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1                                              TRALI has primarily been attributed to passive infusion
2                                              TRALI induction by intact antibody was completely abroga
3                                              TRALI invokes an acute immune response dominated by neut
4                                              TRALI is the third leading cause of transfusion-related
5                                              TRALI is thought to be primarily mediated by donor antib
6                                              TRALI requires an immune priming step followed by transf
7                                              TRALI was associated with older platelets (P =.014).
8                                              TRALI was frequently underdiagnosed and underreported in
9                                              TRALI, like the acute respiratory distress syndrome, may
10                                              TRALI, like the adult respiratory distress syndrome, may
11                     We report a series of 90 TRALI reactions in 81 patients secondary to transfusion
12 the roles of the F(ab')2 and Fc regions of a TRALI-inducing immunoglobulin G anti-major histocompatib
13 o induce TRALI from RBCs and may represent a TRALI mitigation step.
14 tion even when administered 90 minutes after TRALI onset.
15 elationship between leukocyte antibodies and TRALI is more compelling if concordance between the anti
16 tion, and treatment with ATL in both LPS and TRALI models protected from ALI.
17 al and radiologic manifestations of TACO and TRALI are similar.
18                                     TACO and TRALI are the leading causes of transfusion-related fata
19 el is generally assumed to underlie TACO and TRALI disease pathology, where the first hit represents
20 ins very challenging to distinguish TACO and TRALI from underlying causes of lung injury and/or fluid
21                                     TACO and TRALI have emerged as important causes of posttransfusio
22 ch is required to better understand TACO and TRALI pathophysiology, and more biomarker studies are wa
23 e provide an up-to-date overview of TACO and TRALI regarding clinical definitions, diagnostic strateg
24 ciated with antibodies have been reported as TRALI and an association with passive infusion of lipids
25 associated with multiple transfusions can be TRALI, because each unit of blood or blood component can
26                       First, at the bedside, TRALI causes hypoxia and noncardiogenic pulmonary edema,
27                 All blood products can cause TRALI, and no specific treatment is available.
28  days) but not fresh platelets (1 day) cause TRALI via ceramide-mediated endothelial barrier dysfunct
29  exposure to blood components that may cause TRALI are also discussed.
30 a donor whose blood products may have caused TRALI in several transfusion recipients.
31 TRALI syndrome." DATA SYNTHESIS: The classic TRALI syndrome is an uncommon condition characterized by
32            In both experimental and clinical TRALI, an immune priming step is generally necessary to
33 PS) as the priming step, whereas in clinical TRALI the specific priming events are currently being de
34 plement activation was increased in clinical TRALI.
35 ttractive therapeutic approach for combating TRALI.
36 es is necessary before initiation of complex TRALI workup.
37 s to what should be considered to constitute TRALI.
38                 Both the classic and delayed TRALI syndromes are among the most important complicatio
39 e management of both the classic and delayed TRALI syndromes is essentially supportive.
40  and to define the newly recognized "Delayed TRALI syndrome." DATA SYNTHESIS: The classic TRALI syndr
41                            While the delayed TRALI syndrome can develop after the transfusion of a si
42                                This "delayed TRALI syndrome" is common, occurring in up to 25% of cri
43 resistant to antibody-mediated PMN-dependent TRALI induction.
44                                 To determine TRALI incidence by prospective, active surveillance and
45 re is no sentinel feature that distinguishes TRALI from TACO.
46 e suggest that NETs form in the lungs during TRALI, contribute to the disease process, and thus could
47                          In the experimental TRALI model, targeting platelet activation with either a
48        A common theme among the experimental TRALI models is the central importance of neutrophils in
49 s than in red blood cell products (the fatal TRALI incidence for plasma is 1:2-300 000 products; plat
50 reexisting inflammation is a risk factor for TRALI and neutrophils (polymorphonuclear neutrophils [PM
51 s inflammation are known to be important for TRALI initiation.
52          Since 2004, preventive measures for TRALI and TAS have been implemented, but their implement
53 Two proposed pathophysiologic mechanisms for TRALI have received the most attention: the antibody hyp
54 storage may present promising strategies for TRALI prevention.
55 nd DNase1, both of which protected mice from TRALI.
56 I mAb, there was significant protection from TRALI compared with nonbarrier mice.
57 cted in the lungs of mice that suffered from TRALI.
58 interleukin-8, a known risk factor for human TRALI.
59 tected NETs in the lungs and plasma of human TRALI and in the plasma of patients with acute lung inju
60 ies has replicated several features of human TRALI, focusing prominently on the role of neutrophils.
61                                           In TRALI, the first hit can, for example, be represented by
62 role of Fc-mediated complement activation in TRALI, with a direct relation to macrophage trafficking
63                       Recent developments in TRALI secondary to antibodies to HNA-3a antigen span dia
64 potential therapeutic strategy to explore in TRALI patients.
65 AMPs could serve as a priming "first hit" in TRALI.
66 in platelet concentrates (PCs) implicated in TRALI or control PCs that did not elicit a transfusion r
67                            PCs implicated in TRALI reactions contained significantly higher sCD40L le
68 a containing HNA-3a antibodies implicated in TRALI, and their ability to prime the oxidase was measur
69 to biologic response modifiers implicated in TRALI.
70 ibodies to HNA-3a are commonly implicated in TRALI.
71 i-HNA-3a antibodies previously implicated in TRALI.
72   We investigated whether OPN is involved in TRALI induction by promoting PMN recruitment to the lung
73   In this study, the role of these lipids in TRALI was investigated using an isolated, perfused rat l
74 roup to identify areas of research needed in TRALI.
75 e we show that NET biomarkers are present in TRALI patients' blood and that NETs are produced in vitr
76 sures have led to a significant reduction in TRALI, and TACO prevention is increasingly highlighted w
77 , which, in a susceptible patient, result in TRALI (2-hit hypothesis).
78 uct-derived factors and appears to result in TRALI by binding directly to pulmonary endothelium as we
79 tigated the role of the complement system in TRALI.
80 lity complex class I antibodies were used in TRALI mouse models, in combination with analyses of plas
81 lammatory activity and the ability to induce TRALI from RBCs and may represent a TRALI mitigation ste
82  priming activity, and the ability to induce TRALI in an animal model were measured.
83 a TLR9 antagonist blocked the mtDAMP-induced TRALI response, whereas 2 FPR antagonists did not, under
84  EV-dependent sphingolipid shuttling induces TRALI.
85 ng of transfusion related acute lung injury (TRALI) and transfusion associated circulatory overload (
86       Transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (
87 ) and transfusion-related acute lung injury (TRALI) are syndromes of acute respiratory distress that
88       Transfusion-related acute lung injury (TRALI) is a form of posttransfusion acute pulmonary insu
89       Transfusion-related acute lung injury (TRALI) is a hazardous transfusion complication with an a
90       Transfusion-related acute lung injury (TRALI) is a leading cause of transfusion-related mortali
91       Transfusion-related acute lung injury (TRALI) is a life-threatening complication of hemotherapy
92       Transfusion-related acute lung injury (TRALI) is a serious complication of hemotherapy.
93       Transfusion-related acute lung injury (TRALI) is a syndrome of respiratory distress triggered b
94       Transfusion-related acute lung injury (TRALI) is a syndrome that includes dyspnea, hypotension,
95       Transfusion-related acute lung injury (TRALI) is now the leading cause of transfusion-associate
96       Transfusion-related acute lung injury (TRALI) is one of the leading causes of transfusion-relat
97       Transfusion-related acute lung injury (TRALI) is one of the leading causes of transfusion-relat
98       Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion death.
99       Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated mo
100       Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related death
101       Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related morta
102       Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related morta
103       Transfusion-related acute lung injury (TRALI) is the most common cause of transfusion-related m
104       Transfusion-related acute lung injury (TRALI) remains a significant cause of transfusion-relate
105 rding transfusion-related acute lung injury (TRALI) through the bedside to bench and back to the beds
106  term transfusion-related acute lung injury (TRALI) was coined in 1983 to describe a constellation of
107       Transfusion-related acute lung injury (TRALI), a form of noncardiogenic pulmonary edema that de
108 el of transfusion-related acute lung injury (TRALI), a life-threatening complication of transfusions
109 el of transfusion-related acute lung injury (TRALI), Boc2 also reversed ASA protection, and treatment
110 e US, transfusion-related acute lung injury (TRALI), hemolytic transfusion reactions (HTRs), and tran
111 ions, transfusion-related acute lung injury (TRALI), transfusion-associated graft-versus-host disease
112 s) in transfusion-related acute lung injury (TRALI), which is the leading cause of death after transf
113 ethal transfusion-related acute lung injury (TRALI).
114 to as transfusion-related acute lung injury (TRALI).
115 ed in transfusion-related acute lung injury (TRALI).
116 to as transfusion-related acute lung injury (TRALI).
117 event transfusion-related acute lung injury (TRALI).
118 fatal transfusion-related acute lung injury (TRALI).
119 is of transfusion-related acute lung injury (TRALI).
120                Only additional research into TRALI prevention will provide the answers on how to best
121 ng male predominant plasma programs to limit TRALI, and preliminary evidence suggests that this is a
122  FcgammaRs, in the onset of 34-1-2S-mediated TRALI in mice.
123 whether CRP affects murine antibody-mediated TRALI induced by the anti-major histocompatibility compl
124 ion was related to in vivo antibody-mediated TRALI induction, which was correlated with increased mac
125 est a two-step process for antibody-mediated TRALI induction: the first step involves antibody bindin
126                   A murine antibody-mediated TRALI model was used to elucidate the roles of the F(ab'
127 y predispose recipients to antibody-mediated TRALI reactions and support the notion that modulating C
128 reviewed and contrasted to antibody-mediated TRALI.
129 may predispose patients to antibody-mediated TRALI.
130 veoli of mice experiencing antibody-mediated TRALI.
131 reviously, we established an immune-mediated TRALI mouse model, wherein mice with cognate antigen wer
132 of lipid priming activity and lipid-mediated TRALI.
133                             The OPN-mediated TRALI response seemed dependent on macrophages, likely t
134 ces in pulmonary and critical care medicine, TRALI is now considered to be one of the leading causes
135 e formed in a murine, 2-hit model, mimicking TRALI with lipopolysaccharide and C5a stimulation.
136                      Thus, steps to mitigate TRALI are in place, but a complete mechanistic understan
137 fer a novel therapeutic strategy to mitigate TRALI risk.
138            Experimental studies have modeled TRALI by using anti-major histocompatibility complex ant
139 d for sphingolipids, and applied in a murine TRALI model in vivo and for endothelial barrier assessme
140        Using a previously established murine TRALI model, we found that in contrast to wild-type (WT)
141 ed for induction of antibody-mediated murine TRALI through localization to the lungs and stimulation
142 an immunoglobulin G 1 variants of the murine TRALI-inducing antibody 34-1-2S, either unable to activa
143 Superimposed illness prevented assessment of TRALI in 14 patients.
144 ld to develop and standardize definitions of TRALI so that epidemiologic and research aspects of this
145                       Because development of TRALI is associated with donor antibodies (Abs) reactive
146                   Second, the development of TRALI requires a hit from the patient and from the produ
147               To examine the epidemiology of TRALI, we completed a nested case-control study of the f
148 pted clinical (mainly pulmonary) features of TRALI, the treatment options, and the excellent long-ter
149                  The two major hypotheses of TRALI, passively transfused neutrophil and human leukocy
150  be effective in decreasing the incidence of TRALI and which could have significant drawbacks.
151 early promise in decreasing the incidence of TRALI from high plasma volume blood products.
152 n explanation for the increased incidence of TRALI in patients with immune priming conditions, and we
153  antibodies, have decreased the incidence of TRALI.
154 review are to summarize current knowledge of TRALI with an emphasis on issues pertinent to the intens
155     These data suggest a 2-step mechanism of TRALI: priming of hematopoietic cells, followed by vascu
156 all of the proposed pathogenic mechanisms of TRALI is increased pulmonary capillary permeability, whi
157 s in the pathogenesis of this mouse model of TRALI and show ultrastructural evidence of pulmonary vas
158                 A new in vivo mouse model of TRALI based on major histocompatibility complex (MHC) I
159                The proposed two-hit model of TRALI is also supported by animal studies.
160 rux and Sachs clarified the two-hit model of TRALI pathogenesis.
161                          In a mouse model of TRALI that is neutrophil and platelet dependent, NETs ap
162 a clinically relevant in vivo mouse model of TRALI using an MHC I mAb, the mechanism of lung injury w
163                       The two-event model of TRALI, which is identical to the pathogenesis of the acu
164  second event in a 2-event in vitro model of TRALI.
165 n was evaluated in a 2-event animal model of TRALI.
166 g injury is common to all existing models of TRALI.
167  an anti-OPN antibody prevented the onset of TRALI induction.
168 anistic understanding of the pathogenesis of TRALI and of which patients are at highest risk remains
169               To explore the pathogenesis of TRALI, we developed an in vivo mouse model based on the
170  have been implicated in the pathogenesis of TRALI.
171  for establishing the pretest probability of TRALI as opposed to TACO.
172 o, are discussed as well as human studies of TRALI.
173 port both the antibody and lipid theories of TRALI.
174 ications for the prevention and treatment of TRALI.
175 thelium, which reframes our understanding of TRALI as a rapid-onset vasculitis.
176  but because of gaps in our understanding of TRALI, blood-bankers do not know how beneficial these in
177 between hydrostatic (TACO) and permeability (TRALI) pulmonary edema after transfusion is difficult, i
178 MNs, causing endothelial damage and possibly TRALI in predisposed patients.
179 red blood cell (RBC) supernatant and prevent TRALI.
180 rtality, and thus determining how to prevent TRALI is extremely important.
181                                   Preventing TRALI poses a difficult challenge for blood-banking expe
182  an effective therapeutic strategy to reduce TRALI severity.
183 om female donors was concurrent with reduced TRALI incidence: 2.57 (95% CI, 1.72-3.86) in 2006 versus
184 s report, clinicians can diagnose and report TRALI cases to the blood bank; importantly, researchers
185 vide potential targets for reducing residual TRALI.
186 ), and compared with pretransfusion samples, TRALI patients' plasma demonstrated increases in both in
187                             We conclude that TRALI is the result of 2 events with the second events c
188                             We conclude that TRALI may be more frequent than previously recognized an
189 consensus conference helped demonstrate that TRALI is likely underreported.
190                          We hypothesize that TRALI requires 2 events: (1) the clinical condition of t
191                    The major concept is that TRALI is defined as new acute lung injury occurring duri
192                                          The TRALI definition developed at the 2004 consensus confere
193 response modifiers responsible for 51 of the TRALI cases, including human leukocyte antigen (HLA) cla
194 PN to the OPN KO mice, however, restored the TRALI response and pulmonary PMN accumulation.
195       The biologic processes contributing to TRALI are poorly understood.
196 ens in the recipient does not always lead to TRALI.
197 ids in components may predispose patients to TRALI.
198  with 34-1-2s or CRP alone were resistant to TRALI, however mice injected with 34-1-2s together with
199 d thus could be targeted to prevent or treat TRALI.
200                                    A typical TRALI serologic workup consists of tests for HLA class I
201 well as mitigating antibody-mediated in vivo TRALI.
202 ary hydrostatic (cardiogenic) edema, whereas TRALI presents as pulmonary permeability edema (noncardi
203 e conferences have set out criteria by which TRALI is distinguished from other causes of acute lung i
204 , as well as how to deal with cases in which TRALI and TACO are both present.
205 HC), a mouse model has been studied in which TRALI-like disease is caused by injecting mice with anti
206 s were sequestered in the lungs of mice with TRALI, and retention of platelets was neutrophil depende
207 nt activation in the plasma of patients with TRALI (n = 53), which correlated with elevated neutrophi
208 -control study of the first 46 patients with TRALI compared with 225 controls who had received transf
209 nalyses of plasma samples from patients with TRALI.

 
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