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1 1 activation by thrombin can be inhibited by aprotinin.
2 let aggregation (P<0.001) in the presence of aprotinin.
3 ed by the plasmin/serine protease antagonist aprotinin.
4 5.4 U, P<0.002) than patients not prescribed aprotinin.
5 ta by TSP, but not by the plasmin inhibitor, aprotinin.
6 ition of bovine plasminogen and inhibited by aprotinin.
7 se was completely inhibited by DesPro2-Arg15-Aprotinin.
8 Galardin and the serine protease inhibitor, aprotinin.
9 or inhibitor-1 and serine protease inhibitor aprotinin.
10 me inhibitors, and the intraoperative use of aprotinin.
11 r permeability and is effectively blocked by aprotinin.
12 more effective than the reference inhibitor aprotinin.
13 ncludes bestatin, leupeptin, E64, AEBSF, and aprotinin.
15 ion, we prospectively assessed three agents (aprotinin [1295 patients], aminocaproic acid [883], and
16 on during CPB (n=17) and (2) those receiving aprotinin (2x10(6) kallikrein inhibitor units [KIU] in p
17 s with operating-room charges for the use of aprotinin (33,517 patients) or aminocaproic acid (44,682
18 The treatment group (n=7) was administered aprotinin (40,000 kallikrein inhibitor units [KIU]/kg lo
22 A total of 1343 patients (13.2%) received aprotinin, 6776 patients (66.8%) received aminocaproic a
23 sulfoxide (DMSO)/Ringer's solution, 300 KIU aprotinin (a serine protease inhibitor), 0.05% or 0.10%
24 These processes were similarly sensitive to aprotinin, a potent inhibitor of serine proteases, inclu
26 taneously treated with the plasmin inhibitor aprotinin, a significant reduction in the size of necrot
27 revealed by engineering the binding loop of aprotinin, a small protein with high affinity for DENV p
28 e protease inhibitors (camostat mesylate and aprotinin), affords protection against neutrophil elasta
32 f Abeta40 with the serine protease inhibitor aprotinin also increased diffuse extracellular depositio
34 ts were randomized to receive intraoperative aprotinin, an inhibitor of several serine proteinases, o
36 cardiac surgery, the odds ratio (OR) between aprotinin and an increased risk of renal dysfunction wit
42 ntinue to suggest the virtual equivalence of aprotinin and lysine analogues in reducing bleeding and
44 of LIMA grafts between patients who received aprotinin and placebo, both groups were analyzed collect
45 s extend the clinical mechanism of action of aprotinin and provide the first proof of principle that
47 nding of apoE-beta VLDL, lipoprotein lipase, aprotinin, and lactoferrin to megalin in a concentration
48 nogen and Spl in the presence of 100 micro M aprotinin, and plasminogen activation by pro-uPA alone w
49 rtic cross-clamp time, use of intraoperative aprotinin, and preoperative use of statin, we found that
50 iproteinase inhibitor, alpha2-macroglobulin, aprotinin, and soybean inhibitor, using trypsin as the i
52 A recent highly publicized report implicated aprotinin as an independent causal factor for postoperat
53 a binary test set of proteins (lysozyme and aprotinin) at a pH not employed in the training set were
58 ted by plasminogen activator inhibitor-1 and aprotinin but not by tissue inhibitor of metalloproteina
60 cleaved PAR1 receptors, was preserved in the aprotinin but not the placebo group (P<0.05), and (3) su
61 was critical for the degradation process as aprotinin, but not alpha(2)-antiplasmin, prevented colla
62 e inhibitors, diisopropylfluorophosphate and aprotinin, but not by soybean or lima bean trypsin inhib
63 t been realized with the discontinued use of aprotinin, but rather increased blood product use has oc
64 mbin generation in humans to examine whether aprotinin can inhibit platelet PAR1 activation clinicall
66 etic mobility were observed upon raising the aprotinin concentration, allowing determination of their
67 nhibitor, hirudin, or the plasmin inhibitor, aprotinin, consistent with the interpretation that matri
70 han and phosphoramidon), serine proteinases (aprotinin), cysteine proteinases (leupeptin) and urokina
75 in by both PA culture broths by 99%, whereas aprotinin did not significantly reduce the protease acti
76 with epsilon-aminocaproic acid and low-dose aprotinin (each with a 35% reduction versus placebo, P<0
79 in a double-blind study to receive high-dose aprotinin, epsilon-aminocaproic acid, or saline placebo.
82 that the peptidic inhibitors, leupeptin and aprotinin, exhibited similar potencies in inhibiting fac
84 akdown, rats were treated intravenously with aprotinin, followed by intravitreal injection of VEGF(16
85 ilon-aminocaproic acid may be preferred over aprotinin for reducing hemorrhage with cardiac surgery.
86 analyzed from the International Multicenter Aprotinin Graft Patency Experience (IMAGE) trial in whic
92 stimated risk of death was 64% higher in the aprotinin group than in the aminocaproic acid group (rel
104 study describes the incidence and impact of aprotinin hypersensitivity reactions in children undergo
107 ication of the proposed method for measuring aprotinin in pretreated plasma samples is also reported.
111 nduced and early diabetic BRB breakdown with aprotinin indicates that azurocidin may be an important
117 nt studies suggest that the antifibrinolytic aprotinin is associated with increased renal and vascula
121 The risk of hypersensitivity reactions to aprotinin is low in children undergoing cardiothoracic s
123 ogen variants showed similar affinity toward aprotinin (Kd's of 3-9 muM), which were not significantl
124 ion of factor XIa activation of factor IX by aprotinin (Ki 0.89 +/- 0.52 microM) was non-competitive,
125 p-aminobenzamidine (Ki 28 +/- 2 microM) and aprotinin (Ki 1.13 +/- 0.07 microM) in a classical compe
126 lipoprotein (beta VLDL), lipoprotein lipase, aprotinin, lactoferrin, and the receptor-associated prot
127 the binding of apoE-beta VLDL, lactoferrin, aprotinin, lipoprotein lipase, and RAP to megalin is eit
129 of endogenous serine protease activity with aprotinin markedly decreased ENaC-mediated currents and
131 PI) domain of tick anticoagulant protein, an aprotinin mutant (6L15), amyloid beta-protein precursor,
133 he use of epsilon-aminocaproic acid (n=9) or aprotinin (n=46) in patients undergoing cardiac surgery
134 pective review of our entire experience with aprotinin (n=865), 681 first exposures, 150 second expos
137 cting each patient's likelihood of receiving aprotinin on the basis of preoperative characteristics a
138 were treated simultaneously with plasmin and aprotinin or a tissue inhibitor of metalloproteinases, T
140 e and dog mast cell protease (dMCP)-3, i.e., aprotinin or bis(5-amidino-2-benzimidazolyl) methane (BA
141 KD1-L17R was equally or more effective than aprotinin or tranexamic acid, which have been used as an
142 may mediate BRB breakdown in early diabetes, aprotinin or vehicle was injected intravenously each day
147 anner by agents that inhibited plasmin, e.g. aprotinin, or that inhibited plasminogen activation, e.g
148 te quantification of recombinantly expressed aprotinin out of its host cell protein background using
152 ot affected by TIMP-1 or protease inhibitors aprotinin, pepstatin, or leupeptin but was inhibited in
154 activated receptor, and we hypothesized that aprotinin preserves myocardial cellular junctions and pr
155 tivity of plasmin-like serine proteases with aprotinin prevented beta1 integrin/CDCP1 complexing and
157 ti-uPAR or anti-uPA Abs or plasmin inhibitor aprotinin prior to coculturing with healthy cardiocytes
164 these results, the serine protease inhibitor aprotinin reproduced the effects of FAEEs and prevented
167 s resist antiproteases, including leupeptin, aprotinin, serpins, and alpha2-macroglobulin, suggesting
168 t transfused PRBC in the model suggests that aprotinin significantly impacts ARF (P=0.008; OR=1.5).
172 was 1.6% (180/11,198) and was higher in the aprotinin subset (2.6%, 72/2757 versus 1.3%, 108/8441; P
174 lysis were more frequent among recipients of aprotinin than among recipients of aminocaproic acid.
175 hese data suggest that the administration of aprotinin to patients treated with DHCA does not increas
178 nhibition with the affinity of leupeptin and aprotinin to the factor XIa-factor IX complex only appro
180 e of renal dysfunction in patients receiving aprotinin, tranexamic acid, or no antifibrinolytic treat
182 Procrit), by maximizing red cell counts, and aprotinin (Trasylol), by inhibiting fibrinolysis, are tw
185 ed acute renal and vascular safety concerns, aprotinin use is associated with an increased risk of lo
186 nocaproic acid or no antifibrinolytic agent, aprotinin use was also associated with a larger risk-adj
187 n between perioperative variables, including aprotinin use, and renal dysfunction was assessed by ANO
191 logistic regression (C-index, 0.72), use of aprotinin was associated with a doubling in the risk of
192 ors and undergoing off-pump cardiac surgery, aprotinin was associated with a greater than two-fold in
194 ilure seen in patients who were administered aprotinin was directly related to increased number of tr
195 e instrumental-variable analysis, the use of aprotinin was found to be associated with an excess risk
197 ither with propensity adjustment or without, aprotinin was independently predictive of 5-year mortali
200 -fused variant of the fibrinolysis inhibitor aprotinin was used to control the hydrogel degradation r
203 esisting tryptic peptidase inhibitors (e.g., aprotinin), while favoring angiotensin destruction at Ty
205 rvival was worse among patients treated with aprotinin, with a main-effects hazard ratio for death of
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