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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.
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       We also show that surface coating with aprotinin and manual addition of aprotinin yield similar
44 sponse to cardiopulmonary bypass (CPB) using aprotinin and modified ultrafiltration.
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
47                      The association between aprotinin and serious end-organ damage indicates that co
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
54 duction/multidesulfurization of linaclotide, aprotinin, and wheat protein.
55                                   rHuEPO and aprotinin are now being used with increasing frequency 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
59  mixture of proteinase inhibitors, including aprotinin, BB-94, pepstatin, and E64.
60                        Because the inhibitor aprotinin binds strongly with trypsin at alkaline pH, th
61                               In presence of aprotinin, both free and aprotinin-bound trypsinogen wer
62      In presence of aprotinin, both free and aprotinin-bound trypsinogen were detected revealing a 1:
63 ted by plasminogen activator inhibitor-1 and aprotinin but not by tissue inhibitor of metalloproteina
64                                              Aprotinin but not epsilon-aminocaproic acid appears to a
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
71 pared by copolymerization of the PEG-trypsin-aprotinin complex during the gel-casting step.
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
74                                     Although aprotinin costs more than its alternatives, its costs ma
75 ts with high, medium, or low affinity toward aprotinin could be successfully discriminated.
76 han and phosphoramidon), serine proteinases (aprotinin), cysteine proteinases (leupeptin) and urokina
77             Compared head to head, high-dose aprotinin demonstrated significant reduction in total bl
78 t sensitivity and lowest detection limit for aprotinin detection.
79 t a microsensor dual-coated with both TF and aprotinin detects the hemostatic rescue in the tPA-induc
80                                              Aprotinin did not have an effect on NCD or levels of MBI
81                                              Aprotinin did not increase the likelihood of postoperati
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
84 benzenesulfonyl fluoride (AEBSF), but not by aprotinin, EDTA, or pepstatin.
85      We conducted a meta-analysis to compare aprotinin, epsilon-aminocaproic acid, and tranexamic aci
86 in a double-blind study to receive high-dose aprotinin, epsilon-aminocaproic acid, or saline placebo.
87                                  In the post-aprotinin era, with the exclusive use of lysine analogue
88 duct utilization would affected in this post-aprotinin era.
89  that the peptidic inhibitors, leupeptin and aprotinin, exhibited similar potencies in inhibiting fac
90 nexplained cardiopulmonary instability after aprotinin exposure, Type B).
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
94 nin levels were significantly greater in the aprotinin group (all P<0.05).
95 urs after CPB, but this was preserved in the aprotinin group (P<0.001).
96  activity was approximately 30% lower in the aprotinin group (P=0.007).
97                                          The aprotinin group demonstrated decreased myocardial tissue
98             During the operative period, the aprotinin group received a greater number of units of pl
99 stimated risk of death was 64% higher in the aprotinin group than in the aminocaproic acid group (rel
100 ed relative risk of in-hospital death in the aprotinin group was 1.78 (95% CI, 1.56 to 2.02).
101 sk for renal dysfunction was observed in the aprotinin group.
102                        Patients who received aprotinin had a higher mortality rate and larger increas
103                epsilon-Aminocaproic acid and aprotinin had no effect on risks of postoperative myocar
104 d loss during liver hepatectomy, while 1 and aprotinin had no effect.
105 ges, as treatment with the plasmin inhibitor aprotinin had no effect.
106                                              Aprotinin has been demonstrated to prevent activation of
107                              Of note is that aprotinin has been reintroduced into the Canadian market
108                                              Aprotinin has recently been associated with adverse outc
109 nolytics, e.g., tranexamic acid (TXA, 1) and aprotinin, has been challenging.
110                Hypersensitivity reactions to aprotinin have been reported in adult cardiac surgical p
111  study describes the incidence and impact of aprotinin hypersensitivity reactions in children undergo
112                                         Anti-aprotinin IgE was undetectable in 7 of 8 reactor cases t
113               We support the targeted use of aprotinin in adult cardiac surgery patients at high risk
114 ication of the proposed method for measuring aprotinin in pretreated plasma samples is also reported.
115                            Similarly, use of aprotinin in the latter group was associated with a 55 p
116 cid, we support their use as alternatives to aprotinin in those at high risk for bleeding.
117 leeding or stroke, and discourage the use of aprotinin in those at high risk for renal failure.
118 nduced and early diabetic BRB breakdown with aprotinin indicates that azurocidin may be an important
119 etting of DHCA because of concerns regarding aprotinin-induced renal dysfunction.
120                                              Aprotinin inhibited azurocidin-induced BRB breakdown by
121                The serine protease inhibitor aprotinin inhibited this activation of MMPs by plasminog
122 ough its first loop, in the same manner that aprotinin inhibits trypsin.
123                                    (Although aprotinin is a serine protease inhibitor, here we use th
124 nt studies suggest that the antifibrinolytic aprotinin is associated with increased renal and vascula
125       The proposed electrochemical assay for aprotinin is examined further using trypsin, plasmin, an
126                                              Aprotinin is frequently used in high-risk cardiac surger
127                                     Although aprotinin is known to be effective in reducing postopera
128    The risk of hypersensitivity reactions to aprotinin is low in children undergoing cardiothoracic s
129                                              Aprotinin is used during cardiac surgery for its blood-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
135                  The design was based on two aprotinin loops and aimed to leverage both key specific
136  of endogenous serine protease activity with aprotinin markedly decreased ENaC-mediated currents and
137                                     However, aprotinin may not ameliorate the problem of perioperativ
138 PI) domain of tick anticoagulant protein, an aprotinin mutant (6L15), amyloid beta-protein precursor,
139 traoperative variables in patients receiving aprotinin (n=325) or lysine analogues (n=456).
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
142         Therefore, we assessed the affect of aprotinin on both blood transfusion requirements and ren
143                We investigated the effect of aprotinin on renal dysfunction in cardiac surgery, consi
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
146  on insulin aggregation but was not seen for aprotinin or albumin.
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
150 R, 0.32; 95% CI, 0.15 to 0.69) and high-dose aprotinin (OR, 0.28; 0.22 to 0.37).
151 tatistically significant only with high-dose aprotinin (OR, 0.39; 0.24 to 0.61).
152 nexamic acid), the serine protease inhibitor aprotinin, or no antibleeding agent.
153 lso were inhibited by AEBSF and not by EDTA, aprotinin, or pepstatin.
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
156 tenuates the purported independent affect of aprotinin (P=0.231) on ARF.
157                 A cocktail containing AEBSF, aprotinin, pancreatic trypsin inhibitor, leupeptin, anti
158                                              Aprotinin, pepstatin A, and E-64 did not affect TSF acti
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
161                                              Aprotinin preserves adherens junctions after regional is
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
164             Immunfluorescence confirmed that aprotinin prevented loss of coronary endothelial adheren
165 ti-uPAR or anti-uPA Abs or plasmin inhibitor aprotinin prior to coculturing with healthy cardiocytes
166       No adverse sequelae were attributed to aprotinin reaction.
167                    Similarly, patients given aprotinin received more cryoprecipitate in the intensive
168                   In all, 1512 of the 33,517 aprotinin recipients (4.5%) and 1101 of the 44,682 amino
169                               Only high-dose aprotinin reduced the rate of reexploration (relative ri
170                                              Aprotinin reduced tyrosine phosphorylation in myocardial
171                Furthermore, as compared with aprotinin, renal toxicity was not observed with KD1-L17R
172 these results, the serine protease inhibitor aprotinin reproduced the effects of FAEEs and prevented
173 sequences and the entropic advantage driving aprotinin's high affinity.
174                  Our results have shown that aprotinin seems to be safe during on-pump cardiac surger
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).
177                           However, high-dose aprotinin significantly increased the risk of renal dysf
178                        Compared with saline, aprotinin significantly reduced IL-10 (P=0.02) and peak
179                  Furthermore, treatment with aprotinin significantly suppressed VEGF-induced BRB brea
180  was 1.6% (180/11,198) and was higher in the aprotinin subset (2.6%, 72/2757 versus 1.3%, 108/8441; P
181                 It is found that the trypsin-aprotinin system offers the highest sensitivity and lowe
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
185  fibrinogen and human thrombin that includes aprotinin to reduce fibrinolysis.
186           Addition of the protease inhibitor aprotinin to the cell culture and graft perfusion media
187 nhibition with the affinity of leupeptin and aprotinin to the factor XIa-factor IX complex only appro
188        The binding of the protease inhibitor aprotinin to trypsinogen was used as protein-protein aff
189 e of renal dysfunction in patients receiving aprotinin, tranexamic acid, or no antifibrinolytic treat
190                                              Aprotinin (Trasylol) is used to mitigate bleeding during
191 Procrit), by maximizing red cell counts, and aprotinin (Trasylol), by inhibiting fibrinolysis, are tw
192                                              Aprotinin treatment (223 deaths among 1072 patients [20.
193                                              Aprotinin use does not independently increase the risk o
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
197 sk-adjusted assessment of ARF in relation to aprotinin use.
198 .06; 95% CI, 0.02 to 0.22) were lower in the aprotinin versus lysine analog group (all P<0.05).
199                                              Aprotinin was a commonly used pharmacological agent for
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
202                           However, high-dose aprotinin was associated with a statistically significan
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
205                                      (99m)Tc-Aprotinin was found to be useful in detecting cardiac am
206 ither with propensity adjustment or without, aprotinin was independently predictive of 5-year mortali
207                         To block azurocidin, aprotinin was injected intravenously before the intravit
208                                              Aprotinin was used in 24.6% (2757/11,198).
209 -fused variant of the fibrinolysis inhibitor aprotinin was used to control the hydrogel degradation r
210                   As expected, leupeptin and aprotinin were competitive with respect to the tripeptid
211 caproic acid, 4-aminomethylbenzoic acid, and aprotinin were developed in the 1960s without the struct
212                                              Aprotinin, when compared to placebo, significantly decre
213 esisting tryptic peptidase inhibitors (e.g., aprotinin), while favoring angiotensin destruction at Ty
214 in affects the interactions of leupeptin and aprotinin with the active site.
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

 
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