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1 elial barrier but does not necessarily cause plasma leakage.
2 f the VE biomarkers with the severity of the plasma leakage.
3 074) had an adjusted association with severe plasma leakage.
4 laudin-5 are strongly associated with severe plasma leakage.
5 for exacerbated dengue pathogenesis, notably plasma leakage.
6 yte-associated FITC-gelatin fluorescence and plasma leakage.
7 re significantly associated with significant plasma leakage.
8  openings in the endothelium without causing plasma leakage.
9 rrhagic manifestations, and 23% had signs of plasma leakage.
10  with high viremia and increased severity of plasma leakage.
11 icoagulant suppression, vascular injury, and plasma leakage.
12 es, specifically mast cell degranulation and plasma leakage.
13  vessels and protects them from VEGF-induced plasma leakage.
14  total VEGF-A in DHF patients at the time of plasma leakage.
15 ilder form of dengue virus infection without plasma leakage.
16 acterized by a transient period of localized plasma leakage.
17 and tight and adherens junction markers with plasma leakage.
18 ere correlated with the degree of subsequent plasma leakage.
19 u and Monastral blue as a tracer to quantify plasma leakage.
20 sed the risk of developing severe dengue and plasma leakage.
21 ubsequent platelet count, severe dengue, and plasma leakage.
22 on status, and disease severity, measured by plasma leakage.
23 engue hemorrhagic fever, is characterized by plasma leakage and derangements in hemostasis.
24    These changes were accompanied by reduced plasma leakage and improved vascular integrity in metast
25                                              Plasma leakage and keratinocyte chemoattractant producti
26  that salmeterol pretreatment can reduce the plasma leakage and leukocyte adhesion in early- and late
27 ergic receptor agonist, on ovalbumin-induced plasma leakage and leukocyte adhesion in tracheal blood
28 s vascular remodeling in inflammation, where plasma leakage and leukocyte influx are prominent featur
29 ire the phenotype of venules specialized for plasma leakage and leukocyte recruitment.
30 uctural protein 1 (NS1; anti-NS1 Igs) induce plasma leakage and mortality in mice with warfarinized a
31 viremia levels correlated with the degree of plasma leakage and thrombocytopenia.
32 vere dengue cases, 701 (12.4%) patients with plasma leakage, and 1441 of 4008 (40.0%) patients recrui
33 rations occur in dengue, are associated with plasma leakage, and are correlate with molecules of endo
34 droitin sulfate are strongly associated with plasma leakage, and elevated levels of syndecan-1 and cl
35 clinically relevant endpoints-severe dengue, plasma leakage, and hospitalization-in the dengue-confir
36                    Vascular permeability and plasma leakage are immune-pathologies of severe dengue v
37 ts resulted in both early and late phases of plasma leakage as measured with Evans blue.
38 dly reduced neutrophil (PMN) recruitment and plasma leakage at dermal sites with LTB(4).
39 and a potent inducer of inflammation causing plasma leakage at the site of infection.
40 duced airway hyperresponsiveness and mucosal plasma leakage but had no effect on inflammatory cells o
41 as also able to inhibit neutrophil-dependent plasma leakage, but had no effect on the response induce
42 eans, binds to endothelial cells at sites of plasma leakage, but little is known about the amount and
43 el structure and blood perfusion and blocked plasma leakage by enhanced endothelial barrier function
44   Treatments with the anti-NS1-DR4 Ig led to plasma leakage, coagulopathy, and morality in mice with
45 significantly lower for patients with severe plasma leakage compared to those with no leakage (1.46 v
46 sistance to injury, characterized by reduced plasma leakage, decreased leucocyte adhesion and amelior
47 the relationship between pericytes and blood plasma leakage during photothrombotic occlusion of corti
48 eased vascular permeability and pathological plasma leakage during viral hemorrhagic fevers are large
49 other inflammatory diseases when the rate of plasma leakage from blood vessels exceeds the drainage t
50 y; this has been proposed as a mechanism for plasma leakage in dengue hemorrhagic fever.
51  expression may be an important mechanism of plasma leakage in DHF.
52  and has been hypothesized to play a role in plasma leakage in diabetic retinopathy.
53 r the bradykinin B2 receptor (B2R) inhibited plasma leakage in hamster cheek pouch topically exposed
54                              The severity of plasma leakage in patients inversely correlated with pla
55 ough the infection had no effect on baseline plasma leakage, in both strains it potentiated the leaka
56  contribute to both early and late phases of plasma leakage induced by antigen, but most leakage occu
57 ful vascular protective effects: suppressing plasma leakage, inhibiting vascular inflammation, and pr
58  in extensive microvascular permeability and plasma leakage into tissues and organs.
59 ial (VE) components in dengue infection with plasma leakage is unknown.
60 dengue virus (DV) infection characterized by plasma leakage, is more common in secondary DV infection
61  by early and late phases of vasodilatation, plasma leakage, leukocyte influx, and bronchoconstrictio
62 ia, consistent with circulatory collapse and plasma leakage, likely impairing oxygen delivery and dis
63 lar endothelial cells producing disseminated plasma leakage, manifesting as nonspecific fever, headac
64 x events such as bronchoconstriction, airway plasma leakage, mucus secretion and cough.
65 essation of capillary flow, we observed that plasma leakage occurred with three times greater frequen
66  of several viral hemorrhagic fevers, severe plasma leakage occurs at the time of viral clearance and
67 /NO bioavailability is associated with worse plasma leakage, occurs early in dengue illness and corre
68                                       Severe plasma leakage or shock was more common among children a
69          Severe dengue was defined as severe plasma leakage or shock, severe bleeding, or organ invol
70 ed in arterioles also occurs in venules, (2) plasma leakage persists well beyond red cell escape and
71                                              Plasma leakage results from gaps between endothelial cel
72 y may play a role in the pathogenesis of the plasma leakage seen in dengue hemorrhagic fever and deng
73             The main outcome of interest was plasma leakage severity.
74 se its presentation can resemble more common plasma leakage syndromes, including angioedema or system
75 imiting febrile illness to one manifested by plasma leakage that can lead to vascular collapse and de
76 athophysiological hallmark of DHF and DSS is plasma leakage that leads to enhanced vascular permeabil
77 , particularly the mechanisms underlying the plasma leakage that results in hypovolaemic shock in a s
78 ion with a dengue virus, is characterized by plasma leakage, thrombocytopenia, and hepatic inflammati
79 neutrophil-induced endothelial pores prevent plasma leakage through actomyosin-based pore confinement
80                                              Plasma leakage was preceded by rapid activation of matri
81                                       Severe plasma leakage was the most common presentation among ch
82 .025-1.307) had an adjusted association with plasma leakage, whereas levels of syndecan-1 (OR = 1.004
83                 The ability of Ang1 to block plasma leakage without producing angiogenesis may be the