Coagulation Model Research Articles

Planetesimal formation during protoplanetary disk buildup (Corrigendum)

Models of dust coagulation and subsequent planetesimal formation are usually computed on the backdrop of an already fully formed protoplanetary disk model. At the same time, observational studies suggest that planetesimal formation should start early, possibly even before the protoplanetary disk is fully formed. In this paper, we investigate under which conditions planetesimals already form during the disk buildup stage, in which gas and dust fall onto the disk from its parent molecular cloud. We couple our earlier planetesimal formation model at the water snow line to a simple model of disk formation and evolution. We find that under most conditions planetesimals only form after the buildup stage when the disk becomes less massive and less hot. However, there are parameters for which planetesimals already form during the disk buildup. This occurs when the viscosity driving the disk evolution is intermediate ($\alpha_v \sim 10^{-3}-10^{-2}$) while the turbulent mixing of the dust is reduced compared to that ($\alpha_t \le 0.03 \cdot \alpha_v$), and with the assumption that water vapor is vertically well-mixed with the gas. Such $\alpha_t \ll \alpha_v$ scenario could be expected for layered accretion, where the gas flow is mostly driven by the active surface layers, while the midplane layers, where most of the dust resides, are quiescent.

Peptides Derived from a Plant Protease Inhibitor of the Coagulation Contact System Decrease Arterial Thrombus Formation in a Murine Model, without Impairing Hemostatic Parameters.

Several plant protein inhibitors with anticoagulant properties have been studied and characterized, including the Delonix regia trypsin inhibitor (DrTI). This protein inhibits serine proteases (trypsin) and enzymes directly involved in coagulation, such as plasma kallikrein, factor XIIa, and factor XIa. In this study, we evaluated the effects of two new synthetic peptides derived from the primary sequence of DrTI in coagulation and thrombosis models to understand the mechanisms involved in the pathophysiology of thrombus formation as well as in the development of new antithrombotic therapies. Both peptides acted on in vitro hemostasis-related parameters, showing promising results, prolonging the Partially Activated Thromboplastin Time (aPTT) and inhibited platelet aggregation induced by adenosine diphosphate (ADP) and arachidonic acid. In murine models, for arterial thrombosis induced by photochemical injury, and platelet-endothelial interactions monitored by intravital microscopy, both peptides at doses of 0.5 mg/kg significantly extended the time of artery occlusion and modified the platelet adhesion and aggregation pattern with no changes in bleeding time, demonstrating the high biotechnological potential of both molecules.

Control of positive systems with an unknown state-dependent power law input delay and input saturation

This paper is motivated by a class of positive systems with an input that is subject to an unknown state-dependent power law delay as well as saturation. For example, biological networks have non-negative protein concentration states. Mass action kinetics in these systems result in power law behavior, while complex interactions cause signal propagation delays. Incomplete network characterization makes delay state-dependence unknown. Manipulating network activity via modulated protein concentrations to attain desired performance is restricted by upper-bounds on concentration actuator authority. Here, an innovative control law exploits system dynamics to compensate for control domain restrictions. A Lyapunov stability analysis establishes that the reference tracking error of the closed-loop system is uniformly ultimately bounded. Numerical simulations on a human coagulation model show controller efficacy and better performance compared to the relevant literature. This example application steps toward personalized, closed-loop treatments for trauma coagulopathy, which currently has 30% mortality with open-loop clinical approaches.

A neural network parametrized coagulation rate model for

Coagulation is a key factor governing the size distribution of nanoclusters during the high temperature synthesis of metal oxide nanomaterials. Population balance models are strongly influenced by the coagulation rate coefficient utilized. Although simplified coagulation models are often invoked, the coagulation process, particularly for nanoscale particles, is complex, affected by the coagulating nanocluster sizes, the surrounding temperature, and potential interactions. Toward developing improved models of nanocluster and nanoparticle growth, we have developed a neural network (NN) model to describe titanium dioxide (TiO2) nanocluster coagulation rate coefficients, trained with molecular dynamics (MD) trajectory calculations. Specifically, we first calculated TiO2 nanocluster coagulation probabilities via MD trajectory calculations varying the nanocluster diameters from 0.6 to 3.0nm, initial relative velocity from 20 to 700ms-1, and impact parameter from 0.0 to 8.0nm. Calculations consider dipole-dipole interactions, dispersion interactions, and short-range repulsive interactions. We trained a NN model to predict whether a given set of nanocluster diameters, impact parameter, and initial velocity would lead to the outcome of coagulation. The accuracy between the predicted outcomes from the NN model and the MD trajectory calculation results is >95%. We subsequently utilized both the NN model and MD trajectory calculations to examine coagulation rate coefficients at 300 and 1000K. The NN model predictions are largely within the range 0.65-1.54 of MD predictions, and importantly NN predictions capture the local minimum coagulation rate coefficients observed in MD trajectory calculations. The NN model can be directly implemented in population balances of TiO2 formation.

Mechanisms involved in regulation of blood coagulation: history of research and perspectives

Blood clotting is the most important physiological response in the body to disruption to vascular structure or vessel wall abnormalities. This process is non-stationary, involving many not fully established mechanisms of spatial regulation, and an understanding of this process is essential for the prevention of a large number of life-threatening conditions. This review is focused on investigations into the research of blood clotting processes by a team of biophysicists, alumni and employees of the Biophysics Department of the Faculty of Physics, Lomonosov Moscow State University, who created one of the leading Russian scientific schools for experimental and theoretical approaches to the study of the hemostasis system. The review describes the main directions of research, which included many diverse aspects of the problem - from the development of theoretical models of blood coagulation to the development and clinical studies of new methods for assessing the state of the hemostasis system.

Instantaneous gelation and non-existence of weak solutions for the Oort–Hulst–Safronov coagulation model

The possible occurrence of instantaneous gelation to the Oort–Hulst–Safronov (OHS) coagulation equation is investigated for a certain class of unbounded coagulation kernels. The existence of instantaneous gelation is confirmed by showing the non-existence of mass-conserving weak solutions. Finally, it is shown that for such kernels, there is no weak solution to the OHS coagulation equation at any time interval.

"iPSC-derived liver organoids and inherited bleeding disorders: Potential and future perspectives".

The bleeding phenotype of hereditary coagulation disorders is caused by the low or undetectable activity of the proteins involved in hemostasis, due to a broad spectrum of genetic alterations. Most of the affected coagulation factors are produced in the liver. Therefore, two-dimensional (2D) cultures of primary human hepatocytes and recombinant overexpression of the factors in non-human cell lines have been primarily used to mimic disease pathogenesis and as a model for innovative therapeutic strategies. However, neither human nor animal cells fully represent the hepatocellular biology and do not harbor the exact genetic background of the patient. As a result, the inability of the current in vitro models in recapitulating the in vivo situation has limited the studies of these inherited coagulation disorders. Induced Pluripotent Stem Cell (iPSC) technology offers a possible solution to overcome these limitations by reprogramming patient somatic cells into an embryonic-like pluripotent state, thus giving the possibility of generating an unlimited number of liver cells needed for modeling or therapeutic purposes. By combining this potential and the recent advances in the Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 technology, it allows for the generation of autologous and gene corrected liver cells in the form of three-dimensional (3D) liver organoids. The organoids recapitulate cellular composition and organization of the liver, providing a more physiological model to study the biology of coagulation proteins and modeling hereditary coagulation disorders. This advanced methodology can pave the way for the development of cell-based therapeutic approaches to treat inherited coagulation disorders. In this review we will explore the use of liver organoids as a state-of-the-art methodology for modeling coagulation factors disorders and the possibilities of using organoid technology to treat the disease.

Consideration of Tissue Deformation through an Electrode Displacement in a Monopolar Coagulation Model

In today's surgery, high-frequency electrical currents are often used to achieve various effects, one important being the heating of tissue to stop bleeding. However, the physical processes of tissue heating are complex and not fully understood. This complicates medical device approval with the settings used for such applications. Therefore, a simulation approach can help provide evidence. In this contribution, we present a modification of a model already presented and described in a previous investigation. By incorporating continuum mechanics into our model, we were able to simulate the deformation of the tissue due to electrode displacement. The resulting deformed configuration was then used to simulate Joule heating by applying a constant direct current voltage and to analyze the effect of varying the electrode displacement depth on the heat distribution result. Our results show that the contact area of the electrode to the tissue plays a crucial role in heating the tissue. This is because the tissue heats up more slowly with a large contact area than with a small one, resulting in significantly greater heat propagation to deeper tissue regions.

Evolution of the Soot-Particle Size Distribution Function in the Cylinder and Exhaust System of Piston Engines: Simulation

A computational tool for simulating the temporal evolution of the soot-particle size distribution function (SDF) in the internal combustion engine (ICE) and in the attached exhaust pipe is developed and tested against available experimental data on the soot-particle SDF at the outlet of the exhaust system. Firstly, a database of soot particle properties (particle mean diameter, dispersion, total particle number density vs. time for different fuels, fuel-to-air equivalence ratios, temperatures, pressures, and exhaust gas recirculation) is developed based on the thoroughly validated detailed model of soot formation under ICE conditions. The database is organized in the form of look-up tables. Secondly, the soot-particle SDF in the database is approximated using the log-normal SDF, which is directly used in the multidimensional calculations of the ICE operation process. Thirdly, the coagulation model of soot particles is developed, which includes three coagulation mechanisms: Brownian, turbulent–kinetic, and turbulent–diffusion. This model is applied for simulating the evolution of the soot-particle SDF in the exhaust pipe after opening the exhaust valve. Calculations show that the coagulation process of soot particles in the exhaust pipe has a significant effect on the mean size of particles at the outlet of the exhaust system (the mean particle diameter can increase by almost an order of magnitude), and the dominant mechanism of particle coagulation in the exhaust system of a diesel engine is the Brownian mechanism. The objective, approach, and obtained results are the novel features of the study.

Learning Coagulation Processes With Combinatorial Neural Networks

AbstractSimulating the evolution of a coagulating aerosol or cloud of droplets in a key problem in atmospheric science. We present a proof of concept for modeling coagulation processes using a novel combinatorial neural network (CombNN) architecture. Using two types of data from a high‐detail particle‐resolved aerosol simulation, we show that CombNN models outperform standard neural networks and are competitive in accuracy with traditional state‐of‐the‐art sectional models. These CombNN models could have application in learning coarse‐grained coagulation models for multi‐species aerosols and for learning coagulation models from observed size‐distribution data.

Rapid formation of massive planetary cores in a pressure bump

Context. Models of planetary core growth by either planetesimal or pebble accretion are traditionally disconnected from the models of dust evolution and formation of the first gravitationally bound planetesimals. State-of-the-art models typically start with massive planetary cores already present. Aims. We aim to study the formation and growth of planetary cores in a pressure bump, motivated by the annular structures observed in protoplanetary disks, starting with submicron-sized dust grains. Methods. We connect the models of dust coagulation and drift, planetesimal formation in the streaming instability, gravitational interactions between planetesimals, pebble accretion, and planet migration into one uniform framework. Results. We find that planetesimals forming early at the massive end of the size distribution grow quickly, predominantly by pebble accretion. These few massive bodies grow on timescales of ~100 000 yr and stir the planetesimals that form later, preventing the emergence of further planetary cores. Additionally, a migration trap occurs, allowing for retention of the growing cores. Conclusions. Pressure bumps are favourable locations for the emergence and rapid growth of planetary cores by pebble accretion as the dust density and grain size are increased and the pebble accretion onset mass is reduced compared to a smooth-disc model.

Systems Biology Approach for Personalized Hemostasis Correction.

The correction of blood coagulation impairments of a bleeding or thrombotic nature employs standard protocols where the type of drug, its dose and the administration regime are stated. However, for a group of patients, such an approach may be ineffective, and personalized therapy adjustment is needed. Laboratory hemostasis tests are used to control the efficacy of therapy, which is expensive and time-consuming. Computer simulations may become an inexpensive and fast alternative to real blood tests. In this work, we propose a procedure to numerically define the individual hemostasis profile of a patient and estimate the anticoagulant efficacy of low-molecular-weight heparin (LMWH) based on the computer simulation of global hemostasis assays. We enrolled a group of 12 patients receiving LMWH therapy and performed routine coagulation assays (activated partial thromboplastin time and prothrombin time) and global hemostasis assays (thrombodynamics and thrombodynamics-4d) and measured anti-Xa activity, fibrinogen, prothrombin and antithrombin levels, creatinine clearance, lipid profiles and clinical blood counts. Blood samples were acquired 3, 6 and 12 h after LMWH administration. We developed a personalized pharmacokinetic model of LMWH and coupled it with the mechanism-driven blood coagulation model, which described the spatial dynamics of fibrin and thrombin propagation. We found that LMWH clearance was significantly lower in the group with high total cholesterol levels. We generated an individual patient's hemostasis profile based on the results of routine coagulation assays. We propose a method to simulate the results of global hemostasis assays in the case of an individual response to LMWH therapy, which can potentially help with hemostasis corrections based on the output of global tests.

Inhibition of platelet-surface-bound proteins during coagulation under flow II: Antithrombin and heparin

Blood coagulation is a self-repair process regulated by activated platelet surfaces, clotting factors, and inhibitors. Antithrombin (AT) is one such inhibitor that impedes coagulation by targeting and inactivating several key coagulation enzymes. The effect of AT is greatly enhanced in the presence of heparin, a common anticoagulant drug. When heparin binds to AT, it either bridges with the target enzyme or induces allosteric changes in AT leading to more favorable binding with the target enzyme. AT inhibition of fluid-phase enzymes caused little suppression of thrombin generation in our previous mathematical models of blood coagulation under flow. This is because in that model, flow itself was a greater inhibitor of the fluid-phase enzymes than AT. From clinical observations, it is clear that AT and heparin should have strong inhibitory effects on thrombin generation, and thus we hypothesized that AT could be inhibiting enzymes bound to activated platelet surfaces that are not subject to being washed away by flow. We extended our mathematical model to include the relevant reactions of AT inhibition at the activated platelet surfaces as well as those for unfractionated heparin and a low molecular weight heparin. Our results show that AT alone is only an effective inhibitor at low tissue factor densities, but in the presence of heparin, it can greatly alter, and in some cases shut down, thrombin generation. Additionally, we studied each target enzyme separately and found that inactivation of no single enzyme could substantially suppress thrombin generation.

Model reduction of coagulation cascade based on genetic algorithm.

Fibrin is an important product of the coagulation cascade, and plays an eminent role in platelet stabilization. Since coagulation cascade models typically involve the reaction kinetics of dozens of proteins, which will incur burdensome computational costs when coupled to blood flow in complex geometries, researchers often ignore this process when constructing thrombosis models. However, previous studies have shown that fundamental aspects of coagulation can be reproduced with simpler models, which motivated us to obtain a reduced-order model of fibrin generation through a systematic approach. Therefore, we introduced a semi-automatic framework to perform model-reduction of cascade reactions in this study, which consisted of two processes. Specifically, the retained protein species and cascade reactions were determined based on published studies and simulation results from the full cascade model, while the optimal reaction rates for the new cascade network were determined using a genetic algorithm. The framework has been applied to a 19-species coagulation model that triggers fibrin generation in internal fields via reactive boundaries, and a 10-species reduced-order model was obtained to reproduce the kinetics of fibrinogenesis in the full cascade model at different boundary tissue factor concentrations. This reduced-order model of fibrinogenesis would be valuable for thrombosis modeling that considers both the coagulation cascade and platelet activity. Furthermore, the framework proposed herein can also be applied to the reductions of other cascade reaction models.

The Supply Side of Coagulation: Fibrinogen and Bleeding in Liver Disease and Transplantation.

In this issue of Transplantation, Carrier et al1 describe a study that assesses the effect of preoperative fibrinogen levels on perioperative bleeding and outcomes. In 613 patients with end-stage liver disease who underwent liver transplantation between 2008 and 2019, preoperative low fibrinogen levels were associated with more blood loss but not worse 1-y survival in univariate and multivariate statistical models. This effect was most prominent when fibrinogen levels were below 3 g/L before surgery. In any model of coagulation, fibrinogen is the substrate required to create an effective clot and provide hemostasis. Like most components of hemostasis, fibrinogen is synthesized by the liver and reduced in severe liver disease. Additionally, and maybe more commonly‚ dysfibrinogenemia occurs in liver disease resulting in defects of the fibrinogen structure with undetermined effects on hemostasis.2 The coagulation abnormalities associated with liver disease result in dysbalanced hemostasis that can cause impaired clot formation or excessive thrombosis. Conventional coagulation tests cannot detect this dysbalanced hemostasis‚ as they measure only (a part of) the procoagulant side of hemostasis. Viscoelastic testing, now routinely used in many transplant centers‚ may provide a better assessment of all aspects of clot formation by creating a visual representation of changes in the viscosity of blood when a clot forms. Viscoelastic testing can guide transfusion management in many clinical scenarios‚ including liver transplantation‚ but possibly, more importantly, allows us to identify patients who are hypercoagulable even when the conventional coagulation tests are abnormally high. The results of Carrier et al suggest that low preoperative fibrinogen levels may be an indicator that a patient is at risk for increased intraoperative bleeding. This may be particularly useful if perioperative viscoelastic testing is not used or available as with the study center. This risk of bleeding increased when fibrinogen levels were below 3 g/L before surgery, a level that is far higher than what has traditionally been considered a concerning threshold. Most experts and societies, for example, the review on perioperative coagulation management in liver transplant recipients by Bezinover et al here in Transplantation in 2018,3 recommend fibrinogen concentrate and/or cryoprecipitate transfusion for fibrinogen levels below 1.5 to 2 g/L. Although raising new questions, the present study does not provide enough evidence to change this recommendation at this time. An association with bleeding (even in a multivariate model) does not necessarily mean that replacing fibrinogen with levels over 3 g/L will reduce the risk of bleeding. The assumption is that fibrinogen levels that are below 3 g/L before surgery may decrease more during transplantation to a level that actually impairs hemostasis. Excessive transfusion of cryoprecipitate (and, to a lesser degree, fibrinogen concentrates) is not without risk and may increase the risk of thromboembolic complications.4 The results by Carrier et al are raising new questions about fibrinogen thresholds and may provide the impetus for future (prospective) studies but should not necessarily change our current management. The Centre Hospitalier de L’Universite de Montreal (CHUM) has demonstrated for many years with great success what can be achieved with a concerted effort to reduce blood transfusion5: More than 70% of the patients in the present study did not receive any red blood cell transfusion at all! The center undertakes a number of interventions to achieve these remarkable results. For example, over 50% of the patients in this study underwent phlebotomy at the beginning of surgery. I am not aware of any other center that implemented such a vigorous and successful program to reduce blood transplantation. Unfortunately, this also limits the generalizability of the present study (and reduces the statistical power of the study). Furthermore, because viscoelastic testing was not used in this study, we do not know if lower preoperative fibrinogen levels result in deficient fibrinogen contribution to clot strength later during surgery (assessed, for example, using fibrinogen assays such as FIBTEM with rotational thromboelastometry, ROTEM). In summary, Carrier et al provide important insight into the role of fibrinogen in achieving hemostasis during and good outcomes after liver transplantation. Their data encourage us to check for fibrinogen levels whenever we measure conventional or viscoelastic coagulation tests and design future randomized trials of fibrinogen replacement in liver transplantation.

Computational modeling of hypercoagulability in COVID-19

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected more than 100 million people worldwide and claimed millions of lives. While the leading cause of mortality in COVID-19 patients is the hypoxic respiratory failure from acute respiratory distress syndrome, there is accumulating evidence that shows excessive coagulation also increases the fatalities in COVID-19. Thus, there is a pressing demand to understand the association between COVID-19-induced hypercoagulability and the extent of formation of undesired blood clots. Mathematical modeling of coagulation has been used as an important tool to identify novel reaction mechanisms and to identify targets for new drugs. Here, we employ the coagulation factor data of COVID-19 patients reported from published studies as inputs for two mathematical models of coagulation to identify how the concentrations of coagulation factors change in these patients. Our simulation results show that while the levels of many of the abnormal coagulation factors measured in COVID-19 patients promote the generation of thrombin and fibrin, two key components of blood clots, the increased level of fibrinogen and then the reduced level of antithrombin are the factors most responsible for boosting the level of fibrin and thrombin, respectively. Altogether, our study demonstrates the potential of mathematical modeling to identify coagulation factors responsible for the increased clot formation in COVID-19 patients where clinical data is scarce.

Influence of temperature-dependent tissue parameters on monopolar coagulation model

Abstract The use of high-frequency (HF) generators for HF surgical treatment of biological tissue has become an indispensable part of today's surgical applications of all kinds. Generally, HF alternating electric currents between 300 kHz and 1 MHz are used to induce hemostasis by heating at the cellular level. This effect can be attributed to Joule heating, in which a current dissipated conductor converts the electrical energy into thermal energy. However, sound evidence on the reliability and effectiveness of application-specific HF generator modes is not sufficiently available. Usually, the evidence takes place empirically by means of preclinical or clinical studies. Nevertheless, a corresponding empirical data collection is time- and cost-intensive. Therefore, physiological and statistical modeling provides the opportunity to relate tissue response to the applied electrical energy to obtain a prediction of the tissue reaction. In this contribution, we establish a monopolar coagulation model of an already well-known model approach based on Pennes bioheat equation. Additionally, the vaporization of tissue water at the water boiling point is considered. Furthermore, a variation of temperature-dependent tissue parameters was performed to analyze their impact on the model output. The simulation results demonstrate that the initial electrical conductivity has the greatest influence on the temperature distribution as well as on the time until the tissue temperature reached the boiling point of water. In contrast, the tissue water content has the least impact on the model output. Depending on the desired coagulation effect, HF power control as a function of electrical conductivity or its reciprocal, tissue resistance, must be added next in an improved model.

Coagulation sedimentation performance and model optimization of ultra-fine tailings overflow from hydrocyclone

In order to study the sedimentation characteristics of ultra-fine tailings overflow from hydrocyclone in a coagulation environment, the sedimentation velocity of overflow ultra-fine tailings under different coagulant dosage, pulp pH and temperature conditions were analyzed experimentally in this study. The results indicate that with the increase in sedimentation time, the sedimentation velocity of the coagulant first increases, followed by a decline before becoming flat. When the ferric chloride coagulant dosage is 90 mg/L, the pH of the pulp is 9. The sedimentation velocity reaches the maximum value of 5.57 mm/s, when the temperature of the pulp is 60 °C. According to the sedimentation process of the coagula, the coagulation sedimentation model of total tailings was extended and modified. The average absolute error between the corrected settlement velocity and the actual velocity was found as 0.0034, with the root mean square error is as 0.0088, which is relatively small. The results obtained from the theoretical calculations are consistent with the experimental data. The modified and optimized coagulation sedimentation model is important in promoting the theoretical research on the coagulation and sedimentation of such ultra-fine mineral particles.

Zeolite fly ash-enhanced coagulation treatment of oil recovery wastewater from polymer flooding.

Herein, an enhanced coagulation model is proposed in which zeolite is used as a crystal nucleus to promote flocs. The zeolite is prepared from fly ash by microwave-assisted hydrothermal synthesis. Scanning electron microscopy (SEM), X-ray diffraction (XRD), and specific surface area and pore size analysis (BET) characterization confirmed the successful synthesis of ZFA, and improved the surface properties. Thus, the adsorption capacity of ZFA as crystal nucleus was improved, which enabled it to achieve better results in the process of enhanced coagulation. Compared with those of conventional coagulation, the oil content and SS removal rate of ZFA-enhanced coagulation increased by 85% and 44%, respectively. Compared with that of CFA-enhanced coagulation, the oil removal efficiency increased by 4%, and the SS removal efficiency increased by 9%. The optimal conditions of ZFA-enhanced coagulation were as follows: ZFA dosage of 100mg/L, pH value of 5-8, ZFA particle size range of 60-75μm, temperature of 40-50 ℃, and precipitation time of 30min.

Application of Dragon Fruit Peel’s Mucilage in Coagulation – Flocculation Process to Remove Turbidity from Water

The study determined flocculation activity of mucilage extracted from dragon fruit peel (Hylocereus undatus) and its ability in reducing synthetic coagulant polyaluminium chloride (PAC) used in coagulation – flocculation process to remove turbidity of different types of water. Investigated waters were turbid waters made from kaolin suspension (KS), suspension of river water with hill soil (FW), and To Lich river water (TL). Turbidity removal was assessed in a sequent coagulation and flocculation model using PAC and mucilage extracted from dragon fruit peel in Jar-tests. Optimal coagulation conditions of PAC with PAC dosage of 20-50 mg/L and pH range of 6-8 regardless of water types and resulted in maximum turbidity removal of about 98%. In order to obtain a comparable turbidity removal, 50%-68% of the required PAC was reduced if mucilage was used. The presence of mucilage enhanced turbidity removal of PAC by 13-22% total efficiency. Mucilage extracted from dragon fruit peel has shown its flocculation ability and its potential as a green material in water treatment.