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 alized predominantly to endothelial cells in occlusive and plexiform vascular lesions.

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

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

6 Thirty-two healthy subjects underwent occlusive application of 0.1% capsaicin cream (or placeb

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

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

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

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

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

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

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

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

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

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

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

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

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

20 We compared post-occlusive blood oxygenation time-course of femoral/popli

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

22 Unheralded vaso-occlusive cardiovascular events (myocardial infarction,

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

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

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

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

27 ressure and hypertrophy and pulmonary artery occlusive changes.

28 issue before bulk dissolution of potentially occlusive clots.

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

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

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

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

33 celerated advanced atherosclerosis featuring occlusive coronary atherosclerosis, vulnerable plaque, a

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

35 Major occlusive coronary events were equally strongly associat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 as a link with acute chest syndrome and vaso-occlusive crisis.

54 The use of thrombolysis for occlusive deep vein thrombosis, in attempt to reduce the

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

56 24-3.33]; P = .002), and peripheral arterial occlusive disease (adjusted HR, 2.15 [95% CI, 1.26-3.66]

57 ), GVHD (OR, 2.4; 95% CI, 1.8-3.3), and veno-occlusive disease (OR, 2.2; 95% CI, 1.4-3.6).

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

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

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

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

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

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

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

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

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

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

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

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

70 2) per day after recognition of hepatic veno-occlusive disease (VOD).

71 Atherosclerotic arterial occlusive disease affecting the lower extremities is als

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

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

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

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

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

77 ypertension and differentiate pulmonary veno-occlusive disease from pulmonary arterial hypertension.

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

79 her heterozygosity of Nf1 would lead to vaso-occlusive disease in genetically engineered mice in vivo

80 is an effective therapy for atherosclerotic occlusive disease in the coronary and peripheral circula

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

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

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

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

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

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

87 Veno-occlusive disease occurred twice with cyclophosphamide.

88 No additional cases of veno-occlusive disease occurred.

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

90 initiation of pulmonary vasodilators in veno-occlusive disease often leads to increased mortality.

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

92 Vascular occlusive disease poses a threat to kidney viability, bu

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

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

95 Treosulfan causes less veno-occlusive disease than busulfan and does not require pha

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

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

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

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

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

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

108 of lumen enlargement (growth/remodeling) in occlusive disease, show remarkably wide variation among

109 17 patients (3%) had hepatic veno-occlusive disease.

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

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

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

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

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

115 ped severe hepatotoxicity suggestive of veno-occlusive disease.

116 ge differences in tissue injury in models of occlusive disease.

117 rminants of the severity of tissue injury in occlusive disease.

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

119 patients with symptomatic atherosclerotic VB occlusive disease.

120 m that protects against ischemia in arterial occlusive disease.

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

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

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

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

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 ant pathological process in several vascular occlusive diseases, including atherosclerosis and resten

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

130 in linking vascular inflammation and thrombo-occlusive diseases.

131 th both asymptomatic and symptomatic carotid occlusive diseases.

132 creased proliferation of SMCs contributed to occlusive diseases.

133 apeutic target for the treatment of vascular occlusive diseases.

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

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

136 d VSMCs is a potential strategy against vaso-occlusive disorders such as in-stent restenosis, vein-gr

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

138 schemia differ among various ocular arterial occlusive disorders.

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

140 hc is a potential therapeutic target in vaso-occlusive disorders.

141 esions in different types of ocular arterial occlusive disorders.

142 By contrast, occlusive dressing control wounds showed generalized hyp

143 ent with physiological function, compared to occlusive dressing control wounds that showed formation

144 more physiological blood vessels compared to occlusive dressing control wounds.

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

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

147 rrhagic venous infarctions, all secondary to occlusive DVST.

148 g platelets and myeloid leukocytes fostering occlusive DVT formation.

149 We study occlusive dynamics within a model microvascular network:

150 ac syndrome is a multisystemic microvascular occlusive endotheliopathy with suspected immune-mediated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 clinical efficacy for preventing acute vaso-occlusive events in severely affected adults.

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

167 s of uncertain net value as the reduction in occlusive events needs to be weighed against any increas

168 Tissue damage from vascular occlusive events results in the replacement of contracti

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

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

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

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

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

174 ration of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patien

175 course of tranexamic acid on death, vascular occlusive events, and the receipt of blood transfusion i

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

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

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

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

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

181 with poor outcomes following acute vascular occlusive events.

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

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

184 , nilotinib, and ponatinib increase vascular occlusive events.

185 children and adolescents with recurrent vaso-occlusive events; recent evidence documents sustained lo

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

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

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

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

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

191 ts, and reversibility of plexiform and other occlusive lesions in pulmonary arterial hypertension.

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

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

194 s associated with angiographically minimally occlusive lesions.

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

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

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

198 blood rheology and plays a key role in vaso-occlusive manifestations of sickle cell disease.

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

200 erstitial fibrosis, cardiac hypertrophy, and occlusive neointima development.

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

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

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

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

205 % confidence interval [CI], 0.06-0.91), vaso-occlusive pain episodes (11 studies, 1219 participants;

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

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

208 Acute, vaso-occlusive pain is the most characteristic complication o

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

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

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

212 ination of antiangiogenic treatment and vaso-occlusive PDT.

213 The clinical consequences of occlusive peripheral arterial disease include intermitte

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

215 id vessel injury stimulates the formation of occlusive platelet thrombi in mice but not in the size-

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

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

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

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

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

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

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

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

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

225 tomized rats included glomerular hemorrhage, occlusive red blood cell casts, and acute tubular injury

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

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

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

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

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

231 Hemorrhagic occlusive retinal vasculitis is a rare, potentially deva

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

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

234 e important in governing whether or not vaso-occlusive sickle cell crises will occur.

235 obleeds, suggesting that they result from an occlusive small-vessel arteriopathy.

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

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

238 acilitated by applying the allergen under an occlusive tape.

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

240 80% of GSK3beta+/- mice (n=10) formed stable occlusive thrombi after ferric chloride carotid artery i

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

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

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

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

245 Vav3 together may prevent the development of occlusive thrombi in mice fed a high-fat diet.

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

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

248 The formation of occlusive thrombi is complex, involving the integration

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

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

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

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

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

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

255 3 exhibited significantly prolonged times to occlusive thrombosis compared to WT mice indicating a pr

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

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

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

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

260 pendently of their ability to participate in occlusive thrombosis.

261 ivo neoangiogenesis, plaque development, and occlusive thrombosis.

262 ty-four (55%) of the 98 sinuses or bulbs had occlusive thrombosis.

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

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

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

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

267 may rupture with subsequent formation of an occlusive thrombus and result in an acute coronary syndr

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

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

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

271 The identification of strategies to suppress occlusive thrombus formation without undermining normal

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

273 to promote effective hemostasis and prevent occlusive thrombus formation.

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

275 e test assesses the time required to form an occlusive thrombus, the occlusion time (OT), and the tim

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

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

278 Post-occlusive transient changes in venous blood oxygenation

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

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

281 e collateral circulation to lessen injury in occlusive vascular disease depends on the density and ca

282 net benefit for many people who already have occlusive vascular disease.

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

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

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

286 formation and neointimal thickening in other occlusive vascular diseases.

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

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

289 standard statin regimens reduces the risk of occlusive vascular events in a wide range of individuals

290 similar predictive values for incident major occlusive vascular events.

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

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

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

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

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

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

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

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

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

300 5-HT-LTD is mutually occlusive with dopamine/endocannabinoid-dependent LTD, s