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At least 1,081 records · Page 60Linked to original sources
PubMed1994

Role of plasminogen activator and of 92-KDa type IV collagenase in glioblastoma invasion using an in vitro matrigel model.

The invasive nature of human gliomas represents a major factor in preventing their total resection. The exact nature of the underlying mechanisms of tumor cell invasion are still unclear. In this study, we have quantitatively assayed a glioblastoma cell line for its ability to migrate through a polycarbonate filter coated with matrigel which contains a complex of multiple basement membrane components. At 48 h the glioblastoma cell line (U251) showed a rate of invasiveness of 42% and also dependent on the concentration of matrigel. The U251 cell line produced a urokinase type plasminogen activator and a 92-KDa type IV collagenase. Both enzymes were inhibited by the addition of uPA and 92-KDa type IV collagenase antibodies. Those same antibodies reduced the invasion rate of U251 cells from 42% to 12 and 21%, respectively. Similarly, the addition of epsilon-aminocaproic acid (a plasmin inhibitor) or tissue inhibitor of metalloprotease (TIMP2, a collagenase inhibitor) reduced the invasiveness of U251 cells from 42% to 14% and 10%, respectively. Additionally, the other two glioblastoma cell lines (LG11, UWR1) and astrocytes showed a rate of invasiveness at 41%, 61% and 12%, respectively. Finally, the addition of hyaluronic acid to the matrigel, a constituent of brain extracellular matrix, enhanced the rate of invasion. These findings provide evidence for the role of serine proteases and metalloproteases in facilitating the invasion of extracellular matrix components by glioblastoma cell line and suggest a therapeutic role for protease inhibitors in attempting to minimize the invasive propensity of gliomas.

Aminocaproic Acid↗
PubMed1976

[Diphenoloxidases: presence in the membrane of human erythrocyte (author's transl)].

Diphenoloxidases, enzymes which accelerate the auto-oxidation of epinephrine and Dopa, have been described by one of us in blood platelets. Earlier we identified these enzymes in different animal species and particularly in human red blood cells. With the object of localising these enzymes and of understanding their function in vivo, we separated the ghosts of red blood cells according to the method described by Fairbanks G., Steck, T.L. and Wallach, D.F.H. (1971) (Biochemistry 1, 2606) and using the protease inhibitors diisopropylfuorophosphate (DFP) (10(-3) M) and 6-aminocaproic acid 10(-2) M in sodium phosphate buffer, 5 X 10(-3) M (pH 8). These ghosts, totally free of haemoglobin, were first of all pulverised in liquid nitrogen then treated ultrasonically. The supernant shows the presence of a band of diphenoloxidase activity on starch gel electrophoresis and two bands on isoelectrofocusing in polyacrylamide gel pH 5 to pH 8 after incubation with 0.02 M Dopa, 0.076 M Tris, 0.005 M citric acid, 0.004 M magnesium, pH 8.7 for 2 h at 37 degrees C. These enzymes differ from (Na, K)-ATPase in that they are neither inhibited by DFP (10(-1) M) nor by EDTA (10(-2) M) but are inhibited by lead acetate 10(-2) M. Like (Na, K)-ATPase diphenoloxidases are present at membranes level. The role in vivo of these diphenoloxidases in ATPase activity of red blood cells is discussed.

Adenosine Triphosphatases↗
PubMed1977

[Prevention of complications of histamine liberation occurring after administration of anesthetic agents and adjuvants].

To protect the organism against histamine liberated during anesthesia specific premedication is used including:--hydroxyzine (Atarax) which blocks the H1 histamine receptors, and is an anxiolytic,--tritoqualine (Hypostamine) which inhibits histamine synthesis,--epsilon aminocaproic acid (Hemocaprol) which prevents the antigen-antibody reaction and blocks the alternate route of complement. Twenty five patients were thus premedicated, 25 others received no premedication. All were put to sleep with Alfatesine. The results were judged on the clinical symptoms and the variations of histamine in whole blood. This premedication seems very efficacious, in particular in subjects with a high risk of histamine liberation.

Adjuvants, Anesthesia↗
PubMed2003

Human lipoprotein (a)-induced reduction of platelet aggregation is not mediated by apolipoprotein A's lysine-binding regions.

Intact lipoprotein (a) (Lp (a)) is known to decrease collagen-stimulated platelet aggregation in vitro, though the nature of the interaction between this lipoprotein and stimulated platelets is unknown. Lysine binding regions of Lp (a) facilitate binding between it and at least one cell type. Epsilon aminocaproic acid (EACA) renders Lp (a)'s lysine binding regions incapable of cellular interaction using those regions. Washed human platelets were presented vehicle alone or with varying concentrations of Lp (a) either not exposed or previously exposed to increasing levels of EACA. In all experiments, EACA failed to affect the impact of Lp(a) on platelet aggregation. It is concluded that the lysine binding regions of Lp (a) do not mediate the intact Lp(a)-induced reduction of collagen-stimulated platelet aggregation in vitro.

Aminocaproic Acid↗
PubMed1986

Postoperative anatrophic nephrolithotomy bleeding.

We reviewed 530 patients treated with anatrophic nephrolithotomy during a 14.5-year period. Significant postoperative renal bleeding occurred in 34 cases (6.4 per cent). The average postoperative blood transfusion requirement in this group was 5,279 cc. Bleeding patients were significantly older and they had worse renal function compared to the nonbleeding group. If bleeding did not begin immediately it usually started 5 to 8 days postoperatively. Bleeding dyscrasias were identified in 6 patients and correction allowed nonoperative management in 4. Epsilon aminocaproic acid was helpful only in the treatment of patients with slow, lower volume bleeding. Eight patients required 9 open renal explorations to control bleeding. Two arteriovenous fistulas and 1 false aneurysm were identified. An attempt at angiographic embolization of an arteriovenous fistula was unsuccessful. Only 1 patient required a nephrectomy (1 of 34 or 2.9 per cent) and there was no mortality. A treatment plan for this complication is described.

Adult↗
PubMed1997

Enhancement of fibrin binding and activation of plasminogen by staplabin through induction of a conformational change in plasminogen.

Staplabin (0.3-0.6 mM), a fungal triprenyl phenol, enhanced 3-fold the plasminogen activator-catalyzed activation of Glu-plasminogen and Lys-plasminogen as well as their binding to fibrin. Staplabin was not stimulatory to the amidolytic activity of plasmin and plasminogen activators. Even in the presence of epsilon-aminocaproic acid (EACA) and fibrinogen fragments, allosteric effectors for Glu-plasminogen, staplabin increased the activation of both forms of plasminogen. In size-exclusion chromatography of Glu-plasminogen and Lys-plasminogen, the molecular elution time, which varies as the conformation of a protein changes, was shortened by staplabin. These results suggest that staplabin causes plasminogens to be more susceptible to activation and fibrin binding by inducing a conformational change that is, at least in part, different from that induced by EACA and fibrinogen fragments.

Allosteric Regulation↗
PubMedDate not supplied

[Kinin antagonists in the treatment of acute stenosing laryngotracheitis in children].

The treatment of 97 infants aged from 3 months to 2 years included: nasotracheal intubation (56 patients); i. v. injection, drops (77 patients) or aerosol inhalations (20 cases) of trasylol, kontrikal or gordox; inhalations of epsilon aminocaproic acid (12 cases); glucocorticoids (locally, inhalations, laryngeal drop infusions); local and oral bioantioxidants; noradrenaline for local vasoconstriction. The addition of antikinin medication to the complex of pathogenetically differentiated means which are also proteolytic enzyme inhibitors reduced the frequency and duration of tracheal intubation, duration of laryngeal stenosis by half. Systemic and local administration of antikinin drugs is advocated starting on the first post-diagnosis days, except cases of advanced acute inflammation in the presence of infiltrates in the cavum infraglotticum when antikinin, antihistamine and vasoconstrictors proved ineffective.

Acute Disease↗
PubMed1996

Evidence that the fibrinogen binding domain of Apo(a) is outside the lysine binding site of kringle IV-10: a study involving naturally occurring lysine binding defective lipoprotein(a) phenotypes.

It is now established that the lysine binding site (LBS) of apo(a) kringle IV-10, and particularly Trp72, plays a dominant role in the binding of lipoprotein(a) [Lp(a)] to lysine. To determine the role of the LBS in the binding of Lp(a) to fibrinogen, we examined the binding to plasmin-modified (PM) fibrinogen of human and rhesus monkey Lp(a) species classified as either Lys' or Lys- based on their capacity to bind lysine Sepharose and to have Trp or Arg, respectively, in position 72 of the LBS of kringle IV-10. We also examined the free apo(a)s obtained by subjecting their corresponding parent Lp(a)s to a mild reductive procedure developed in our laboratory. Our results show that both Lyst and Lys- Lp(a)s and their derived apo(a)s, bound to PM-fibrinogen with similar affinities (Kds: 33-100 nM), whereas the B(max) values were threefold higher for apo(a)s. Both the lysine analog epsilon-aminocaproic acid and L-proline inhibited the binding of Lp(a) and apo(a) to PM fibrinogen. We conclude that the LBS of kringle IV-10 is not involved in this process and that apo(a) binds to PM-fibrinogen via a lysine-proline-sensitive domain located outside the LBS and largely masked by the interaction of apo(a) with apoB100. The significant difference in the PM fibrinogen binding capacity also suggests that apo(a) may have a comparatively higher athero-thrombogenic potential than parent Lp(a).

Adult↗
PubMed1996

Safety and efficacy of purified factor IX concentrate and antifibrinolytic agents for dental extractions in hemophilia B.

This study evaluated the safety and efficacy of combined treatment with epsilon-aminocaproic acid or tranexamic acid and monoclonal antibody purified factor IX (MAb factor IX) for prophylaxis against bleeding in eight hemophilia B patients undergoing nine dental extraction procedures. All patients achieved excellent hemostasis without clinical evidence of thrombosis. There were no significant changes in hemoglobin or hematocrit or in markers of hemostatic system activation (prothrombin fragment F1+2, fibrinopeptide A, and fragment B beta 15-42) after surgery. Thus, a highly purified factor IX concentrate and antifibrinolytic therapy can be effectively and safely combined in hemophilia B patients undergoing dental extractions.

Adult↗
PubMed1984

Metabolism of fibrinogen in children with acute lymphoblastic leukaemia.

The metabolism and in vivo kinetics of fibrinogen were studied using homologous 125I-labelled fibrinogen in 21 children with acute lymphoblastic leukaemia (ALL). Ten patients were undergoing induction therapy, 11 children were in complete remission on maintenance therapy. Results in the patients undergoing induction therapy were: plasma fibrinogen levels were normal in all except one patient, the plasma fibrinogen pool was elevated in six cases, seven patients had a shortened fibrinogen half-life and increased fractional catabolic rate for fibrinogen. The absolute catabolic rate for fibrinogen was elevated in six cases. This shortened fibrinogen half-life together with the correcting effect of heparinisation on the fibrinogen turnover indicated that fibrinogen was consumed by chronic disseminated intravascular coagulation. Inhibition of the fibrinolytic system with epsilon-aminocaproic acid in five patients had no influence on the fibrinogen half-life in three of them but resulted in its prolongation in two patients. All except two children in complete remission had normal fibrinogen levels. Six patients had elevated plasma fibrinogen pools and in all of the cases survival and fractional catabolic rate of fibrinogen were normal. The absolute catabolic rate for fibrinogen was normal in eight, elevated in three of the patients. This observation indicates that fibrinogen synthesis remains accelerated in some cases of ALL in complete remission, but the cause of this is not known.

Adolescent↗
PubMed1977

Ruptured intracranial aneurysms. Case morbidity and mortality.

The authors review 100 consecutive cases of ruptured intracranial aneurysms to assess the overall morbidity and mortality. Patients were placed on a regimen of bed rest, sedation, control of blood pressure, anticonvulsants, and antifibrinolytic therapy. Surgery was performed on 86 patients with hypotensive anesthesia and microsurgical techniques. The incidence of early rebleeding while on epsilon aminocaproic acid and control of blood pressure was 11.8%. The overall surgical mortality was 8.1%, and the surgical mortality of patients in Grades 1, 2, and 3 was 6.3%. Of the 100 patients, 60 were able to return to their prior activities, and 25 had moderate neurological deficits that required limitation of their activities. The total case mortality was 15%. The evidence presented indicates that the regimen of active medical treatment before microsurgical intervention has improved the overall case morbidity and mortality, as well as the chance for long-term survival.

Adult↗
PubMed1985

[Comparative evaluation of various methods of immunosuppressive therapy in severe bronchial asthma].

Altogether 216 patients with grave infection-dependent (49.5%) and autoimmune (50.5%) bronchial asthma received 311 courses of immunosuppressant therapy, with follow up periods up to 8 years. According to the clinico-immunologic data the patients were distributed into 4 groups. The basic drugs were (1) azathioprin, (2) azathioprin and prednisolone, (3) prednisolone, (4) delagil combined with heparin and epsilon-aminocaproic acid. Evaluation of the sort-term results of the treatment showed that the highest percentage of a clinical remission was attained with basic therapy including azathioprin combined with delagil and heparin. The immunosuppressants produced side effects in 14.2-31.3% of patients. These effects (dyspepsia, cytopenia, allergy) were of transitory nature. The long-term results were worse as compared with the short-term ones. The lethality for the whole group of patients amounted to 10.1%. It was caused by the status asthmaticus and cardiopulmonary insufficiency. Indications and contraindications for use of immunosuppressant therapy are provided.

Adolescent↗
PubMed1977

Properties of a factor increasing monocytopoiesis (FIM) occurring in serum during the early phase of an inflammatory reaction.

A factor increasing monocytopoiesis (FIM) has been demonstrated during the onset of an acute inflammatory reaction caused by an intraperitoneal injection of polystyrene latex particles. It is protein in nature, does not contain a carbohydrate moiety essential for its function, and is very probably not a glycoprotein. The molecular weight of FIM lies between 18,000 and 24,000 daltons (determined with both ultrafiltration membranes and gel filtration on Sephadex G100). The monocytosis induced by FIM is dose dependent. FIM is thermolabile, having a half-time of about 20 min at 37 degrees C in serum; temperature inactivation can be delayed by the addition of epsilon-aminocaproic acid, the half-time at 37 degrees C then being about 45 min. In vitro treatment of normal murine blood with the inducers of the inflammatory reaction does not result in FIM activity in the serum. FIM dose not have chemotactic activity toward macrophages, is not a clotting factor, is not a biologically active fragment of the complement system, and has no colony-stimulating or-enhancing activity in the vitro bone marrow colony assay. On the basis of these results, a mechanism is postulated for the humoral regulation of monocytopoiesis.

Aminocaproic Acid↗
PubMed1989

Plasminogen interactions with immobilized fibrinogen.

This report describes the binding of plasminogen to fibrinogen adsorbed onto polystyrene wells. Binding was determined by enzyme linked immunosorbent assay. Both glu- and lys-plasminogen bound to immobilized fibrinogen in a dose-dependent fashion. However, more lys- than glu-plasminogen bound when equal concentrations of either were added to immobilized fibrinogen. Plasminogen binding was inhibited by epsilon aminocaproic acid indicating that binding was mediated via lysine-binding regions of plasminogen. Soluble fibrinogen added in excess of immobilized fibrinogen did not compete for plasminogen binding but fibrinogen fragments produced by plasmin digestion of fibrinogen did. Treatment of immobilized fibrinogen with thrombin caused a small but significant (p less than 0.01) increase in plasminogen binding. These studies demonstrate that immobilized fibrinogen binds both glu- and lys-plasminogen and that binding is mediated via lysine-binding regions. These interactions may facilitate plasminogen binding to fibrinogen adsorbed on to surfaces and to cells such as platelets which bind fibrinogen.

Aminocaproic Acid↗
PubMed2001

Neuritogenesis and the nerve growth factor-induced differentiation of PC-12 cells requires annexin II-mediated plasmin generation.

One of the key morphological changes associated with the nerve growth factor (NGF)-induced differentiation of rat adrenal pheochromocytoma (PC-12) cells is the growth of axon-like processes called neurites. A growing body of evidence suggests that this process may be dependent upon plasmin, a serine protease generated from plasminogen (Plg) by either urokinase Plg activator (u-PA) or tissue Plg activator (t-PA). Prior work in our laboratory has identified annexin II (Ann-II) as a co-receptor for Plg and t-PA that promotes and localizes plasmin generation near the cell surface. In the present study, we report a 3-9-fold increase in Ann-II protein and message levels in NGF-treated PC-12 cells. Message stability and nuclear run-on assays suggest that this induction occurs at the level of gene transcription. Neurite outgrowth assays on and within a three-dimensional matrix demonstrate the inhibition of NGF-induced PC-12 cell differentiation by polyclonal and monoclonal antibodies directed against Ann-II as well as by the overexpression of antisense Ann-II mRNA. Neuritogenesis is also impaired by alpha(2)-plasmin inhibitor, antibodies directed against t-PA and u-PA, and epsilon-aminocaproic acid, a lysine analog that inhibits Plg activation and the binding of Plg to Ann-II. Plasmin generation assays reveal a 2-fold increase in plasmin production on NGF-treated PC-12 cells, which can be blocked by a polyclonal antibody directed against the tail region of Ann-II. From these data, we conclude that Ann-II is transcriptionally up-regulated by NGF and that Ann-II-mediated plasmin generation may play an important role during neurite development in the differentiating PC-12 cell.

Aminocaproic Acid↗
PubMed1992

Binding of fibrin fragments to one-chain and two-chain tissue-type plasminogen activator.

To explore whether fibrin fragments have binding affinity for the tissue-type plasminogen activator (t-PA) molecule, the interactions were studied of (DD)E complex and fragments DD, E1, and E3 with one-chain and two-chain t-PA. For this purpose, a solid-phase binding assay was developed using microtiter plates with nitrocellulose filters. It was found that (DD)E complex and fragments DD and E3 retained the t-PA binding function of the parent fibrin molecule, thus demonstrating that t-PA binds to both the D and E domains of fibrin. Unexpectedly, fragment E1 did not bind t-PA. Fibrin fragments had different binding properties for one-chain and two-chain t-PA. (DD)E complex had the highest and fragment E3 the lowest affinity for one-chain t-PA, both binding curves being consistent with one class of binding sites. However, binding of the fragments with two-chain t-PA was distinguished by more than one class of binding sites, with fragment E3 having the highest affinity for this form of the activator. epsilon-Aminocaproic acid, even at 50 mmol/L concentration, had only minimal effect on binding of (DD)E complex or fragment DD to either one-chain or two-chain t-PA. The potentiating effect of fibrin fragments on plasminogen activation by t-PA was measured by a chromogenic substrate assay. Fragment DD was the most effective stimulator of plasminogen activation by t-PA. In conclusion, (DD)E complex and fragment DD retained most of the regulatory functions of fibrin, which included t-PA binding and t-PA-mediated acceleration of plasminogen activation to plasmin.

Aminocaproic Acid↗
PubMed1981

Anti-fibrinolytic treatment in the pre-operative management of subarachnoid haemorrhage caused by ruptured intracranial aneurysm.

One hundred consecutive patients treated with epsilon aminocaproic acid 24 grams daily prior to surgery for ruptured intracranial aneurysms have been compared with the previous 100 patients managed similarly but without anti-fibrinolytic drugs. No other alterations in management were made and the two series are closely comparable in all other respects. Fewer episodes of recurrent haemorrhage and deaths from this cause occurred in the treated patients, but more cases of cerebral ischaemia occurred. Neither difference is statistically significant and overall more deaths occurred in the patients treated with antifibrinolytic drugs. The value of this method of treatment in the management of aneurysmal subarachnoid haemorrhage is questioned.

Adolescent↗