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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.
14 8.0) containing increasing concentrations of aprotinin (0-300 muM).
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
19 ction versus placebo, P<0.001) and high-dose aprotinin (53% reduction, P<0.001).
20                    The rhK4 was inhibited by aprotinin (6 kDa), forming an equimolar 27 kDa complex.
21 ction versus placebo, P<0.010) and high-dose aprotinin (62% reduction, P<0.001).
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
25                                     Although aprotinin, a serine protease inhibitor, reduces blood lo
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
29                        Patients who received aprotinin alone on the day of CABG surgery had a higher
30                                 An optimized aprotinin-alpha2-PI1-8 concentration ensured ideal degra
31                                              Aprotinin, already approved for clinical use to reduce t
32 f Abeta40 with the serine protease inhibitor aprotinin also increased diffuse extracellular depositio
33                                       Use of aprotinin among patients undergoing CABG surgery does no
34 ts were randomized to receive intraoperative aprotinin, an inhibitor of several serine proteinases, o
35                  However, the combination of aprotinin and ACE inhibitors during off-pump cardiac sur
36 cardiac surgery, the odds ratio (OR) between aprotinin and an increased risk of renal dysfunction wit
37                                         Both aprotinin and epsilon-aminocaproic acid decreased blood
38                      These data suggest that aprotinin and epsilon-aminocaproic acid differ in their
39               Antifibrinolytic drugs such as aprotinin and epsilon-aminocaproic acid have been effect
40           This study examined the effects of aprotinin and epsilon-aminocaproic acid on plasma levels
41                                              Aprotinin and fresh whole blood were administered during
42 ntinue to suggest the virtual equivalence of aprotinin and lysine analogues in reducing bleeding and
43 sponse to cardiopulmonary bypass (CPB) using aprotinin and modified ultrafiltration.
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
46                      The association between aprotinin and serious end-organ damage indicates that co
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
51                                   rHuEPO and aprotinin are now being used with increasing frequency t
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
54  mixture of proteinase inhibitors, including aprotinin, BB-94, pepstatin, and E64.
55                        Because the inhibitor aprotinin binds strongly with trypsin at alkaline pH, th
56                               In presence of aprotinin, both free and aprotinin-bound trypsinogen wer
57      In presence of aprotinin, both free and aprotinin-bound trypsinogen were detected revealing a 1:
58 ted by plasminogen activator inhibitor-1 and aprotinin but not by tissue inhibitor of metalloproteina
59                                              Aprotinin but not epsilon-aminocaproic acid appears to a
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
65 pared by copolymerization of the PEG-trypsin-aprotinin complex during the gel-casting step.
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
68                                     Although aprotinin costs more than its alternatives, its costs ma
69 ts with high, medium, or low affinity toward aprotinin could be successfully discriminated.
70 han and phosphoramidon), serine proteinases (aprotinin), cysteine proteinases (leupeptin) and urokina
71             Compared head to head, high-dose aprotinin demonstrated significant reduction in total bl
72 t sensitivity and lowest detection limit for aprotinin detection.
73                                              Aprotinin did not have an effect on NCD or levels of MBI
74                                              Aprotinin did not increase the likelihood of postoperati
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
77 benzenesulfonyl fluoride (AEBSF), but not by aprotinin, EDTA, or pepstatin.
78      We conducted a meta-analysis to compare aprotinin, epsilon-aminocaproic acid, and tranexamic aci
79 in a double-blind study to receive high-dose aprotinin, epsilon-aminocaproic acid, or saline placebo.
80                                  In the post-aprotinin era, with the exclusive use of lysine analogue
81 duct utilization would affected in this post-aprotinin era.
82  that the peptidic inhibitors, leupeptin and aprotinin, exhibited similar potencies in inhibiting fac
83 nexplained cardiopulmonary instability after aprotinin exposure, Type B).
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
87 nin levels were significantly greater in the aprotinin group (all P<0.05).
88 urs after CPB, but this was preserved in the aprotinin group (P<0.001).
89  activity was approximately 30% lower in the aprotinin group (P=0.007).
90                                          The aprotinin group demonstrated decreased myocardial tissue
91             During the operative period, the aprotinin group received a greater number of units of pl
92 stimated risk of death was 64% higher in the aprotinin group than in the aminocaproic acid group (rel
93 ed relative risk of in-hospital death in the aprotinin group was 1.78 (95% CI, 1.56 to 2.02).
94 sk for renal dysfunction was observed in the aprotinin group.
95                        Patients who received aprotinin had a higher mortality rate and larger increas
96                epsilon-Aminocaproic acid and aprotinin had no effect on risks of postoperative myocar
97 d loss during liver hepatectomy, while 1 and aprotinin had no effect.
98 ges, as treatment with the plasmin inhibitor aprotinin had no effect.
99                                              Aprotinin has been demonstrated to prevent activation of
100                              Of note is that aprotinin has been reintroduced into the Canadian market
101                                              Aprotinin has recently been associated with adverse outc
102 nolytics, e.g., tranexamic acid (TXA, 1) and aprotinin, has been challenging.
103                Hypersensitivity reactions to aprotinin have been reported in adult cardiac surgical p
104  study describes the incidence and impact of aprotinin hypersensitivity reactions in children undergo
105                                         Anti-aprotinin IgE was undetectable in 7 of 8 reactor cases t
106               We support the targeted use of aprotinin in adult cardiac surgery patients at high risk
107 ication of the proposed method for measuring aprotinin in pretreated plasma samples is also reported.
108                            Similarly, use of aprotinin in the latter group was associated with a 55 p
109 cid, we support their use as alternatives to aprotinin in those at high risk for bleeding.
110 leeding or stroke, and discourage the use of aprotinin in those at high risk for renal failure.
111 nduced and early diabetic BRB breakdown with aprotinin indicates that azurocidin may be an important
112 etting of DHCA because of concerns regarding aprotinin-induced renal dysfunction.
113                                              Aprotinin inhibited azurocidin-induced BRB breakdown by
114                The serine protease inhibitor aprotinin inhibited this activation of MMPs by plasminog
115 ough its first loop, in the same manner that aprotinin inhibits trypsin.
116                                    (Although aprotinin is a serine protease inhibitor, here we use th
117 nt studies suggest that the antifibrinolytic aprotinin is associated with increased renal and vascula
118       The proposed electrochemical assay for aprotinin is examined further using trypsin, plasmin, an
119                                              Aprotinin is frequently used in high-risk cardiac surger
120                                     Although aprotinin is known to be effective in reducing postopera
121    The risk of hypersensitivity reactions to aprotinin is low in children undergoing cardiothoracic s
122                                              Aprotinin is used during cardiac surgery for its blood-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
128                  The design was based on two aprotinin loops and aimed to leverage both key specific
129  of endogenous serine protease activity with aprotinin markedly decreased ENaC-mediated currents and
130                                     However, aprotinin may not ameliorate the problem of perioperativ
131 PI) domain of tick anticoagulant protein, an aprotinin mutant (6L15), amyloid beta-protein precursor,
132 traoperative variables in patients receiving aprotinin (n=325) or lysine analogues (n=456).
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
135         Therefore, we assessed the affect of aprotinin on both blood transfusion requirements and ren
136                We investigated the effect of aprotinin on renal dysfunction in cardiac surgery, consi
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
139  on insulin aggregation but was not seen for aprotinin or albumin.
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
143 R, 0.32; 95% CI, 0.15 to 0.69) and high-dose aprotinin (OR, 0.28; 0.22 to 0.37).
144 tatistically significant only with high-dose aprotinin (OR, 0.39; 0.24 to 0.61).
145 nexamic acid), the serine protease inhibitor aprotinin, or no antibleeding agent.
146 lso were inhibited by AEBSF and not by EDTA, aprotinin, or pepstatin.
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
149 tenuates the purported independent affect of aprotinin (P=0.231) on ARF.
150                 A cocktail containing AEBSF, aprotinin, pancreatic trypsin inhibitor, leupeptin, anti
151                                              Aprotinin, pepstatin A, and E-64 did not affect TSF acti
152 ot affected by TIMP-1 or protease inhibitors aprotinin, pepstatin, or leupeptin but was inhibited in
153                                              Aprotinin preserves adherens junctions after regional is
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
156             Immunfluorescence confirmed that aprotinin prevented loss of coronary endothelial adheren
157 ti-uPAR or anti-uPA Abs or plasmin inhibitor aprotinin prior to coculturing with healthy cardiocytes
158       No adverse sequelae were attributed to aprotinin reaction.
159                    Similarly, patients given aprotinin received more cryoprecipitate in the intensive
160                   In all, 1512 of the 33,517 aprotinin recipients (4.5%) and 1101 of the 44,682 amino
161                               Only high-dose aprotinin reduced the rate of reexploration (relative ri
162                                              Aprotinin reduced tyrosine phosphorylation in myocardial
163                Furthermore, as compared with aprotinin, renal toxicity was not observed with KD1-L17R
164 these results, the serine protease inhibitor aprotinin reproduced the effects of FAEEs and prevented
165 sequences and the entropic advantage driving aprotinin's high affinity.
166                  Our results have shown that aprotinin seems to be safe during on-pump cardiac surger
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).
169                           However, high-dose aprotinin significantly increased the risk of renal dysf
170                        Compared with saline, aprotinin significantly reduced IL-10 (P=0.02) and peak
171                  Furthermore, treatment with aprotinin significantly suppressed VEGF-induced BRB brea
172  was 1.6% (180/11,198) and was higher in the aprotinin subset (2.6%, 72/2757 versus 1.3%, 108/8441; P
173                 It is found that the trypsin-aprotinin system offers the highest sensitivity and lowe
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
176  fibrinogen and human thrombin that includes aprotinin to reduce fibrinolysis.
177           Addition of the protease inhibitor aprotinin to the cell culture and graft perfusion media
178 nhibition with the affinity of leupeptin and aprotinin to the factor XIa-factor IX complex only appro
179        The binding of the protease inhibitor aprotinin to trypsinogen was used as protein-protein aff
180 e of renal dysfunction in patients receiving aprotinin, tranexamic acid, or no antifibrinolytic treat
181                                              Aprotinin (Trasylol) is used to mitigate bleeding during
182 Procrit), by maximizing red cell counts, and aprotinin (Trasylol), by inhibiting fibrinolysis, are tw
183                                              Aprotinin treatment (223 deaths among 1072 patients [20.
184                                              Aprotinin use does not independently increase the risk o
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
188 sk-adjusted assessment of ARF in relation to aprotinin use.
189 .06; 95% CI, 0.02 to 0.22) were lower in the aprotinin versus lysine analog group (all P<0.05).
190                                              Aprotinin was a commonly used pharmacological agent for
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
193                           However, high-dose aprotinin was associated with a statistically significan
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
196                                      (99m)Tc-Aprotinin was found to be useful in detecting cardiac am
197 ither with propensity adjustment or without, aprotinin was independently predictive of 5-year mortali
198                         To block azurocidin, aprotinin was injected intravenously before the intravit
199                                              Aprotinin was used in 24.6% (2757/11,198).
200 -fused variant of the fibrinolysis inhibitor aprotinin was used to control the hydrogel degradation r
201                   As expected, leupeptin and aprotinin were competitive with respect to the tripeptid
202                                              Aprotinin, when compared to placebo, significantly decre
203 esisting tryptic peptidase inhibitors (e.g., aprotinin), while favoring angiotensin destruction at Ty
204 in affects the interactions of leupeptin and aprotinin with the active site.
205 rvival was worse among patients treated with aprotinin, with a main-effects hazard ratio for death of

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