal thickening in other occlusive vascular diseases.

286 tic aneurysms, acute aortic dissections, and occlusive vascular diseases.

287 y depend on an individual's absolute risk of occlusive vascular events and the absolute reduction in

288 similar predictive values for incident major occlusive vascular events.

289 hear responsiveness in vitro, and attenuated occlusive vascular remodeling in chronically hypoxic Sug

290 Immune dysregulation has been linked to occlusive vascular remodeling in pulmonary arterial hype

291 orcine vessel for 18 d is demonstrated while occlusive vascular remodeling occurs.

292 inical entities were commonly noted: retinal occlusive vasculitis (21/77; 27%) and serpiginoid choroi

293 sitive quantiferon were diverse, but retinal occlusive vasculitis and serpiginoid choroiditis were co

294 at presentation occurred in 61 eyes (26.3%), occlusive vasculitis in 59 eyes (25.4%), and macular ede

295 th focal retinitis and poor in patients with occlusive vasculitis.

296 ation, blunted vascular repair, and worsened occlusive vasculopathy in mice.

297 (Kohlmeier-Degos disease) is a rare thrombo-occlusive vasculopathy that can affect multiple organ sy

298 Mutants are unable to form occlusive venous and arterial thrombi in response to end

299 To test this, we generated occlusive VWF-rich thrombi in the middle cerebral artery

300 Two days after siRNA injection, thrombi (occlusive) were observed in vessels (large and medium-si