Relevant bibliographies by topics / Insect residue adhesion

Academic literature on the topic 'Insect residue adhesion'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Insect residue adhesion"

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Kok, Mariana, Tobias Mertens, Dominik Raps, and Trevor M. Young. "Influence of surface characteristics on insect residue adhesion to aircraft leading edge surfaces." Progress in Organic Coatings 76, no. 11 (November 2013): 1567–75. http://dx.doi.org/10.1016/j.porgcoat.2013.06.013.

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Wohl, Christopher J., Joseph G. Smith, Ronald K. Penner, Tyler M. Lorenzi, Conrad S. Lovell, and Emilie J. Siochi. "Evaluation of commercially available materials to mitigate insect residue adhesion on wing leading edge surfaces." Progress in Organic Coatings 76, no. 1 (January 2013): 42–50. http://dx.doi.org/10.1016/j.porgcoat.2012.08.009.

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Suderman, Richard J., Andrea J. Pruijssers, and Michael R. Strand. "Protein tyrosine phosphatase-H2 from a polydnavirus induces apoptosis of insect cells." Journal of General Virology 89, no. 6 (June 1, 2008): 1411–20. http://dx.doi.org/10.1099/vir.0.2008/000307-0.

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The family Polydnaviridae is a large group of immunosuppressive insect viruses that are symbiotically associated with parasitoid wasps. The polydnavirus Microplitis demolitor bracovirus (MdBV) causes several alterations that disable the cellular and humoral immune defences of host insects, including apoptosis of the primary phagocytic population of circulating immune cells (haemocytes), called granulocytes. Here, we show that MdBV infection causes granulocytes in the lepidopteran Spodoptera frugiperda to apoptose. An expression screen conducted in the S. frugiperda 21 cell line identified the MdBV gene ptp-H2 as an apoptosis inducer, as indicated by cell fragmentation, annexin V binding, mitochondrial membrane depolarization and caspase activation. PTP-H2 is a classical protein tyrosine phosphatase that has been shown previously to function as an inhibitor of phagocytosis. PTP-H2-mediated death of Sf-21 cells was blocked by the pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-(O-methyl) Asp-fluoromethylketone (Z-VAD-FMK), but cells maintained in this inhibitor still exhibited a suppressed phagocytic response. Mutagenesis experiments indicated that the essential catalytic cysteine residue required for the phosphatase activity of PTP-H2 was required for apoptotic activity in Sf-21 cells. Loss of adhesion was insufficient to stimulate apoptosis of Sf-21 cells. PTP-H2 expression, however, did significantly reduce proliferation of Sf-21 cells, which could contribute to the apoptotic activity of this viral gene. Overall, our results indicate that specific genes expressed by MdBV induce apoptosis of certain insect cells and that this activity contributes to immunosuppression of hosts.
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Podda, Gianmarco, James R. Roberts, Richard A. McClintock, and Zaverio M. Ruggeri. "Distinct Functional Conformations of von Willebrand Factor A1 Domain in Support of Platelet-Surface or Platelet-Platelet Interactions." Blood 110, no. 11 (November 16, 2007): 5182. http://dx.doi.org/10.1182/blood.v110.11.5182.5182.

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Abstract The adhesive protein, von Willebrand factor (VWF), is generally considered a key substrate for platelet adhesion to the vessel wall, yet its role in platelet cohesion (aggregation) may be equally important for normal thrombus formation. In either case, the function of VWF is mediated by the primary interaction of the VWF A1 domain (VWF-A1) with glycoprotein (GP) Ibα, a component of the GPIb-IX-V receptor complex on the platelet membrane. Because normal plasma VWF in solution and GPIb coexist in circulating blood without any appreciable interaction, it has been postulated that conformational changes occur when VWF becomes immobilized and/or under the effect of pathologically elevated shear stress, such that binding to the receptor becomes possible and resultis in platelet tethering to a surface and shear-induced aggregation. Changes of the molecular shape of VWF, from coiled to extended, have been shown under the effect of hemodynamic forces, but evidence for conformational changes within VWF-A1 has remained elusive. The crystal structure of VWF-A1 in complex with a GPIbα amino terminal fragment has revealed that the VWF-A1 residues involved in the interaction are comprised between positions 544–614 and, in particular, do not include several positively charged Arg and Lys residues located in helices α4 and 5 (residues 627–668). The latter appear as likely candidates to interact with negatively charged residues in GPIbα as a consequence of potential conformational changes induced by tensile stress on the bond following an initial ligand-receptor contact. We tested this hypothesis by evaluating the ability of selected VWF-A1 mutants to support platelet adhesion or aggregation, respectively, under controlled flow conditions. Methods. We expressed in insect cells and purified a series of VWF-A1 fragments comprising residues 445–733. One fragment had native sequence and 8 had single or multiple substitutions of positively charged amino acid residues in helices α4 and/or α5. None of the substituted residues contribute to contacts with GP Ibα in the known crystal structures of the corresponding complex, and all except one were between 8 and 20 angstroms away from the closest GPIbα residue. All the fragments were dimeric (d) owing to the presence of interchain disulfide bond(s). Results: Native dVWF-A1 in solution supported platelet aggregation in a laminar flow field. Of the 8 mutants, 5 had variably decreased function (up to 95% less aggregation) and 2 had increased function (up to 200% increase in aggregation). The same results were observed with platelet-rich plasma in suspension or by measuring platelet aggregate formation with blood cells perfused over immobilized VWF-A1 at wall shear rates as high as 10,000 1/s. In contrast, as judged by the number of tethered platelets and their rolling velocities, all mutants supported adhesion as well as or better that the native VWFA-1 at all shear rates tested (500–25,000 1/s). Conclusions: These results provide structural evidence for the existence of different VWF-A1 conformers that can modulate adhesive properties with distinct effects on platelet adhesion to a surface or platelet aggregation.
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Khan, Abdul Ghafoor, Johannes Pichler, Anke Rosemann, and Dieter Blaas. "Human Rhinovirus Type 54 Infection via Heparan Sulfate Is Less Efficient and Strictly Dependent on Low Endosomal pH." Journal of Virology 81, no. 9 (February 14, 2007): 4625–32. http://dx.doi.org/10.1128/jvi.02160-06.

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ABSTRACT K-type major-group human rhinoviruses (HRVs) (including HRV54) share a prominent lysine residue in the HI surface loop of VP1 with all minor-group HRVs. Despite the presence of this residue, they cannot use members of the low-density lipoprotein receptor family for productive infection. Reexamining all K-type viruses for receptor usage, we noticed that HRV54 is able to replicate in RD cells that lack the major-group receptor intercellular adhesion molecule 1 (ICAM-1). By using receptor blocking assays, inhibition of sulfation, enzymatic digestion, and proteoglycan-deficient cell lines, we show here that wild-type HRV54, without any adaptation, uses heparan sulfate (HS) proteoglycan as an alternate receptor. However, infection via HS is less efficient than infection via ICAM-1. Moreover, HRV54 has an acid lability profile similar to that of the minor-group virus HRV2. In ICAM-1-deficient cells its replication is completely blocked by the H+-ATPase inhibitor bafilomycin A1, whereas in ICAM-1-expressing cells it replicates in the presence of the drug. Thus, use of a “noncatalytic” receptor requires the virus to be highly unstable at low pH.
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Connell, John W., Christopher J. Wohl, Allison M. Crow, William T. Kim, Michelle H. Shanahan, Jereme R. Doss, and Yi Lin. "Synthesis and characterization of copolyimides containing fluorine and silicon surface-modifying agents." High Performance Polymers 30, no. 3 (March 17, 2017): 355–64. http://dx.doi.org/10.1177/0954008317698315.

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Understanding the effects that monomer chemistries have on material properties allows for fine tuning of polymer synthesis for current and future applications. In order to develop polymeric-based coatings that have minimal surface adhesion characteristics when exposed to a variety of contaminants, a more thorough understanding of fundamental structure–property relationships is needed. In the aeronautics field, one concept to improve fuel efficiency of future aircraft is to modify the wing design to enable laminar flow. There is a concern that contaminants such as insect residue and other debris will adhere to airflow surfaces and have sufficient height to disrupt laminar flow thereby increasing drag with concomitant loss of fuel efficiency. One potential solution would be a polymer surface or coating that prevents or minimizes adhesion of such contaminants. As part of a structure–property relationship study involving modification of surface properties, a series of copolyimides containing both fluorine and silicon surface-modifying agents (SMAs) were prepared and characterized. Based on knowledge of structure–property relationships with polyimides containing either type of SMA, it was hypothesized that the combination of two different SMAs may lead to unique surface properties as the two SMAs competed for surface area at the polymer–air interface. Copolyimides for this study were prepared through a multistep synthesis using an aromatic dianhydride with equimolar amounts of diamino functionalities comprised of an aromatic diamine along with two SMAs. Films were cast from copoly(amide acid) solutions that were subsequently thermally imidized under a nitrogen atmosphere. Polyimide films and coatings were characterized using differential scanning calorimetry, Fourier transform infrared spectroscopy, ultraviolet–visible spectroscopy, contact angle goniometry, scanning electron microscopy, and energy-dispersive X-ray spectroscopy to determine chemical, thermal, and surface properties. Select samples were subject to high velocity insect impacts in a small-scale wind tunnel and the resulting residues were characterized for height and surface area and compared to those of a control surface.
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ROBERTSON, Alexis, Gavin S. MacCOLL, Julia A. B. NASH, Mark K. BOEHM, Stephen J. PERKINS, and Pierre-Marc G. BOULOUX. "Molecular modelling and experimental studies of mutation and cell-adhesion sites in the fibronectin type III and whey acidic protein domains of human anosmin-1." Biochemical Journal 357, no. 3 (July 25, 2001): 647–59. http://dx.doi.org/10.1042/bj3570647.

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Anosmin-1, the gene product of the KAL gene, is implicated in the pathogenesis of X-linked Kallmann's syndrome. Anosmin-1 protein expression is restricted to the basement membrane and interstitial matrix of tissues affected in this syndrome during development. The anosmin-1 sequence indicates an N-terminal cysteine-rich domain, a whey acidic protein (WAP) domain, four fibronectin type III (FnIII) domains and a C-terminal histidine-rich region, and shows similarity with cell-adhesion molecules, such as neural cell-adhesion molecule, TAG-1 and L1. We investigated the structural and functional significance of three loss-of-function missense mutations of anosmin-1 using comparative modelling of the four FnIII and the WAP domains based on known NMR and crystal structures. Three missense mutation-encoded amino acid substitutions, N267K, E514K and F517L, were mapped to structurally defined positions on the GFCC′ β-sheet face of the first and third FnIII domains. Electrostatic maps demonstrated large basic surfaces containing clusters of conserved predicted heparan sulphate-binding residues adjacent to these mutation sites. To examine these modelling results anosmin-1 was expressed in insect cells. The incorporation of the three mutations into recombinant anosmin-1 had no effect on its secretion. The removal of two dibasic motifs that may constitute potential physiological cleavage sites for anosmin-1 had no effect on cleavage. Peptides based on the anosmin-1 sequences R254–K285 and P504–K527 were then synthesized in order to assess the effect of the three mutations on cellular adhesion, using cell lines that represented potential functional targets of anosmin-1. Peptides (10μg/ml) incorporating the N267K and E514K substitutions promoted enhanced adhesion to 13.S.1.24 rat olfactory epithelial cells and canine MDCK1 kidney epithelial cells (P<0.01) compared with the wild-type peptides. This result was attributed to the introduction of a lysine residue adjacent to the large basic surfaces. We predict that two of the three missense mutants increase the binding of anosmin-1 to an extracellular target, possibly by enhancing heparan sulphate binding, and that this critically affects the function of anosmin-1.
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Martin, M., C. Andréoli, A. Sahuquet, P. Montcourrier, M. Algrain, and P. Mangeat. "Ezrin NH2-terminal domain inhibits the cell extension activity of the COOH-terminal domain." Journal of Cell Biology 128, no. 6 (March 15, 1995): 1081–93. http://dx.doi.org/10.1083/jcb.128.6.1081.

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Overexpression in insect cells of the full coding sequence of the human membrane cytoskeletal linker ezrin (1-586) was compared with that of a NH2-terminal domain (ezrin 1-233) and that of a COOH-terminal domain (ezrin 310-586). Ezrin (1-586), as well as ezrin (1-233) enhanced cell adhesion of infected Sf9 cells without inducing gross morphological changes in the cell structure. Ezrin (310-586) enhanced cell adhesion and elicited membrane spreading followed by microspike and lamellipodia extensions by mobilization of Sf9 cell actin. Moreover some microspikes elongated into thin processes, up to 200 microns in length, resembling neurite outgrowths by a mechanism requiring microtubule assembly. Kinetics of videomicroscopic and drug-interference studies demonstrated that mobilization of actin was required for tubulin assembly to proceed. A similar phenotype was observed in CHO cells when a comparable ezrin domain was transiently overexpressed. The shortest domain promoting cell extension was localized between residues 373-586. Removal of residues 566-586, involved in in vitro actin binding (Turunen, O., T. Wahlström, and A. Vaheri. 1994. J. Cell Biol. 126:1445-1453), suppressed the extension activity. Coexpression of ezrin (1-233) with ezrin (310-586) in the same insect cells blocked the constitutive activity of ezrin COOH-terminal domain. The inhibitory activity was mapped within ezrin 115 first NH2-terminal residues. We conclude that ezrin has properties to promote cell adhesion, and that ezrin NH2-terminal domain negatively regulates membrane spreading and elongation properties of ezrin COOH-terminal domain.
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Chinthalapudi, Krishna, Erumbi S. Rangarajan, David T. Brown, and Tina Izard. "Differential lipid binding of vinculin isoforms promotes quasi-equivalent dimerization." Proceedings of the National Academy of Sciences 113, no. 34 (August 8, 2016): 9539–44. http://dx.doi.org/10.1073/pnas.1600702113.

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The main cause of death globally remains debilitating heart conditions, such as dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM), which are often due to mutations of specific components of adhesion complexes. Vinculin regulates these complexes and plays essential roles in intercalated discs that are necessary for muscle cell function and coordinated movement and in the development and function of the heart. Humans bearing familial or sporadic mutations in vinculin suffer from chronic, progressively debilitating DCM that ultimately leads to cardiac failure and death, whereas autosomal dominant mutations in vinculin can also provoke HCM, causing acute cardiac failure. The DCM/HCM-associated mutants of vinculin occur in the 68-residue insert unique to the muscle-specific, alternatively spliced isoform of vinculin, termed metavinculin (MV). Contrary to studies that suggested that phosphoinositol-4,5-bisphosphate (PIP2) only induces vinculin homodimers, which are asymmetric, we show that phospholipid binding results in a domain-swapped symmetric MV dimer via a quasi-equivalent interface compared with vinculin involving R975. Although one of the two PIP2 binding sites is preserved, the symmetric MV dimer that bridges two PIP2 molecules differs from the asymmetric vinculin dimer that bridges only one PIP2. Unlike vinculin, wild-type MV and the DCM/HCM-associated R975W mutant bind PIP2 in their inactive conformations, and R975W MV fails to dimerize. Mutating selective vinculin residues to their corresponding MV residues, or vice versa, switches the isoform’s dimeric constellation and lipid binding site. Collectively, our data suggest that MV homodimerization modulates microfilament attachment at muscular adhesion sites and furthers our understanding of MV-mediated cardiac remodeling.
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Rosenzweig, W. D., D. Premachandran, and D. Pramer. "Role of trap lectins in the specificity of nematode capture by fungi." Canadian Journal of Microbiology 31, no. 8 (August 1, 1985): 693–95. http://dx.doi.org/10.1139/m85-131.

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Seven adhesive-producing nematode-trapping fungi were tested for their ability to capture nine different nematodes. The nematodes included species that are free living as well as plant and insect parasites. The fungi displayed no selectivity. Each fungus was able to trap and consume all of the different nematodes tested. A study of cuticle surface saccharides of five of the nematodes revealed the presence on all the nematodes of glucose–mannose and N-acetylgalactosamine residues. L-Fucose residues were not found on any of the nematodes. The involvement of lectins in the capture of prey by nematode-trapping fungi is discussed.
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Book chapters on the topic "Insect residue adhesion"

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"predicting the permissible external loading that a diamond-coated cutting tool can withstand without premature de-bonding. 3.1.6. Wear mechanisms. The failure of CVD diamond-coated inserts during machining can be in the form of flaking (interfacial failure) or abrasive wear (gradual cohesive failure) [22]. Ideally, a test of superb adhesion is when the diamond coating fully deteriorates by wear rather than flaking. Flaking will occur primarily due to poor adhesion between the diamond coating and the carbide substrate [6]. Therefore, flaking is clearly undesirable because the benefit of using a diamond coating is lost, except for the chip breaking assistance of faceted diamond crystals at the rake surface [29, 75]. If the adhesion strength of the CVD diamond coating is sufficient to withstand the machining stresses, then the abrasive action between the workpiece material and the diamond coating becomes the primary failure mechanism. Unless the CVD diamond coating is polished, a two-step wear mechanism is ex­ pected to occur. The first step is caused by the initial high surface roughness of the CVD diamond coating in which crack initiation occurs at the surface. The mecha­ nism that describes such behavior was proposed by Gunnars and Alahelisten [56]. They described a three-zone wear model as shown in Fig. 6. In this model, the role of residual stresses becomes significant in controlling crack propagation from the surface to the interface that could lead to interface failure (flaking). As outlined earlier, the high total compressive residual stress present in CVD diamond coatings on carbide inserts was assumed to be biaxial and oriented parallel to the interface. Wear starts to occur at the surface, which, because of geometry, allows stress to relax. A crack is more likely to initiate at protruding grains in zone I and propa­ gate preferentially along the (111) easy cleavage planes of diamond. The geometry at deeper depths, however, prevents the compressive residual stress from relaxing. Therefore, as the crack propagates deeper in the coating, it encounters higher com­ pressive stresses that cause the cracks to redirect their paths deviating from cleavage planes to a direction parallel to the interface in region II. The high compressive stress now causes cracks to propagate fast parallel to the interface resulting in a smooth surface in region III. Due to the smoother surface, fewer asperities will be present and it becomes harder to nucleate cracks." In Adhesion Aspects of Thin Films, Volume 1, 100–139. CRC Press, 2014. http://dx.doi.org/10.1201/b11971-20.

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Conference papers on the topic "Insect residue adhesion"

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Wohl, Christopher, Joseph Smith, John Connell, Emilie Siochi, Ronald Penner, and John Gardner. "Engineered Surfaces for Mitigation of Insect Residue Adhesion." In 51st AIAA Aerospace Sciences Meeting including the New Horizons Forum and Aerospace Exposition. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2013. http://dx.doi.org/10.2514/6.2013-413.

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Taher, Mahmoud A., William F. Schmidt, and Ajay P. Malshe. "3-D FEM of Residual Stresses in CVD Diamond-Coated Carbide Cutting Inserts for Process Optimization." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-1056.

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Abstract The high thermal strains that generate during chemical vapor deposition (CVD) of diamond coatings on carbide inserts result in high compressive thermal residual stresses in the diamond near the coating interface. These stresses are believed to increase the strain energy at the interface leading to coating failure. To help predict CVD diamond adhesion characteristics to carbide inserts, quantifying such residual stresses becomes important. A three dimensional finite element model was constructed for a commercial cemented carbide tool insert coated with a 20μm film of CVD diamond and the interfacial thermal residual stresses at the rake and flank regions computed. A 2-D axi-symmetric contact model was constructed to evaluate the effectiveness of mircohardness indentation as an appropriate adhesion test for CVD diamond coatings. Superposition of the residual stresses and the stresses generated by indentation just before cohesive brittle failure of the coating revealed that the combined shear and peel stresses were lower than those originally present due to residual stresses alone indicating that the indentation method may not be a useful technique for determining adhesion.
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Yoon, Sung-Hwan, Jun S. Lee, Ji-Sun Im, Xugang Xiong, Nam-Goo Cha, Joey L. Mead, and Carol M. F. Barry. "Effect of Tooling Surface Roughness in Micro-Injection Molding." In ASME 2008 International Manufacturing Science and Engineering Conference collocated with the 3rd JSME/ASME International Conference on Materials and Processing. ASMEDC, 2008. http://dx.doi.org/10.1115/msec_icmp2008-72093.

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Quality of tooling surface has been considered as one of the important factors defining the injection molded part quality. Therefore, surface polishing has been an important and relatively expensive step in conventional mold making process. Although the poor surface quality impacts the product quality when molding macroscale parts, it becomes more significant with sub-micrometer features. Previous micro injection molding research result has indicated that rough tooling surface may cause polymer adhesion on the tooling surface. To evaluate the effect of roughness, optical grade polycarbonate was molded using silicon inserts with artificially generated surface roughness (root-mean-square roughness: 3∼143 nm) by dry etching. The silicon and molded parts surface were characterized using atomic force and scanning electron microscopy. Filling and ejection of the parts as well as residual polymer on the tooling correlated surface roughness of the tooling.
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Lopez, J. A., D. W. Chung, K. Fujikawa, F. S. Hagen, T. Papavannopoulou, and G. J. Roth. "MOLECULAR CLONING OF HUMAN PLATELET GLYCOPROTEIN Ib." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642927.

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Glycoprotein Ib (GPIb) mediates von Willebrand factor-dependent platelet adhesion and participates in the resulting platelet activation process. In the present investigation, the primary structure of human platelet GPIb was studied. GPIb and its proteolytic fragment glycocalicin were purified to near homogeneity from human platelets by affinity chromatography using wheat germ agglutinin and anti-GPIb monoclonal antibody (D. Nugent, University of Washington) coupled to Sepharose. GPIba chain, β chain, and glycocalicin were isolated, reduced and carboxymethylated, and then fragmented by trypsin and S. aureus V8 protease. Peptides were isolated by HPLC and subjected to amino acid sequence analysis. Approximately 200 amino acid residues were identified. Affinity purified rabbit antibodies directed against the a chain, the ft chain, and glycocalicin were prepared and shown to be monospecific by Western blot analysis. Total RNA was prepared from human erythroleukemia cells grown in the presence of phorbol acetate. Poly(A)+ RNA was selected and used to prepare a cDNA library in λgt11. The library was screened with [125]I-labeled polyclonal antibody to glycocalicin. The clone with the largest cDNA insert was sequenced and shown to code for amino acid sequences corresponding to those determined by Edman degradation of glycocalicin. The predicted amino acid sequence contains at least six tandem repeats of 24 amino acids that are highly homologous with 13 repeats present in leucine rich α2 glycoprotein of human plasma. Another region in the protein contains a second repeat rich in threonine and serine, which shows some homology to a 9 amino acid repeat in the connecting region of human factor V. This region is probably the major site of attachment of clusters of O-linked carbohydrate in GPIbα. These results indicate that human platelet glycoprotein Ibα has a multi-domain structure composed of a number of repetitive sequences. Supported in part by grants from the American Heart Association, Robert Wood Johnson Foundation, Veterans Administration, and National Institutes of Health.
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Alzate Mosquera, Sara Lizeth. "Icopor, resina y plástico para la preparación de mampuestos." In Nuevas realidades para la educación en ingeniería: currículo, tecnología, medio ambiente y desarrollo. Asociación Colombiana de Facultades de Ingeniería - ACOFI, 2022. http://dx.doi.org/10.26507/paper.2323.

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Con el paso del tiempo se han evidenciado los avances tecnológicos, así como la aplicación de nuevas tecnologías y la elaboración de prototipos innovadores en los cuales las lecciones aprendidas de aciertos y desaciertos marcan la pauta de la evolución. El crecimiento de la población genera exigencias para un mejor sostenimiento de los estilos de vida en las comunidades, no obstante, este aumento conlleva a un mayor consumo en productos de materia prima y, por consiguiente, se generan grandes cantidades de desechos en el sector, contaminación atmosférica, hídrica y del suelo, cambios de clima, situación exacerbada por las grandes industrias, el uso automotriz y las actividades de construcción. En Colombia el gran consumo de plástico aumenta con el transcurso del tiempo, de este modo, se evidencian cifras en crecimiento del 2019-2022. En este estudio se plantea una solución desde la óptica de la ingeniería civil, así pues, produciendo el prototipo del mampuesto. Este primer modelo de mampuesto con magnitudes comerciales fue elaborado con materiales reciclables y materiales químicos. Para su construcción artesanal se empleó núcleo de icopor recubierto con trozos de papel periódico para ofrecer cumplimiento a los requisitos del mampuesto comercial. Se le insertó al icopor astillas de madera, se agregó una capa envases plásticos anteriormente lavados y cortados, y resina epóxica de alta efectividad como adhesivo. La resina proporciona a los residuos embebidos rigidez y seguridad. El peso del mampuesto producido fue de 1.414 kilogramo y una resistencia a flexo-tracción de 0,53MPa.
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