No description available.

The use of synthetic materials for tissue and organ reconstruction, i. e. tissue engineering, has become a promising alternative to current surgical therapies and may overcome the shortcomings of the methods in use today. The challenge is in the design and reproducible fabrication of biocompatible and bioresorbable polymers, with suitable surface chemistry, desirable mechanical properties, and the wanted degradation profile. These material properties can be achieved in various manners, including the synthesis of homo- and copolymers along with linear and star-shaped architectures. In many applications the materials’ three-dimensional structure is almost as important as its composition and porous scaffolds with high porosity and interconnected pores that facilitate the in-growth of cells and transportation of nutrients and metabolic waste is desired. In this work linear and star-shaped polymers have been synthesized by ring-opening polymerization using a stannous-based catalyst and a spirocyclic tin initiator. A series of linear copolymers with various combinations of 1,5-dioxepane-2-one (DXO), Llactide (LLA) and ε-caprolactone (CL) have been polymerized using stannous octoate as catalyst. It is shown that the composition of the polymers can be chosen in such a manner that the materials’ mechanical and thermal properties can be predetermined. A solvent-casting and particulate leaching scaffold preparation technique has been developed and used to create three-dimensional structures with interconnected pores. The achieved physical properties of these materials’ should facilitate their use in both soft and hard tissue regeneration. Well defined star-shaped polyesters have been synthesized using a spirocyclic tin initiator where L-lactide was chosen as a model system for the investigation of the polymerization kinetics. Neither the temperature nor the solvent affects the molecular weight or the molecular weight distribution of the star-shaped polymers, which all show a molecular weight distribution below 1.19 and a molecular weight determined by the initial monomer-to-initiator concentration. / QC 20101217

No description available.

The purpose of this study was to investigate the use of instructional activities that take place before reading, during reading, and after reading in guided reading and shared reading routines in elementary school classrooms in Utah school districts. This project used extant data from classroom observations to answer questions about how the observed activities were used as part of guided and shared reading routines in second and third grades within the five school districts of the Brigham Young University-Public School Partnership. The results of this study showed that there were differences in how teachers implemented the before reading, during reading, and after reading activities for guided and shared reading. The average teacher devoted more time to instructional activities during the reading portion of guided or shared reading than to instructional activities used before reading or after reading as part of the guided reading or shared reading routines. Differences between frequencies for instructional activities done after reading in guided reading differed significantly between second and third grade classrooms in the study. This study determined that school districts in the study had significantly different frequencies for instructional activities implemented before, during, and after reading in guided reading. These significant results and the results of other comparisons were used to provide insights about the possible implications of this study.

I det här utvecklas en reproducerbar polymerisationsmetod för att uppnå en stabil produktion av poly(ε-caprolakton-co-p-dioxanon) (PCLDX), skala upp filamenttillverkningen för att producera 1.75 mm långa filament och optimera 3D-utskriftsprocessen för att tillverka ställningar/anordningar för mjukvävnadsteknik. PCLDX, med högre nedbrytningshastighet och bättre flexibilitet jämfört med poly(ε-caprolactone) (PCL), syntetiserades på ett reproducerbart sätt genom sampolymerisering. Den syntetiserade PCLDX uppvisade önskvärd sammansättning (85 mol% CL : 15 mol% DX), molmassa (cirka 40 kg∙mol-1), dispersitet (cirka 1.8) och relativt låg smältpunkt (cirka 45 ℃). För att tillverka tredimensionella matriser av PCLDX utformades och optimerades två processer, filamenttillverkning och 3D printning. För filamenttillverkningsprocessen användes låg extruderingstemperatur (65 och 80 ℃) och låg extruderingshastighet (100 cm∙min-1) för att spara energi och minimera nedbrytningen. PCLDX-filament med en jämn diameter på 1.75 mm tillverkades genom att använda en passande partikelstorlek (diameter på 3-4 mm) och en kylmetod (blandning av vatten och torris, 0 ℃). De erhållna filamenten uppvisade lägre Youngs modul (25 % lägre än PCL), PCLDX batch oberoende termiska egenskaper, god ytkvalitet och printbarhet. Den termiska nedbrytningen av PCLDX under processen var försumbar och molmassan var nästintill oförändrad. Processen har skalats upp för att producera stora mängder PCLDX-filament, vars produktivitet nådde upp till 140 g∙h-1. Tredimensionella matriser tillverkades genom att printa önskad design genom manuell matning och låg printhastighet (5 mm/s). En isplatta användes för att kyla ner maskinen under printningen för att undvika bucklingproblem. Det optimerade printprotokollet genererade ingen termisk nedbrytning av polymeren, påverkade inte polymerens molmassa eller dispersitet. De producerade matriserna hade samma termiska egenskaper oavsett polymerbatch och god ytkvalitet. Det optimerade printprotokollet användes också framgångsrikt för att skriva ut komplicerade prototyper, t.ex. menisk och knäprotes för potentiella biomedicinska tillämpningar. / In this project, we develop a reproducible polymerization method to achieve stable production of poly(ε-caprolactone-co-p-dioxanone) (PCLDX), scale-up the filament fabrication to produce 1.75 mm filaments and optimize 3D printing process to manufacture scaffolds/devices for soft tissue engineering. PCLDX, with a higher degradation rate and better pliability compared to poly(ε-caprolactone) (PCL), was successfully synthesized by reproducible copolymerization of ε-caprolactone (CL) and p-dioxanone (DX). The synthesized PCLDX exhibited a polymer composition of 85 mol% CL : 15 mol% DX, molar mass around 40 kg∙mol-1, dispersity around 1.8, and relatively low melting point around 45 ℃. From PCLDX particles to final scaffolds, two processes, including filament fabrication and scaffold manufacturing, were designed and optimized. For the filament fabrication process, low extrusion temperature (65 and 80 ℃) and low extrusion speed (100 cm∙min-1) were applied to save energy and minimize degradation. PCLDX filaments with an even diameter of 1.75 mm were fabricated using suitable particle sizes (diameter of 3-4 mm) and a cooling method (mixture of water and dry ice, 0℃). The obtained filaments exhibited lower young’s modulus (25% lower than PCL), consistent thermal properties, good surface quality, and printability. The thermal degradation of PCLDX during the process was negligible, and the molar mass was kept almost unchanged. The process has been scaled up to produce high amounts of PCLDX filaments, whose productivity rate reached up to 140 g∙h-1. For the scaffold manufacturing process, porous scaffolds were manufactured by feeding manually and printing slowly (5 mm/s). The printability was assessed and validated using produced PCL/PCLDX filaments and commercial PCL filaments. The optimized printing protocol maintained the molar mass and dispersity of the material. The produced scaffolds possessed consistent thermal properties independent on polymer batches and good surface quality. The optimized printing protocol was also successfully applied to print complicated prototypes, such as meniscus and knee prosthesis for potential biomedical applications.

La fusion des myoblastes est une étape cruciale pour une bonne formation musculaire pendant l'embryogenèse et après une blessure à l'âge adulte. Le système génétique simpliste des mouches a été largement utilisé dans le passé pour identifier les acteurs essentiels impliqués dans la fusion des myoblastes. Chez la drosophile, la protéine d'échafaudage Antisocial (Ants)/Rols7 joue un rôle essentiel dans la fusion des myoblastes en connectant les protéines de surface d'adhésion cellulaire au cytosquelette. Même si la plupart des voies moléculaires régissant la fusion des myoblastes sont évolutives conservées entre les mammifères et les mouches, les contributions relatives de Tanc1 et Tanc2, les orthologues mammifères de Ants/Rols7, dans la fusion de myoblastes n'ont pas été établies. Le premier objectif de la thèse était d'évaluer les contributions potentielles de Tanc1 et Tanc2 dans la fusion de myoblastes en utilisant la lignée cellulaire de myoblastes murins C2C12 comme modèle de différenciation et de fusion de myoblastes. Nous avons constaté que l'expression de Tanc1 et Tanc2 n'est pas modulée lors de la différenciation C2C12, mais que les deux échafaudages sont enrichis au niveau du cortex lors de la prolifération des myoblastes. De plus, le knockdown de Tanc1 ou Tanc2 a altéré la fusion des myoblastes sans affecter la différenciation des myoblastes. Notamment, l'expression du défaut de fusion humain entièrement restauré Tanc1 ou Tanc2 observé dans les cellules C2C12 épuisées pour Tanc1 ou Tanc2 suggérant qu'un niveau seuil de leur expression est critique pour une fusion efficace des myoblastes. De plus, ni Tanc1 ni Tanc2 n'ont pu se substituer à Ants/Rols7 lors de la fusion des myoblastes chez la drosophile, ce qui suggère que différents acteurs pourraient être impliqués dans la régulation de la fusion des myoblastes chez les mammifères. Le deuxième objectif de la thèse était de caractériser davantage le rôle de Tanc1 et Tanc2 dans la fusion de myoblastes en utilisant des modèles murins de souris. À cette fin, des souris knock-out Tanc1 totales (Tanc1 KO) et des souris knock-out Tanc2 conditionnelles (Tanc2 cKO) ont été générées. Bien que les souris Tanc2 KO aient été précédemment signalées comme étant mortelles sur le plan embryonnaire, nous rapportons ici que ces souris sont viables contrairement à ce qui a été rapporté. L'expression de Tanc1 et Tanc2 a été détectée dans les somites ainsi que dans les fibres musculaires primaires. L'analyse du phénotype musculaire au stade embryonnaire a révélé une différenciation normale des somites et la formation de fibres musculaires chez les souris Tanc1 KO et Tanc2 cKO. De plus, lors de l'analyse au stade adulte, aucune différence dans la section transversale des fibres musculaires entre les souris de type sauvage et les souris mutantes n'a été détectée. Cela pourrait-il impliquer une redondance potentielle entre Tanc1 et Tanc2 dans la régulation de la myogenèse ? Pour répondre à cette question, des souris double knockout Tanc1 et Tanc2 sont actuellement en cours de génération. En conclusion, nous avons identifié dans cette étude un nouveau rôle pour les protéines d'échafaudage Tanc1 et Tanc2 dans la fusion de myoblastes chez les mammifères. L'identification de nouveaux acteurs essentiels dans la fusion des myoblastes nous rapproche de sa compréhension et de son ciblage thérapeutique à long terme. / Myoblast fusion is a crucial step for proper muscle formation during embryogenesis and after in injury during adulthood. The simplistic genetic system of flies has been extensively used in the past to identify essential players involved in myoblast fusion. In Drosophila, the scaffold protein Antisocial (Ants)/Rols7 plays an essential role in myoblast fusion by connecting the cell adhesion surface proteins to the cytoskeleton. Even though most molecular pathways governing myoblast fusion are evolutionary conserved between mammals and flies, the relative contributions of Tanc1 and Tanc2, the mammalian orthologs of Ants/Rols7, in myoblast fusion have not been established. The first aim of the thesis was to assess the potential contributions of Tanc1 and Tanc2 in myoblast fusion by using the murine myoblast C2C12 cell line as a model for myoblasts differentiation and fusion. We found that Tanc1 and Tanc2 expression is not modulated during C2C12 differentiation, but that both scaffolds are enriched at the cortex during myoblast proliferation. Furthermore, the knockdown of either Tanc1 or Tanc2 impaired myoblast fusion without affecting myoblast differentiation. Notably, the expression of human Tanc1 or Tanc2 fully restored fusion defect observed in C2C12 cells depleted for Tanc1 or Tanc2 suggesting that a threshold level of their expression is critical for efficient myoblast fusion. Furthermore, neither Tanc1 nor Tanc2 could substitute for Ants/Rols7 during Drosophila myoblast fusion suggesting that different players might be involved in regulating myoblast fusion in mammals. The second aim of the thesis was to further characterize the role of Tanc1 and Tanc2 in myoblast fusion by using murine mice models. For this purpose, total Tanc1 knockout mice (Tanc1 KO) and conditional Tanc2 knockout mice (Tanc2 cKO) were generated. Although Tanc2 KO mice were previously reported to be embryonically lethal, we report here that those mice are viable contrary to what has been reported. Tanc1 and Tanc2 expression was detected in the somites as well as in the primary muscle fibers. Analysis of the muscle phenotype at the embryonic stage revealed normal somites differentiation and muscle fiber formation in both Tanc1 KO and Tanc2 cKO mice. Furthermore, when analyzed at the adult stage, no difference in the cross-sectional area of the muscle fibers between wild-type mice and mutant mice was detected. Could this imply a potential redundancy between Tanc1 and Tanc2 in regulating myogenesis? To answer this question, Tanc1 and Tanc2 double knockout mice are currently being generated. In conclusion, we identified in this study a novel role for the scaffold proteins Tanc1 and Tanc2 in myoblast fusion in mammals. Identifying new and essential players in myoblast fusion brings us a step closer to understanding it and on the long run target it therapeutically.

Les organismes vivants, qu'ils soient simples ou complexes, ont acquis des stratégies pour s'adapter aux changements environnementaux. Ces changements correspondent à un large éventail de signaux chimiques, physiques ou mécaniques qui doivent être transmis en messages intracellulaires. Dans la cellule, des réseaux de signalisation sont modulés avec une grande précision pour transmettre ces messages et générer une réponse cellulaire appropriée. Les protéines d'échafaudage jouent un rôle crucial dans la sélectivité et la modulation spatio-temporelle de la transduction du signal. Par divers mécanismes moléculaires, elles médient l’organisation de complexes multimoléculaires impliqués dans plusieurs processus biologiques. CNK est une protéine d'échafaudage découverte par le biais d’études génétiques chez la drosophile où elle agit comme modulateur positif de la signalisation RAS/MAPK. Cependant, les fonctions physiologiques des homologues de CNK de mammifères (CNK1, CNK2 et CNK3) et leurs contributions aux pathologies humaines sont mal caractérisées. De plus, il existe peu d’évidences rapportant leur implication dans la signalisation RAS/MAPK. Elles ont plutôt été associées à des voies de signalisation contrôlées par les guanosine triphosphatases (GTPases) des familles ARF et RHO. Dans un premier manuscrit, nous avons montré que CNK2 est requise pour la migration et l'invasion des cellules cancéreuses en couplant le récepteur tyrosine kinase (RTK) prométastatique AXL à l'activation de la GTPase ARF6. D'un point de vue mécanistique, la signalisation induite par AXL favorise le recrutement de CNK2 à la membrane plasmique de manière dépendante de PI3K. Ensuite, CNK2 promeut l’activation d’ARF6 via son interaction aux ARF Guanosine exchange factors (GEFs) cytohésines et à la protéine adaptatrice SAMD12. Nous démontrons également qu’ARF6 coordonne l'activité des GTPases RAC1 et RHOA. Enfin, l'ablation génétique de CNK2 ou SAMD12 réduit considérablement les lésions métastatiques hépatiques et pulmonaires dans un modèle de xénogreffe de souris. Dans une série d’expériences de BioID supplémentaires utilisant le mutant gain-de-fonction ARF6 Q67L, nous avons identifié PLD1 et ITGB1 comme candidats potentiels pouvant médier la signalisation RAC1 et RHOA en aval d’ARF6. Dans une autre série d’expériences, nous avons caractérisé l'interaction entre les CNKs et la sous-famille des kinases Misshapen (MSN). Les trois membres de cette sous-famille, MAP4K4, TNIK et MINK1, ont été identifiés comme principaux interacteurs proximaux de CNK2A et CNK3 dans les expériences de BioID. Toutefois, leur interaction ne semble pas être impliquée dans la fonction promigratoire de CNK2A. Par des expériences de cartographie, nous démontrons que les domaines CRIC et DUF1170 de CNK2/3 et la région coiled-coil de MAP4K4 sont importants pour leur interaction. Nos travaux suggèrent également que SAMD10 compétitionne avec MAP4K4 pour se lier à CNK2 et que SAMD10/12 modulent la stabilité de CNK2. Enfin, nos résultats préliminaires suggèrent que MAP4K4 induit la phosphorylation de CNK2/3. Cependant, la pertinence biologique de ces évènements reste à déterminer. Dans l'ensemble, nos travaux révèlent une fonction inattendue de CNK2 dans la régulation de la motilité des cellules cancéreuses et identifient une nouvelle voie de signalisation qui pourrait être ciblée pour limiter les métastases. En outre, nos travaux identifient plusieurs pistes pour approfondir le rôle de CNK dans les cellules de mammifères. / All living organisms, whether simple or complex, have acquired sophisticated strategies to adapt to their changing environment. These environmental changes correspond to a breadth of chemical and mechanical signals that need to be transmitted into intracellular information. In cells, dense signalling networks are put into place and modulated with great precision to transmit messages and generate appropriate cellular responses. Scaffolding proteins play a crucial role in the selectivity and spatiotemporal modulation of signal transduction. Through various molecular mechanisms, they mediate the organization of multimolecular complexes implicated in various biological processes. CNK is a scaffolding protein discovered through genetic studies in drosophila where it acts as an important positive regulator of the highly oncogenic RAS/MAPK pathway. In contrast, the physiological functions of human CNKs and their roles in human diseases are poorly characterized. Moreover, evidence supporting their requirement for RAS/MAPK signalling remains sparse. Rather, they have been linked to signalling pathways controlled by the ARF and RAS homologous (RHO) subfamilies of GTPases. In a first manuscript, we found that mammalian CNK2 promotes cancer cell migration and invasion by coupling the pro-metastatic RTK AXL to downstream activation of ARF6 GTPase. Mechanistically, we showed that AXL signalling induces PI3K-dependent recruitment of CNK2 to the plasma membrane where it stimulates ARF6 via its interaction with the cytohesin ARF GEFs and the adaptor protein SAMD12. We also showed that ARF6 coordinates RAC1 and RHOA GTPase activity. Finally, the genetic ablation of CNK2 or SAMD12 potently reduces liver and lung metastatic lesions in a mouse xenograft model. In a series of supplemental BioID experiments using the gain-of-function ARF6 Q67L mutant, we identified PLD1 and ITGB1 as potential candidates that could mediate RAC1 and RHOA signalling downstream of ARF6. In another study, we characterized the interaction between CNKs and the MSN subfamily of kinases. The three members of this subfamily, namely MAP4K4, TNIK and MINK1, were identified as top proximal interactors of CNK2A and CNK3 in the BioID experiments. However, their interaction does not appear to be involved in the pro-migratory function of CNK2A. Through mapping experiments, we found that the CRIC and DUF1170 domains of CNK2 and CNK3 and the coiled-coil region of MAPK4K4 are important for their interaction. In addition, we found that SAMD10 competes with MAP4K4 for binding to CNK2 and that SAMD10/12 proteins also modulate CNK2 stability. Finally, our preliminary results suggest that MAP4K4 induces CNK2/3 phosphorylation. However, the biological relevance of these interactions and phosphorylation events remains to be addressed. Overall, our work uncovers an unanticipated function of CNK2 in regulating cancer cell motility and identifies a novel signalling pathway that could be targeted to restrain metastasis. Moreover, it identifies several avenues for further study into CNK function in mammalian cells.

<p>This investigation delineates the optimal synthesis and characterization of innovative epoxy-carbon nanotube (CNT) nanocomposite filaments via electrospinning. Electrospinning thermosetting materials such as epoxy resins presents significant challenges due to the polycationic behavior arising from intermolecular noncovalent interactions between epoxide and hydroxyl groups, resulting in a substantial increase in solution surface tension. In this study, electrospinning submicron epoxy filaments was achieved through partial curing of epoxy via a thermal treatment process in an organic polar solvent, circumventing the necessity for plasticizers or thermoplastic binders. The filament diameter can be modulated to as low as 100 nm by adjusting electrospinning parameters.</p> <p><br></p> <p>Integrating a minimal amount of CNT into the epoxy matrix yielded enhanced structural, electrical, and thermal stability. The CNTs were aligned within the epoxy filaments due to the electrostatic field present during electrospinning. The modulus of the epoxy and epoxy-CNT filaments were determined to be 3.24 and 4.84 GPa, respectively, resulting in a 49% improvement. Epoxy-CNT nanofibers were directly deposited onto carbon fiber reinforced polymer (CFRP) prepreg layers, yielding augmented adhesion, interfacial bonding, and significant mechanical property enhancements. The interlaminar shear strength (ILSS) and fatigue resistance demonstrated a 29% and 27% increase, respectively, under intense stress conditions. Up to 45% of the Barely Visible Impact Damage (BVID) energy absorption was increased. In addition, the strategic incorporation of CNT (multi-walled) networks between the layers of CFRP resulted in a significant increase in thermal and electrical conductivities.</p> <p>This study also introduces a scalable fabrication procedure to address large volume processing, reproducibility, accuracy, and electrospinning safety. Electric fields of the experimental multi-nozzle setups were simulated to elucidate the induced surface charges responsible for the Taylor cone formation of the epoxy-CNT solution droplet on the nozzle tips. Electrospinning parameters were subsequently optimized for the multi-nozzle system and analyzed alongside simulated data to improve stability and synthesize fibers with smaller diameters.</p> <p><br></p> <p>Smaller diameter epoxy-CNT nanofibers proved critical as CNTs maintained alignment within the nanofibers when compared to larger diameter nanofibers. This research examines the impact of effective parameters on the diameter of electrospun epoxy-CNT nanofibers using artificial neural networks (ANNs). Consequently, employing a genetic algorithm (GA) and Bayesian optimization (BO) methods enable accurate prediction of epoxy-CNT nanofiber diameters prior to electrospinning. The presented models could aid researchers in fabricating electrospun thermosetting and thermoplastic scaffolds with specified fiber diameters, thereby tailoring these scaffolds for specific applications.</p>

Transforming growth factor beta 3 (TGF3) promotes tenogenic differentiation and may enhance tendon regeneration in vivo. This study aimed to apply TGF3 absorbed in decellularized equine superficial digital flexor tendon scaffolds, and to investigate the bioactivity of scaffold-associated TGF3 in an in vitro model. TGF3 could effectively be loaded onto tendon scaffolds so that at least 88% of the applied TGF3 were not detected in the rinsing fluid of the TGF3-loaded scaffolds. Equine adipose tissue-derived multipotent mesenchymal stromal cells (MSC) were then seeded on scaffolds loaded with 300 ng TGF3 to assess its bioactivity. Both scaffold-associated TGF3 and TGF3 dissolved in the cell culture medium, the latter serving as control group, promoted elongation of cell shapes and scaffold contraction (p < 0.05). Furthermore, scaffold-associated and dissolved TGF3 affected MSC musculoskeletal gene expression in a similar manner, with an upregulation of tenascin c and downregulation of other matrix molecules, most markedly decorin (p < 0.05). These results demonstrate that the bioactivity of scaold-associated TGF3 is preserved, thus TGF3 application via absorption in decellularized tendon scaffolds is a feasible approach.

Abstract  Lack of clinical relevance is assumed to be the main reason behind the high failure rate of medical drugs in the very initial phases of clinical trials. Clinical relevance is difficult to achieve with current tools as they lack the biological and physiological cues found in vivo. Microfluidics, the knowledge of fluid manipulation in small channels, has proven to be a promising science to bridge the gap between the current in vitro and the real in vivo features. In this thesis, a scaffold for the growth of spheroids inside a microfluidic device for potential drug screening was developed. Firstly, the surface of a microfluidic device was coated with the polymers cellulose nanofibrils, polyallylamine hydrochloride, and polyethyleneimine using the Layer-by-Layer technique to achieve an even surface coverage. Here, different chip designs, polymer concentrations, and pressure directions were tested. It was decided that using a negative pressure direction with a polymer concentration of 50 mg/L in a chip design with micropillars was optimal and these conditions were then used for testing the spheroid formation. Secondly, spheroids were grown inside the microfluidic channels using different coatings: the previously mentioned polymer buildup, one non-coated channel, and one coated with attachment factor proteins. These three surface conditions were compared and it was shown that the polymer-based surface cover was indeed superior as a scaffold as it encouraged and promoted cell growth in the spheroid formation of liver cancer cells from the HepG2 cell line. Further development of this cellulose nanofibrils-coated microfluidic device displays a promising future for functioning as an in vitro 3D cell culture model that better mimics the close-to-cell microenvironments by imitating cell proliferation, cell-to-cell, and cell-to-extracellular matrix interactions. / Sammanfattning Den främsta orsaken bakom den höga antal misslyckade kliniska läkemedelsprövningar i de initiala faserna antas bero på brist på klinisk relevans. Klinisk relevans är mycket svår att uppnå med dagens verktyg då de saknar de biologiska och fysiologiska förhållandena som återfinns in vivo. Mikrofluidik, kunskapen om vätskemanipulation i små kanaler har visat sig vara lovande vetenskap för att överbrygga klyftan mellan de nuvarande in vitro och de faktiska in vivo funktionerna. I detta arbete utvecklades en matris för sfäroider att växa på inuti en mikrofluidisk kanal för att potentiellt användas till läkemedelsscreening. Först användes Layer-by-Layer teknologi för att jämnt betäckta ytan inuti en mikrofluidisk kanal med polymererna cellulosananofibriller, polyallylamin hydroklorid samt polyetylenimin. Här testades olika designer på mikrofluidiska chip, polymerkoncentrationer samt tryckriktningar. Utifrån detta gick det att fastställa att negativt tryck med en polymerkoncentration på 50 mg/L i en chippdesign med mikropelare var optimal för en jämn ytbetäckning och dessa förhållanden användes sedan för att pröva sfäroidernas tillväxt. Härnäst testades därmed sfäroidernas tillväxt inuti mikrofluidiska kanaler under tre olika förhållanden: ett med polymerbetäckningen, ett utan betäckning och ett då ytan var täckt med proteiner med fästfaktorer. Dessa tre förhållanden jämfördes sedan med varandra och således gick det att konstatera att den polymerbaseradebetäckningen fungerade överlägset som matris för tillväxt av HepG2 lever cancer cell sfäroider eftersom den tycks främja dess tillväxt och bildning. Det pekar mot att ytterligare utveckling av denna cellulostäckta yta skulle innebära en lovande modell för in vitro 3D cellodling som bättre efterliknar den cellulära mikromiljön genom att imitera cellproliferation, interaktioner celler emellan samt mellan cell och extracellulär matrisen.