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A new computerized bipolar coagulator is described in which tissue heating is switched off automatically when adequate vessel occlusion has been achieved, thus preventing overheating, undue tissue damage, cutting, and sticking of the forceps. Experiments with radiofrequency (rf) heating of albumin or arteries revealed an impedance minimum at the moment of coagulation. The attainment of this impedance minimum is transmitted electronically via a microprocessor to the coagulator, which automatically shuts off the rf energy supply. In experiments, adequate artery strength and avoidance of the drawbacks of conventional coagulation methods were achieved when rf heating was shut off soon after the impedance minimum was reached. Neither irrigation for cooling nor cleaning of the forceps tips was necessary. Electronic feedback through the same cables as used for coagulation enabled the use of conventional bipolar cables and forceps. The bipolar coagulator described can also be used for conventional bipolar coagulation under visual control. The microcomputer enables: 1) automatic coagulation cycles that start when tissue is picked up in the forceps and stop automatically on completion of the seal; 2) the change of power setting from a pedal and activation of automatic cycles by the pedal as described above or surgeon-controlled coagulation, which facilitates the use of alternative debridement with inactive forceps; 3) cable testing; and 4) negligible disturbance of the intraoperative monitoring equipment.
We have characterized Factor VIII coagulant protein, present in normal human plasma, that reacts with a specific human 125I-labeled anti-human VIII:C antigen Fab antibody fragment. Two major Factor VIII coagulant antigen populations were present. The first, approximately 85% of the total antigen, was bound to von Willebrand factor and when tested in a standard one-stage assay had Factor VIII coagulant activity. The second antigenic population, eluting near fibrinogen when plasma was gel filtered, was not bound to von Willebrand protein, did not have Factor VIII coagulant activity unless activated, but did block anti-VIII:C Fab neutralization of clotting activity. The two antigenic populations were separable by cryoprecipitation and agarose gel electrophoresis. Although the two antigenic populations differed in their Factor VIII coagulant activity and in their binding to von Willebrand factor, the principal member of both populations is of mol wt 2.4 X 10(5). Both antigens, when proteolyzed by thrombin, were quickly converted to a 1 X 10(5)-mol wt form in association with the appearance of VIII:C activity. The 1 X 10(5)-mol wt antigen was further slowly degraded to an 8 X 10(4)-mol wt form while Factor VIII coagulant activity declined. These results demonstrate the presence of an inactive Factor VIII coagulant protein in plasma, not associated with von Willebrand factor, that can react with thrombin to yield Factor VIII coagulant activity.
Platelets have been shown to be capable of initiating and promoting some of the reactions in intrinsic coagulation and have been implicated in the pathogenesis of vascular lesions in diabetes mellitus. We have examined the contribution of platelets to the coagulation reactions in 39 patients having diabetes mellitus with and without retinopathy [background retinopathy (BR) or proliferative retinopathy (PR)], 18 patients with nonvascular eye diseases (patient controls), and 38 normal subjects. As compared to control patients, significant elevations were noted in four of the five assays for platelet coagulant activities in diabetic patients with PR and in three of five assays in patients with BR. Thus platelet coagulant hyperactivity is present in diabetics with retinopathy. Significant elevations were noted in two of the assays in patients without retinopathy (NR), suggesting that platelet coagulant hyperactivity may not necessarily be secondary to the vasculopathy. The predominant abnormalities noted were in assays reflecting the contribution of platelets to the early stages of intrinsic coagulation rather than to later stages of prothrombin activation. In addition, the mean platelet volume was found to be significantly greater in patients with PR and BR but not NR than in normal controls. A positive linear correlation (r = 0.81) was noted between the mean of the coagulant activities and platelet volume in diabetic subjects, suggesting a hitherto undescribed relationship between platelet coagulant activities and platelet volume.
A complex of factor VIII coagulant moiety and phospholipid was purified by means of immunoadsorbent chromatography of factor VIII concentrate and consecutive dissociation of the immobilized factor VIII complex by human placental phospholipid (Fibraccel). The complex of factor VIII coagulant moiety and phospholipid displayed factor VIII coagulant activity (VIII C) and factor VIII coagulant antigen (VIII C:Ag), but no factor VIII related antigen (VIII R:Ag). When incubated with factor VIII inhibitor plasma, the complex of factor VIII coagulant moiety and phospholipid exerted higher factor VIII coagulant activity than native factor VIII complex, and than purified factor VIII coagulant moiety alone. Our results prove that in activated prothrombin complex concentrates a complex of factor VIII coagulant moiety and phospholipid is the active mechanism exerting procoagulant activity in factor VIII inhibitor plasma.
Effects of systematic environmental factors and milk production and quality traits on milk coagulation properties (MCP), and on repeatability of those traits were estimated from 979 milk samples collected once a month over a period of 2 years from 83 Finnish Ayrshire cows. Estimation was based on a multitrait animal model and REML methodology. In addition, persistence of non-coagulation of milk in individual cows, and factors associated with it were established from a sub sample of 24 cows producing non-coagulating (NC) milk at least once. MCP were at their best during the first lactation, at the beginning and at the end of lactation, and during grazing seasons. Variation in MCP with systematic environmental factors was partly due to variation in composition and quality of milk, especially in pH and ln (somatic cell count, SCC). Coefficients of repeatability for milk coagulation time and curd firmness were 0.65 and 0.68. These estimates were of the same magnitude as those for protein content, but were higher than those for daily milk yield, fat content, pH, and SCC. Based on the repeatability estimates for the milk coagulation traits and effects of the environmental factors, cows should be sampled at least three times during a lactation to estimate reliably breeding values for the milk coagulation traits. A total of 10% of the milk samples did not coagulate in 30 min after addition of rennet. Cows that produced NC milk at least once (30% of the cows) could be classified into those that produced NC milk only a few times during a lactation and those that produced NC milk at almost every sampling. Based on logistic regression analyses, peak and mid-lactation, high milk yield, low protein and fat content and high pH increased the risk of non-coagulation of milk.
Oxidatively modified low-density lipoprotein (OxLDL) is present in atherosclerotic lesions and has been proposed to play an important role in atherogenesis. Thrombosis is the major mechanism underlying acute complications of atherosclerosis. In the present study, we analyzed the interaction between OxLDL and blood coagulation factors, which are involved in the blood coagulation pathway. We investigated the effect of OxLDL on plasma coagulation by measuring prothrombin time (PT) as a parameter of the extrinsic pathway of blood coagulation and activated partial thromboplastin time (APTT) as a parameter of the intrinsic pathway of blood coagulation following the addition of OxLDL to plasma. OxLDL, but not native LDL, caused prolongation of APTT in a dose- and oxidation time-dependent manner. In addition, the oxidatively modified product of acetylated LDL (AcLDL), but not AcLDL, also caused prolongation of APTT. The inhibition of lysophosphatidylcholine production in OxLDL by phenylmethylsulfonyl fluoride or Pefabloc pretreatment of LDL resulted in a prolongation of APTT, which was equivalent to the effect of OxLDL. Moreover, OxLDL significantly inhibited blood coagulation factor VIII, IX, and XI activity. Furthermore, we demonstrated that recombinant factor VIII binds to OxLDL and that factor VIII associated with OxLDL is detected in the incubation mixture of OxLDL and plasma. These results indicate that the binding of factor VIII to OxLDL affects the intrinsic pathway of the blood coagulation cascade. The present study suggests that the interaction between OxLDL and factor VIII may provide important information on the initiation and progression of atherosclerosis.
A physicochemical treatment (coagulation-flocculation) was applied to a slaughterhouse wastewater, using anionic polyacrylamide as coagulant aid to improve the settling velocity of the flocs formed with the coagulants used: ferric sulphate, aluminium sulphate and polyaluminium chloride. The optimum speed and stirring time for the flocculation stage were ascertained along with the optimum pH and coagulant and coagulant aid doses. The speed and coagulation time were initially set according to recommendations in the literature concerning the treatment of this type of water. Chemical oxygen demand (COD), biochemical oxygen demand at 5 days (BOD5) and total suspended solids (TSS) were recorded at the beginning and end of each experiment in order to monitor the process. Once the optimal conditions had been established, several parameters were measured in order to assess the coagulation-flocculation process: particle number and size, sludge volume, nutrients (ammonia nitrogen, total Kjeldahl nitrogen, albuminoid nitrogen, orthophosphate, total phosphorus) and the residual concentration of iron and aluminium in clarified water. Anionic polyacrylamide, when added with ferric sulphate or polyaluminium chloride led to a significant increase in the settling speed.
Ferric chloride and aluminium sulphate as coagulants and positive charged flocculants PDDMAC ((PDDMAC = poly (diallyldimethylammonium chloride) were used for pre-treatment of water and wastewater for removing humic substance prior to RO membrane filtration. It was found that a combination of flocculant and coagulant enhanced the coagulation-flocculation process and humic acid removal. The optimum conditions of coagulation-flocculation were established in reference to the ratio of humic acid and coagulant. Zeta potential and the ratio of E4/E6 were investigated to explore the possible micro-mechanisms of coagulation-flocculation. The ratios of E4/E6 show the molecular size variations using different coagulants and flocculants, which are expected to benefit membrane-fouling control.
Ovomucoid is a egg white protein which has a strong allergenicity with a unique characteristic in heat-noncoagulable one contrast to heat-coagulable other major egg white proteins. By ELISA and immunoblots analysis, ovomucoid was detected in heat-coagulated egg yolk after immediate boiling of hen's egg for 15 min (boiled egg) at the concentration of 4.8 +/- 0.8 micrograms/g egg yolk, but not detected in raw egg yolk collected by insertion of a needle into the egg yolk cavity. Ovomucoid in heat-coagulated egg yolk was increased by standing the boiled eggs at room temperature for 10, 30, 60 and 120 min at the concentration of 7.5 +/- 3.4, 17.2 +/- 15.1, 28.1 +/- 5.9 and 78.8 +/- 31.3 micrograms/g egg yolk, respectively. The soluble fraction prepared from heat-coagulated egg white of boiled egg contained 37.7 +/- 3.2 mg/ml of proteins including 14.2 +/- 11.9 mg/ml of ovomucoid as a major and miners of detectable ovalbumin and ovotransfferin. These results suggested that the appearance of ovomucoid in coagulated egg yolk of boiled egg was due to passing the soluble fraction rich in ovomucoid in heat-coagulated egg white through into the coagulated egg yolk, which may have notable consequences for the present of ovomucoid as a major egg white allergen in yolk egg of boiled egg.
The coagulant content and thrombin generating potential of synovial fluid from patients with osteoarthritis were studied as a model of extravascular coagulation. The concentrations of individual coagulant proteins were partially correlated with their molecular weight. The levels of the very large coagulants factor V, factor VIII and von Willebrand factor antigen (vWF:ag) are less than 1% of the activities found in a normal pooled reference plasma while smaller coagulants including factors IX, XI and prothrombin range between 9 and 30%. The protease inhibitors antithrombin-III (AT-III) and Alpha-2 macroglobulin in synovial fluid were present at levels of 74% and 13% of plasma, higher than expected based on their molecular weights. Prothrombin was more rapidly activated by tissue thromboplastin than by aPTT reagent. The thrombin activity formed in synovial fluid decreased more rapidly than that formed in dilute plasma. The addition of recombinant factor VIII or bovine factor V to synovial fluid accelerated the thrombin production by APTT but not by tissue thromboplastin. Indicating that the low levels of factor VIII and factor V did limit the rate of thrombin production. The addition of specific antibodies to factor VIII or factor V strongly inhibited thrombin production by aPTT. These data confirm a roughly inverse relationship between the concentrations of coagulation proteins and their molecular weight in synovial fluid and indicate that thrombin can be generated in synovial fluid. The inactivation of thrombin in synovial fluid may be more dependent on antithrombin-III than in plasma because of the increased AT-III/alpha-2 macroglobulin ratio seen in synovial fluid.
The necropsy findings in 21 patients on an intensive care unit, on whom coagulation studies had been performed immediately before death, were assessed. Eleven of the patients were retrospectively studied and 10 were reviewed consecutively in a prospective study. Fifteen patients (eight retrospective and seven prospective) had evidence of disseminated intravascular coagulation. Microthrombi were most often found in the lungs and kidneys. The most common abnormal coagulation tests in patients with necropsy evidence of disseminated intravascular coagulation were raised serum concentrations of fibrinogen and fibrin degradation products, prolonged prothrombin time, and reduced platelet counts. Reduced fibrinogen concentrations and a prolonged thrombin time were the least commonly observed abnormalities. There was no difference in either the prevalence or magnitude of abnormality of any particular coagulation variable test result between those patients with evidence of disseminated intravascular coagulation at necropsy and those without.
BACKGROUND: Disseminated intravascular coagulation (DIC) is a serious complication of acute myeloid leukemia (AML) associated with poor prognosis. In TP53-mutated AML and myelodysplastic syndrome (MDS), however, the classical ISTH criteria rarely identify overt DIC, although bleeding and thrombotic complications are well documented in acute leukaemia. We hypothesized that these patients exhibit a lower-grade, subclinical coagulation activation that is associated with the underlying genomic-instability-related features of TP53-mutant disease. METHODS: We retrospectively analyzed 107 consecutive patients with TP53-mutated AML (n = 52) or high-risk MDS (MDS, n = 55), median age 65 years, diagnosed and initially evaluated at our centre between 2018 and 2025. Seven routine coagulation markers and 46 co-mutated genes were evaluated for associations with overall survival (OS) using univariate and multivariable Cox regression, continuous dose-response modeling, and unsupervised k-means clustering. Internal validity was assessed by 1000 bootstrap resamples. RESULTS: Overt DIC according to ISTH criteria was rare (15%). Subclinical activation was common: 50% of patients had a D-dimer ≥1 μg/mL, 41% a fibrinogen ≥4 g/L, and 29% an INR ≥1.2. In univariate analysis, D-dimer, fibrinogen, INR, prothrombin time, and activated partial thromboplastin time were each associated with OS (HR 1.33-1.38 per SD; all p < 0.05). Complex karyotype correlated with higher D-dimer (median 1.39 vs. 0.60 μg/mL, p = 0.022) and fibrinogen (3.91 vs. 2.53 g/L, p = 0.007), while TP53 variant allele frequency (VAF) showed modest positive correlations with D-dimer (ρ = 0.21), INR (ρ = 0.27), and PT (ρ = 0.27; all p < 0.05). Clustering identified three coagulation phenotypes: Silent (51%), Thrombo-inflammatory (31%), and Consumption-like (18%), showing a graded but statistically non-significant gradient in molecular features and a stepwise decline in median OS (14, 10 and 8 months; log-rank p = 0.041). After adjustment for complex karyotype, TP53 VAF, and favorable co-mutation count, the Consumption-like phenotype was associated with a non-significant increased risk (HR 1.83, 95% CI 0.92-3.65, p = 0.084), whereas favorable co-mutation pathways remained independently protective (HR 0.56, 95% CI 0.35-0.90, p = 0.016). CONCLUSION: In TP53-mutated AML/MDS, coagulation activation intensity is associated with the degree of genomic instability. The three phenotypes may add biological resolution beyond classical DIC and cytogenetic risk groups, but represent laboratory patterns rather than validated bleeding or thrombosis prediction tools. However, after accounting for genomic features, phenotypes were not independent predictors of outcome, with complex karyotype, TP53 VAF, and favorable co-mutation count driving prognosis. Because treatment intensity and other clinical confounders were not available, these survival associations are hypothesis-generating. Coagulation profiling remains inexpensive, widely accessible, and offers a practical window into disease biology that warrants prospective validation.
Lipoprotein-associated coagulation inhibitor produces feed-back inhibition of tissue factor (tissue thromboplastin)-induced coagulation in the presence of factor Xa Recombinant lipoprotein-associated coagulation inhibitor (rLACI) was tested for its ability to modify thromboplastin-induced intravascular coagulation in a rabbit model that allows monitoring of iodine-125 fibrin accumulation/disappearance in the lung and sampling of blood for the measurement of coagulation parameters. Infusion of thromboplastin into the rabbit caused a rapid increase of radioactivity over the lungs, possibly due to the accumulation of 125I fibrin in the lungs, followed by a rapid decline of radioactivity, suggestive of removal of fibrin from the lungs. Thromboplastin also caused a rapid decrease of systemic fibrinogen that was accompanied by a lengthening of the activated partial thromboplastin time and prothrombin time. The effect of coinfusion of rLACI with thromboplastin or bolus injection of rLACI before thromboplastin infusion was studied. At a high dose of rLACI (800 micrograms/kg body weight), the thromboplastin-induced radioactivity increase in the lungs and the systemic fibrinogen decrease were completely suppressed. The activated partial thromboplastin time and prothrombin time of the plasma samples lengthened, possibly due to the presence of thromboplastin in circulation. The thromboplastin-induced radioactivity increase over the lungs was not completely suppressed by lower doses of rLACI (135 to 270 micrograms/kg body weight), but these doses of rLACI prevented systemic fibrinogen decrease. At a bolus dose of 23 micrograms/kg body weight, rLACI provided 50% protection of the fibrinogen consumption (fibrinogen decreased to 82% compared with 65% in rabbits treated with thromboplastin alone). These results show that rLACI is effective in the inhibition of thromboplastin-induced coagulation in vivo.
To improve the ability to predict the occurrence of coagulation disorders in ascites retransfusion and, in addition, to better define the nature of the coagulation disorder, several proteases and antiproteases were analyzed in ascites and plasma before ascites retransfusion in 17 patients. Plasminogen, alpha 2-antiplasmin, antithrombin III, and fibrin(ogen) degradation products in ascites were significantly altered in patients who later developed abnormal coagulation as compared to those who did not. Only plasminogen and alpha 2-antiplasmin in ascites achieved a sufficient predictive value for the occurrence of coagulation abnormalities. The pattern of the coagulation abnormalities observed strongly suggests fibrinolysis induced by the infusion of plasminogen activators as the cause of the coagulation disorder in ascites retransfusion procedures.
Summary. The biphasic waveform is an early marker of disseminated intravascular coagulation (DIC). Neutrophil elastase (NE) cleaves coagulation factors; thus, elevated elastase levels or its dysregulation by alpha-1-protease inhibitor (Alpha1PI) may be linked to DIC. Time courses over a period were determined for factors associated with NE and coagulation in 14 Intensive Care Unit patients with a biphasic waveform who developed DIC. The data were analyzed using a random coefficient linear regression model to predict the variables' mean values on day 0 and their mean rates of change over the period in which the biphasic waveform appeared. The biphasic waveform was normal on day 0, maximized on day 1, and approached normal again by day 4. Alpha1PI/NE complex levels were 2.5-fold greater than normal for the entire period. The A1PI activity, antigen, and specific activity levels were normal on day 0 and increased thereafter by 21.0, 10.5, and 8.9% of normal per day, respectively. Factor II, V, VII, IX, and X activity levels were, respectively, 57, 46, 46, 77, and 46% of normal on day 0, whereas factor VIII and fibrinogen levels were normal. All coagulation factor levels trended upward with time but not significantly. The prothrombin time, but not the activated partial thromboplastin time, was prolonged, and the platelet counts and hematocrits were below normal on day 0 and remained so thereafter. We conclude that events associated with neutrophil activation, elastase release, and perturbations of coagulation precede both the appearance of the biphasic waveform and the diagnosis of DIC in these patients.
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The coagulant iron chloride and the flocculants Polysep 3000 (PO), Superfloc A-1820 (SU) and Praestol 2515 TR (PR) have been used in this study to show the efficiency of coagulation flocculation process in the chemical precipitation method for the removal of organic and colouring matters from the paint industry wastewater. This study also includes the amount of produced sludge. The results indicate that FeCl(3) is efficient at pH range 8-9 and at optimal dose of 650 mgl(-1). Iron chloride allows the removal of 82% of chemical oxygen demand (COD) and 94% of colour. However, sequential addition of coagulant and polymeric additives enhance clearly pollutant removal and produces less decanted sludge compared to the results obtained when the coagulant is used alone. The removal efficiency of COD reaches 91% and that of colour 99%. Coagulation-biflocculation process is more effective than the coagulation-monoflocculation one. The sequential addition of iron chloride, Polysep 3000 (cationic flocculant) and Praestol 2515 TR (anionic flocculant) seems to be the most suitable combination for the treatment of the paint industry wastewaters.