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1 more effective than the reference inhibitor aprotinin.
2 1 activation by thrombin can be inhibited by aprotinin.
3 let aggregation (P<0.001) in the presence of aprotinin.
4 ed by the plasmin/serine protease antagonist aprotinin.
5 5.4 U, P<0.002) than patients not prescribed aprotinin.
6 ta by TSP, but not by the plasmin inhibitor, aprotinin.
7 ition of bovine plasminogen and inhibited by aprotinin.
8 se was completely inhibited by DesPro2-Arg15-Aprotinin.
9 Galardin and the serine protease inhibitor, aprotinin.
10 or inhibitor-1 and serine protease inhibitor aprotinin.
11 me inhibitors, and the intraoperative use of aprotinin.
12 r permeability and is effectively blocked by 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
45 of LIMA grafts between patients who received aprotinin and placebo, both groups were analyzed collect
46 s extend the clinical mechanism of action of aprotinin and provide the first proof of principle that
48 than the gold-standard therapeutic inhibitor aprotinin, and is a promising candidate for development
49 nding of apoE-beta VLDL, lipoprotein lipase, aprotinin, and lactoferrin to megalin in a concentration
50 nogen and Spl in the presence of 100 micro M aprotinin, and plasminogen activation by pro-uPA alone w
51 rtic cross-clamp time, use of intraoperative aprotinin, and preoperative use of statin, we found that
52 iproteinase inhibitor, alpha2-macroglobulin, aprotinin, and soybean inhibitor, using trypsin as the i
53 clonal antibody, epsilon-amino-caproic acid, aprotinin, and the aminoterminal fragment of urokinase-t
56 hibitor, serum alpha-1 antitrypsin, or liver aprotinin, are a class of proteins that competitively bi
57 A recent highly publicized report implicated aprotinin as an independent causal factor for postoperat
58 a binary test set of proteins (lysozyme and aprotinin) at a pH not employed in the training set were
63 ted by plasminogen activator inhibitor-1 and aprotinin but not by tissue inhibitor of metalloproteina
65 cleaved PAR1 receptors, was preserved in the aprotinin but not the placebo group (P<0.05), and (3) su
66 oteolytic activity at the cell surface using aprotinin but was abolished when the gamma-inhibitory tr
67 was critical for the degradation process as aprotinin, but not alpha(2)-antiplasmin, prevented colla
68 e inhibitors, diisopropylfluorophosphate and aprotinin, but not by soybean or lima bean trypsin inhib
69 t been realized with the discontinued use of aprotinin, but rather increased blood product use has oc
70 mbin generation in humans to examine whether aprotinin can inhibit platelet PAR1 activation clinicall
72 etic mobility were observed upon raising the aprotinin concentration, allowing determination of their
73 nhibitor, hirudin, or the plasmin inhibitor, aprotinin, consistent with the interpretation that matri
76 han and phosphoramidon), serine proteinases (aprotinin), cysteine proteinases (leupeptin) and urokina
79 t a microsensor dual-coated with both TF and aprotinin detects the hemostatic rescue in the tPA-induc
82 in by both PA culture broths by 99%, whereas aprotinin did not significantly reduce the protease acti
83 with epsilon-aminocaproic acid and low-dose aprotinin (each with a 35% reduction versus placebo, P<0
86 in a double-blind study to receive high-dose aprotinin, epsilon-aminocaproic acid, or saline placebo.
89 that the peptidic inhibitors, leupeptin and aprotinin, exhibited similar potencies in inhibiting fac
91 akdown, rats were treated intravenously with aprotinin, followed by intravitreal injection of VEGF(16
92 ilon-aminocaproic acid may be preferred over aprotinin for reducing hemorrhage with cardiac surgery.
93 analyzed from the International Multicenter Aprotinin Graft Patency Experience (IMAGE) trial in whic
99 stimated risk of death was 64% higher in the aprotinin group than in the aminocaproic acid group (rel
111 study describes the incidence and impact of aprotinin hypersensitivity reactions in children undergo
114 ication of the proposed method for measuring aprotinin in pretreated plasma samples is also reported.
118 nduced and early diabetic BRB breakdown with aprotinin indicates that azurocidin may be an important
124 nt studies suggest that the antifibrinolytic aprotinin is associated with increased renal and vascula
128 The risk of hypersensitivity reactions to aprotinin is low in children undergoing cardiothoracic s
130 ogen variants showed similar affinity toward aprotinin (Kd's of 3-9 muM), which were not significantl
131 ion of factor XIa activation of factor IX by aprotinin (Ki 0.89 +/- 0.52 microM) was non-competitive,
132 p-aminobenzamidine (Ki 28 +/- 2 microM) and aprotinin (Ki 1.13 +/- 0.07 microM) in a classical compe
133 lipoprotein (beta VLDL), lipoprotein lipase, aprotinin, lactoferrin, and the receptor-associated prot
134 the binding of apoE-beta VLDL, lactoferrin, aprotinin, lipoprotein lipase, and RAP to megalin is eit
136 of endogenous serine protease activity with aprotinin markedly decreased ENaC-mediated currents and
138 PI) domain of tick anticoagulant protein, an aprotinin mutant (6L15), amyloid beta-protein precursor,
140 he use of epsilon-aminocaproic acid (n=9) or aprotinin (n=46) in patients undergoing cardiac surgery
141 pective review of our entire experience with aprotinin (n=865), 681 first exposures, 150 second expos
144 cting each patient's likelihood of receiving aprotinin on the basis of preoperative characteristics a
145 were treated simultaneously with plasmin and aprotinin or a tissue inhibitor of metalloproteinases, T
147 e and dog mast cell protease (dMCP)-3, i.e., aprotinin or bis(5-amidino-2-benzimidazolyl) methane (BA
148 KD1-L17R was equally or more effective than aprotinin or tranexamic acid, which have been used as an
149 may mediate BRB breakdown in early diabetes, aprotinin or vehicle was injected intravenously each day
154 anner by agents that inhibited plasmin, e.g. aprotinin, or that inhibited plasminogen activation, e.g
155 te quantification of recombinantly expressed aprotinin out of its host cell protein background using
159 ot affected by TIMP-1 or protease inhibitors aprotinin, pepstatin, or leupeptin but was inhibited in
160 with physisorption of tissue factor (TF) and aprotinin permits real-time assessment of the coagulatio
162 activated receptor, and we hypothesized that aprotinin preserves myocardial cellular junctions and pr
163 tivity of plasmin-like serine proteases with aprotinin prevented beta1 integrin/CDCP1 complexing and
165 ti-uPAR or anti-uPA Abs or plasmin inhibitor aprotinin prior to coculturing with healthy cardiocytes
172 these results, the serine protease inhibitor aprotinin reproduced the effects of FAEEs and prevented
175 s resist antiproteases, including leupeptin, aprotinin, serpins, and alpha2-macroglobulin, suggesting
176 t transfused PRBC in the model suggests that aprotinin significantly impacts ARF (P=0.008; OR=1.5).
180 was 1.6% (180/11,198) and was higher in the aprotinin subset (2.6%, 72/2757 versus 1.3%, 108/8441; P
182 lysis were more frequent among recipients of aprotinin than among recipients of aminocaproic acid.
183 vity of soybean trypsin inhibitor and bovine aprotinin that they nick supercoiled, circular plasmid D
184 hese data suggest that the administration of aprotinin to patients treated with DHCA does not increas
187 nhibition with the affinity of leupeptin and aprotinin to the factor XIa-factor IX complex only appro
189 e of renal dysfunction in patients receiving aprotinin, tranexamic acid, or no antifibrinolytic treat
191 Procrit), by maximizing red cell counts, and aprotinin (Trasylol), by inhibiting fibrinolysis, are tw
194 ed acute renal and vascular safety concerns, aprotinin use is associated with an increased risk of lo
195 nocaproic acid or no antifibrinolytic agent, aprotinin use was also associated with a larger risk-adj
196 n between perioperative variables, including aprotinin use, and renal dysfunction was assessed by ANO
200 logistic regression (C-index, 0.72), use of aprotinin was associated with a doubling in the risk of
201 ors and undergoing off-pump cardiac surgery, aprotinin was associated with a greater than two-fold in
203 ilure seen in patients who were administered aprotinin was directly related to increased number of tr
204 e instrumental-variable analysis, the use of aprotinin was found to be associated with an excess risk
206 ither with propensity adjustment or without, aprotinin was independently predictive of 5-year mortali
209 -fused variant of the fibrinolysis inhibitor aprotinin was used to control the hydrogel degradation r
211 caproic acid, 4-aminomethylbenzoic acid, and aprotinin were developed in the 1960s without the struct
213 esisting tryptic peptidase inhibitors (e.g., aprotinin), while favoring angiotensin destruction at Ty
215 rvival was worse among patients treated with aprotinin, with a main-effects hazard ratio for death of
216 oating with aprotinin and manual addition of aprotinin yield similar results in inhibiting tissue pla