Tato diplomová práce se zabývá přípravou nových kompozitů na bázi mikrofibrilované celulozy a multi-walls carbon nanotubes (MFC/MWCNTs). Tři různé metody byly použity pro modifikaci MWCNTs. Byl zkoumán vliv použitých modifikací na kvalitu MWCNTs suspense. Dále byly připraveny kompozity obsahující MFC a MWCNTs a vliv MWCNTs na mechanické a elektrické vlastnosti a morfologii byl zkoumán. MWCNTs suspense byly charakterizovány za použití UV-VIS spektrofotometrie, Rastrovacího elektronového mikroskopu (SEM) a Termogravimetrické analýzy (TGA). Elektrické vlastnosti byly měřeny pomocí Keithly Electrometer/High Resistivity Meter. Mechanické vlastnosti v tahu byly měřeny za použití Miniature Materials Tester a pro studium morfologie byl použit SEM. Žádný významný vliv MWCNTs na mechanické vlastnosti nebyl pozorován. Hodnoty získané z měření rezistivity vykazují typický perkolační trend a výrazného snížení rezistivity bylo dosaženo přidáním 1 – 2 wt.% MWCNTs. Nicméně hodnoty se velice liší pro horní a spodní stranu téhož vzorku. Ze získaných výsledků vyplývá, že klíčovým krokem ke zdokonalení vlastností materiálu jsou dobrá suspense MWCNTs a také dosažení vzájemné kompatibility obou složek.

The main topic of this Diploma thesis is the application of low-pressure low-temperature hydrogen plasma for the treatment model samples of rusted brass. Plasmachemical treatment of metallic artifacts is a relatively new way how to remove corrosion of artifacts. The temperature of an object should not exceed 150 °C during the treatment. Corrosion layers were prepared in an ammoniac corrosion atmosphere. The corrosion formation took two weeks. Energy Dispersive X-ray Microanalysis has shown that the corrosion layer was formed by carbon, oxygen, copper, zinc, and lead. The corrosion layers were blue-colored with white crystals on the surface. Except those two colors, brown color was observed on corrosion layers, too. The plasma reactor was a quartz tube with outer copper electrodes and supplied by the RF source of 13.54 MHz. The reactive atomic hydrogen was formed in plasma discharge. This atomic hydrogen reacted with the corrosive layer containing oxygen. This reaction created an unstable OH radical, which emitted light in the region of 305–320 nm. This radiation was detected by the optical emission spectroscopy and it was applied as process monitoring quantity. Rotational temperature and intensity of OH radicals were determined from obtained data. The sample temperature was measured by thermocouple installed inside the sample volume. Rusted samples were treated by low-pressure low-temperature hydrogen plasma. 16 samples were treated at different conditions – plasma power was 100 W, 200 W, 300 W, and 400 W at continuous mode and pulse mode with duty cycle of 25 %, 50 %, and 75 %. The pressure was between 140–160 Pa at hydrogen flow rate of 50 sccm. Samples after plasmachemical treatment were grey colored with white crystals on their surface. Corrosion layers were removed by spatula. The corrosion layers of some samples were easy removable, some others were difficult. Energy Dispersive X-ray Microanalysis, which was carried out after the treatment of 2 selected samples (400 W, 50% pulse mode and 400 W, 75% pulse mode), showed different amounts of carbon, oxygen, copper, zinc, and lead compared to the rusted sample. Other elements in the treated layer were silicon, sulfur, chlorine, and fluorine.

This diploma thesis is focused to the plasma chemical reduction of model corrosion layers prepared on bronze samples. Bronze was the main material for production of the subjects in Bronze Age. First, it was very rare, and therefore was used only for making jewellery and other decorative subjects. Later, the objects of daily use and weapons were produced of bronze. These objects are found and it is necessary to restore him and preserve the cultural heritage for future generations. The research and the optimalization of plasmochemical reduction of model corrosion layers on bronze samples contributes to this. A metallographic grinder was used to create a defined surface, first with the sandpaper P 280 and then after sample 90 degree rotation with the sandpaper P 600. This ensured uniform surface at all bronze samples that is necessary to provide the same corrosion conditions. The grinded samples were washed by ethanol and dried by hot air stream. To prevent contact with the surrounding atmosphere and successive initiation of corrosion, the samples were stored in lockable polyethylene bags. This step was followed by the preparation of model corrosion layers. Hydrochloric and sulfuric acids were chosen as corrosive environments. Petri dish containing 20 ml of the selected acid was placed at the bottom of the desiccator. Samples were placed to the ceramic grate, over the dish, and they were corroded (in vapours of hydrochloric acid for 34 days and in vapours of sulfuric acid for 27 days). The corroded samples were treated using low-pressure hydrogen plasma excited by RF generator. Treatment of samples was carried out in quartz cylindrical reactor (length of 90 cm, inner diameter 9.5 cm) with copper electrodes placed outside. The pressure in the reactor was ranged around 160 Pa at hydrogen flow rate of 50 sccm during the experiments. The continuous and pulse modes (duty cycle of 25%, 50% or 75%) at peak power of 50–300 watts were used for the treatment of 90 minutes duration. The plasma treatment was monitored by optical emission spectroscopy of OH radical using compact Ocean Optics HR4000 spectrometer. Its integral intensity is proportional to the corrosion layer removal. The rotational temperatures of plasma were calculated using selected OH rotational lines, too. The sample temperature during the treatment was measured by thermocouple installed inside the additional non-corroded samples. The reduction of corrosion layer is successful when the maximum of relative intensity of OH radicals is produced and follow gradual decline. The samples which corroded in vapours of sulphuric acid and were treated in pulse modes with duty cycle of 25 % or with delivered power of 50 W has produced no maximum. To the remain samples the maximum although were observed, but reduced corrosion products on the surface were very cohesive. The maximum of relative intensity of OH radicals was observed at all samples corroded in vapours of hydrochloric acid. But there is problem with temperature of sample during experiment. The samples which layer of corrosion product was after experiment incoherent produced the layer of deposit tin. This effect formation at a higher temperature of sample during experiment and therefore with greater deliver energy.

Signal processing from modern microscopes for local characteristics of materials Image processing is more and more important for the advancement of image evaluation taken from microscopes. This thesis engages the problem of artefact detection and removal from images taken by electron microscope, more accurately by low energy electron microscopy (LEEM). It then offers a possible course of processing such images by edge detection and its theoretical use. These operations are all made in MatLAB language.

This thesis concentrates on the methodology of semiconductor samples preparation for low voltage scanning electron microscopy. In the first part a detailed theory of sample imaging using electron beam and difference between classical scanning electron microscopy (SEM) and low voltage scanning electron microscopy (LVSEM) is described. It is given a description of a contrast formation in SEM and LVSEM and theories describing a contrast formation of differently doped semiconductors. The second part contains experimental data. The advantages and disadvantages of cleavage and focused ion beam (FIB) milling as sample preparation techniques are discussed. FIB was found as the best method for sample preparation for the analysis of precisely defined location on the sample. It is necessary to use the lowest possible FIB accelerating voltage for final polishing, ideally 1 kV.

Les dystrophies musculaires sont un groupe de pathologies génétiques qui cause une faiblesse et une perte progressive des muscles squelettiques. Parmi elles, la dystrophie des ceintures de type 2B (LGMD2B) est caractérisée par des mutations dans le gène de la dysferline, entrainant de sévères dysfonctionnements, dont un défaut de réparation membranaire. Les ruptures de la membrane plasmique sont des évènements physiologiques induits par des contraintes mécaniques, comme lors de la contraction des fibres musculaires. Les cellules eucaryotes possèdent donc une machinerie protéique assurant une réparation rapide de larges ruptures membranaires. La liste exhaustive des composants de la machinerie de réparation et leur mode d’action reste à établir.Les annexines (Anx) sont de petites protéines solubles, au nombre de 12 chez les mammifères, qui partagent la propriété de lier les membranes exposant des phospholipides chargés négativement en présence de Ca2+. De nombreuses études ont montré l’implication de certaines Anx (AnxA1, A2, A4, A5, A6 et A7) dans la réparation membranaire de différents types cellulaires (muscle, cancer, endothélium…) et dans différentes espèces (souris, poisson-zèbre, homme…). La présence des Anx dans le muscle squelettique, et la participation de plusieurs membres de cette famille dans la réparation membranaire, soulèvent la question d’un rôle collectif de ces protéines dans la protection et la réparation des ruptures du sarcolemme.Les objectifs de ce travail ont été 1) d’identifier les Anx impliquées dans la réparation membranaire des cellules musculaires squelettiques humaines, 2) développer une stratégie de microscopie corrélative pour étudier le site de rupture et la distribution subcellulaire des Anx à haute résolution, 3) élucider la fonction des Anx dans le mécanisme de réparation, et 4) analyser les Anx dans des cellules musculaires dystrophiques. Avec des approches en biologie cellulaire et moléculaire, et en microscopie de fluorescence et électronique, nous avons donc étudié le comportement des Anx lors d’un dommage du sarcolemme.Nous avons ainsi montré que les AnxA1, A2, A4, A5 et A6 sont exprimées dans les myoblastes et les myotubes humains, et sont recrutées au site de rupture quelques secondes après le dommage, en formant une structure dense à l’extérieur du myotube endommagé appelé domaine « cap ». De plus, nous avons pu déterminer l’ordre relatif de recrutement des Anx au site membranaire endommagé. Les premières Anx à être recrutées sont l’AnxA1, suivies des AnxA6 et A5, les moins sensibles au Ca2+. Les dernières Anx recrutées sont les plus sensibles au Ca2+, les AnxA4 puis A2, qui semblent se lier à des vésicules intracellulaires initialement éloignées du site de rupture. Nous avons également étudié l’ultrastructure du site de rupture à haute résolution. Nos résultats ont révélé que le domaine « cap » correspondait à une accumulation de matériel membranaire qui est associé au Anx. En s’appuyant sur nos résultats et la littérature, nous avons proposé un modèle de réparation membranaire, impliquant les AnxA1, A2, A4, A5 et A6, dans les cellules musculaires squelettiques humaines. Nous nous sommes également intéressés à l’expression des Anx dans des lignées de cellules musculaires dystrophiques issues de patients atteints de dystrophies musculaires des ceintures de type 2B (déficients en dysferline) et 1C (déficients en cavéoline-3). Nous avons ainsi montré que le contexte pathologique perturbait l’expression de certaines Anx, sans en modifier leur localisation subcellulaire.En conclusion, ce travail de thèse montre que plusieurs membres de la famille des Anx sont impliqués dans la réparation membranaire, et agissent de concert pour réparer un dommage de la membrane plasmique. L’implication des Anx dans d’autres pathologies, comme le cancer et la pré-éclampsie, renforce l’intérêt de leur étude dans les processus de réparation membranaire et en font une cible thérapeutique potentielle. / Muscular dystrophy encompasses a group of genetic disorders which cause progressive weakness and wasting of skeletal muscle. Among them, limb girdle muscular dystrophy type 2B (LGMD2B) is characterized by mutations in the dysferlin gene leading to several dysfunctions including a failure in cell membrane repair process. Cell membrane disruption is a physiological phenomenon induced by mechanical stress, such as contraction of muscle fibers. Thus, eukaryotic cells have a repair protein machinery ensuring a rapid resealing of large cell membrane ruptures. The exhaustive list of components of the repair machinery and their interplay remain to be established.The annexin (Anx) family consists of twelve soluble proteins in mammals and share the property of binding to membranes exposing negatively charged phospholipids in a Ca2+-dependent manner. Several studies have shown the involvement of Anx (AnxA1, A2, A4, A5, A6 and A7) in membrane repair of different cell types (muscle, cancer, endothelium…) in different species (mouse, zebrafish, human…). The presence of different Anx in skeletal muscle, together with the participation of several members of the Anx family in membrane repair processes, raise the question of a collective role of these proteins in the protection and repair of sarcolemma injuries.The PhD project aimed 1) at identifying Anx that are essential for membrane repair in human skeletal muscle cells, 2) developing a correlative light and electron microscopy to study the wounded site and the Anx distribution at high resolution, 3) elucidating the function of each Anx in this process and 4) analyzing Anx in dystrophic muscle cells. Using approaches including cellular and molecular biology, fluorescence microscopy and transmission electron microscopy, we studied the behavior of Anx during sarcolemma damage.We showed that AnxA1, A2, A4, A5 and A6 are expressed in human myoblasts and myotubes, and are recruited at the disruption site within seconds after the sarcolemmal damage, forming a dense structure outside the cell, named the “cap” domain. Furthermore, we determined the relative order of Anx recruitment at the disruption site. The first Anx recruited are AnxA1, followed by AnxA6 and A5, the less sensitive to Ca2+. The last Anx recruited are the most sensitive to Ca2+, AnxA4 and A2. AnxA2 and A4 are instead rapidly recruited to intracellular vesicles present deeper in the cytosol. We also studied the ultrastructure of the disruption site at high resolution. Our results revealed that the “cap” domain correspond to a disorganized membrane structure, associated with the Anx. Thanks to our results and the literature, we have proposed a model for membrane repair involving Anx in human skeletal muscle cells. We also looked at the expression of Anx in dystrophic muscle cell lines from patients with limb girdle muscular dystrophy type 2B (dysferline deficient) and 1C (deficient in cadaveoline-3). We have thus shown that the pathological context disrupts the expression of some Anx, without altering their subcellular location.In conclusion, this work shows that several members of the Anx family are involved in membrane repair and act together to repair plasma membrane damage. The implication of Anx in other pathologies, such as preeclampsia or cancer, reinforces the interest of their study in the process of membrane repair.

Le noyau est un organite caractéristique des cellules eucaryotes et les propriétés mécaniques de ce dernier jouent un rôle essentiel dans le comportement de la cellule, notamment sa motilité, sa polarité et sa survie. Le noyau est entouré par une enveloppe comprenant une membrane interne et une membrane externe, ainsi que de nombreuses protéines. Mes objectifs de thèse étaient de comprendre des mécanismes moléculaires déficients dans deux types de maladies génétiques causées par des mutations dans les lamines: la dystrophie musculaire d’Emery-Dreifuss et les syndromes de type progéroïde.Dans un premier temps, nous avons montré que l’émerine s’auto-associe in vitro et en cellules (Herrada et al. ACS Chem. Biol. 2015). J’ai ensuite étudié la structure des oligomères d’émerine, déterminé le fragment protéique minimal nécessaire à la formation de ces oligomères et décrit l’impact de mutations de l’émerine, causant une dystrophie musculaire d’Emery-Dreifuss, sur son auto-assemblage (Samson et al. Biomol NMR Assign. 2016 ; Samson et al. FEBS J. 2016). Puis, j’ai montré que seule cette forme auto-assemblée de l’émerine est capable d’interagir avec la lamine A et que la phosphorylation de l’émerine par la kinase Src, observée suite à un stress mécanique, régule cette interaction entre l’enveloppe nucléaire et le nucléosquelette.Pour finir, j’ai montré que la forme monomérique de l’émerine est capable de former un complexe ternaire avec BAF et la lamine A. Après avoir mesuré les affinités protéine-protéine au sein de ce complexe, identifié les fragments minimaux des différentes protéines permettant de former ce complexe et mis au point un protocole robuste de purification de ce complexe, j’ai pu obtenir des cristaux de ce complexe dans plusieurs conditions. Par la suite, nous avons pu résoudre la structure de ce complexe par remplacement moléculaire avec une résolution de 2 Å. Enfin, j'ai montré que les mutations dans les lamines de type A provoquant des syndromes de type progéroïde pouvaient altérer l'interaction avec BAF in vitro, et nos collaborateurs, l'équipe du Dr B. Buendia (Paris Diderot), ont montré que ces mêmes mutations induisaient une diminution significative de la proximité entre la lamine A et BAF dans les cellules HeLa. Un article, où je suis premier auteur, vient d’être soumis au journal NSMB. / The nucleus is an organelle characteristic of eukaryotic cells and its mechanical properties play an essential role in the behavior of the cell, in particular its motility, polarity and survival. It is surrounded by an envelope comprising an inner membrane and an outer membrane, as well as a large number of proteins. These proteins are either anchored at the nuclear membrane, as emerin, or form a filament meshwork lining the inner nuclear membrane, as lamins. My thesis objectives were to understand molecular mechanisms deficient in two types of genetic diseases caused by mutations in inner nuclear envelope proteins: Emery-Dreifuss muscular dystrophy, associated to mutations in emerin and A-type lamins, and progeroid syndromes caused by mutations in A-type lamins.First, we showed that the emerin protein self-assembles in vitro and in cells (Herrada, Samson et al., ACS Chem. Biol., 2015). I then studied the structure of emerin oligomers, determined the minimal protein fragment necessary for the formation of these oligomers, identify residues forming the structural core of these oligomers by solid-state NMR in collaboration with the group of Prof A. Lange (FMP Berlin), and described the impact of emerin mutations causing Emery-Dreifuss muscular dystrophy on emerin self-assembly (Samson et al., Biomol. NMR Assign. 2016, Samson et al., FEBS J. 2017). Then, I observed, mainly using solution-state NMR, that only the self-assembled form of emerin is able to interact with A-type lamin tail, and that mutants causing Emery-Dreifuss muscular dystrophy and unable to self-assemble are also defective in A-type lamin binding. I also obtained preliminary data showing that phosphorylation of emerin by the Src kinase, observed after a mechanical stress in purified nuclei, regulates the interaction between self-assembled emerin and A-type lamins.Finally, I showed that the monomeric form of emerin is able to form a ternary complex with A-type lamin tail through the chromatin-associated protein Barrier-to-Autointegration Factor (BAF). After having measured the protein-protein affinities within this complex, identified the minimal protein fragments involved in the complex and developed a robust protocol for purification of this complex, I was able to obtain crystals under several conditions. Subsequently, I solved the 3D structure of this complex by molecular replacement at a resolution of 2 Å. Finally, I showed that mutations in A-type lamins causing autosomal recessive progeroid syndromes impair interaction with BAF in vitro, and our collaborators at Univ. Paris Diderot, the team of Dr B. Buendia, showed that these same mutations induce a significant decrease in the proximity between lamin A and BAF in HeLa cells. An article with me as a first author is in preparation that reports all these new data.

Les bactériophages neutralisent les systèmes de défense et détournent les fonctions vitales de leur hôte pour favoriser leur multiplication. Les gènes de phages qui gouvernent cette prise de contrôle de l’hôte restent mal connus, pourtant leur caractérisation présente un intérêt majeur pour mettre à jour des fonctions bactériennes spécifiquement ciblées par les phages et pour concevoir de nouveaux agents antibactériens.Le phage T5 injecte son ADN dans la bactérie Escherichia coli en deux étapes. Seuls les gènes précoces codés par 8% du génome entrent dans la cellule et le transfert s’arrête. Leur expression induit la dégradation du chromosome de l’hôte et l’inactivation de ses systèmes de restriction et de réparation de l’ADN. Après quelques minutes, le reste de la molécule d’ADN est injecté, ce qui permet la production de nouveaux phages. Deux gènes précoces A1 et A2 ont été identifiés comme essentiels pour la reprise du transfert de l’ADN et A1 est également nécessaire pour induire la dégradation de l’ADN de l’hôte. A1 et A2 sont les deux seuls gènes connus pour être impliqués dans la régulation de ce système original d’infection, mais leur fonction n’a jamais été identifiée.Ma thèse porte sur la caractérisation fonctionnelle et structurale des protéines A1 et A2. J’ai purifié A1 et démontré in vitro qu’elle avait une activité DNase dépendante du manganèse. Sa structure atomique a été résolue par cryomicroscopie électronique à 3.01 Å de résolution, montrant une organisation octamérique de symétrie D4 inédite pour une DNase. Chaque monomère (61kDa) contient un domaine exonuclease dont le site actif lie deux ions Mn2+ et qui s’apparente au site catalytique des domaines exonucléases de la DNA polymerase II et des DNAses associées aux systèmes de recombinaison homologue et de réparation de l’ADN comme Mre11. En construisant différents mutants de A1, j’ai identifié certains acides aminés essentiels pour l’activité catalytique et, par des expériences de complémentation fonctionnelle, j’ai montré que cette activité était indispensable pour l’infection. L’ensemble de ces résultats suggèrent que A1 est la DNase, jusqu’ici inconnue, responsable de la dégradation massive du génome de l’hôte au tout début de l’infection. Enfin, j’ai observé que la production de A1 pendant l’infection induit une forte activité recombinase. De nombreux autres bactériophages qui n’appartiennent pas à la famille des T5virus produisent également une protéine similaire à A1 dont la fonction n’a jamais été identifiée. Ce travail est un premier pas vers la compréhension de son rôle dans le mécanisme général d‘infection par les phages. Une deuxième partie de cette thèse porte sur la caractérisation structurale de A2. Des recherches de similarité indiquent la présence d’un domaine Helix-Turn-Helix typique des régulateurs transcriptionnels. J’ai purifié A2 et montré que cette protéine de 14 kDa est un dimère en solution. La caractérisation des propriétés biochimiques de A2 a permis de débuter l’étude de sa structure par RMN.Les résultats de ma thèse ont révélé la structure originale d’une DNase de bactériophage qui contrôle la dégradation du génome bactérien et la régulation du transport de l’ADN viral au début du cycle infectieux. Ces résultats soulèvent des questions intrigantes : comment l’ADN de T5 est-il protégé de l’activité DNase de A1 ? Comment A1 et A2 interagissent-elles lors des étapes de prise de contrôle de l’hôte ? / Bacteriophages defeat bacterial defences and hijack host cell machineries to establish a favourable environment for their multiplication. Early-expressed viral genes that govern host takeover are highly diverse from one phage to another and most of them have no assigned function. They thus represent a pool of novel genes whose products potentially subvert bacterial cell vital functions and could help in designing new antibacterial strategies.T5 phage uses a unique 2-step mechanism to deliver its DNA into its host Escherichia coli. At the onset of the infection, only 8 % of the genome enter the cell before the transfer temporarily stops. Expression of the genes encoded by this DNA portion leads to host chromosome degradation and inactivation of host restriction and DNA mending systems. After a few minutes, T5 DNA transfer resumes, allowing further phage multiplication. A1 and A2 are early genes required for DNA transfer completion and A1 is also necessary to trigger host DNA degradation. A1 and A2 are the only two genes known to be involved in the regulation of this original infection system, but their function yet remains to be characterized.The objectives of this work were to characterize the function and structure of A1 and A2 proteins. I have purified the A1 protein and shown that it has a manganese-dependent DNase activity in vitro. Cryo Electron Microscopy at 3.01 Å resolution unravelled its structure, showing an octameric organization with a D4 symmetry, which is unprecedented for a DNase. Each monomer (61 kDa) carries an exonuclease domain harbouring an active site with two Mn2+ ions. This site is similar to those from the exonuclease domain of the DNA polymerase II and from DNases involved in DNA mending and recombination events like Mre11. I identified essential catalytic residues for the DNase activity and demonstrated that this activity is crucial for infection by engineering A1 mutant proteins and by doing functional complementation assays. Taken together, my results suggest that A1 could then be the elusive DNase responsible for the massive host genome degradation observed during T5 phage infection. Eventually, I uncovered a recombinase activity associated to A1 production during infection. Similar proteins to A1 with unknown functions are produced in several other bacteriophages outside of the T5virus family. This work is a first step towards understanding the role of this protein in the general mechanism of infection by bacteriophages. In a second part, I worked on the structural characterisation of A2 protein. Similarity searches revealed a helix-turn-helix domain typically found in transcriptional regulators. I purified and demonstrated the dimeric organisation of this 14-kDa protein in solution. This initial characterization of A2 has opened avenues for further NMR studies.During my Ph.D., I uncovered the structure of an original bacteriophage DNase that controls bacterial genome degradation and that regulates viral DNA transport at the beginning of the infectious cycle. These results open the intriguing question about the mechanism for T5 DNA protection from A1 DNase activity as well as about the interplay between A1 and A2 during the host takeover.

Le caoutchouc naturel (NR pour Natural Rubber) est une matière première indispensable à la fabrication de milliers de produits !Le choix du latex naturel tient principalement à ses propriétés physico-chimiques intrinsèques bien supérieures à celles des latex synthétiques. Industriellement, le NR est cependant rarement utilisé seul mais associé à des particules de renfort, appelées charges, pour former un matériau composite aux propriétés mécaniques grandement améliorées en particulier la résistance à l’usure.Des études récentes ont mis en évidence que la méthode conventionnelle consistant à introduire les charges sous forme de poudres fines au sein d’un bloc de NR solide ou fondu n’est pas la plus efficace. Une nouvelle approche consistant à mélanger les deux entités, NR et charges, en phase liquide avant séchage s’annonce prometteuse industriellement, mais la littérature à ce sujet est encore très limitée. Ce travail de thèse a visé à parfaire la compréhension des processus gouvernant les interactions NR-charges renforçantes en phase liquide. Pour ce faire nous avons (i) décrit les propriétés physico-chimiques de surface des particules NR en phase liquide, (ii) étudier les effets de la charge renforçante (en termes de taille, composition, fonctionnalisation de surface, concentration) et de la solution (ions valence) sur l'interaction NR-charge et (iii) quantifier les propriétés mécaniques des particules NR.Nous avons été en mesure d’identifier les paramètres clés qui permettent en phase aqueuse diluée, non seulement d’influencer l’interaction particule de NR-charge mais aussi de réguler la dynamique d'interaction et de contrôler la structure des hétéro-agrégats formés.Cette approche originale de l’hétérocoagulation NR-charge en phase liquide ouvre de nombreuses perspectives en vue d’améliorer les propriétés des matériaux composites NR-particules de renfort. / Natural rubber (NR) is an indispensable raw material used in the manufacturing of more than 40,000 products primarily due to its excellent intrinsic physical properties. However, NR is seldom used in its raw state. Often, it needs to be reinforced with particulate fillers (nanoparticles) to further improve its physical strength required for most applications. The precise origin of this mechanical reinforcement effect remains unclear, however, optimal reinforcements appears to depend on the dispersion of filler in the NR matrix and the interaction of NR and filler.It was found that the conventional method of pouring fine powders in a solid block of rubber/melt is not the most efficient way to disperse the fillers. The new alternative approach in which the two components are first dispersed in liquid has shown promising results but available literature is still very limited. Furthermore, the microscopic mechanism involved in the interaction of NR and filler in liquid is still unknown. In this context, we (i) described the physico-chemical surface properties of NR particles in liquid, (ii) identified key filler (size, composition, surface activity, concentration) and solution (ion valence) related parameters to comprehend the structural, morphological, and dynamical evolution of the NR-filler interaction, and (iii) quantified the mechanical properties of the NR particles. With this approach we were able to provide the first reports on the physical processes involved in the interaction of NR and filler. More importantly, a recipe for the basic yet crucial parameters that controls and modulates NR-filler heteroaggregation was established. This could open the way to further understand the reinforcement effect.

abstract: The availability of bulk gallium nitride (GaN) substrates has generated great interest in the development of vertical GaN-on-GaN power devices. The vertical devices made of GaN have not been able to reach their true potential due to material growth related issues. Power devices typically have patterned p-n, and p-i junctions in lateral, and vertical direction relative to the substrate. Identifying the variations from the intended layer design is crucial for failure analysis of the devices. A most commonly used dopant profiling technique, secondary ion mass spectroscopy (SIMS), does not have the spatial resolution to identify the dopant distribution in patterned devices. The possibility of quantitative dopant profiling at a sub-micron scale for GaN in a scanning electron microscope (SEM) is discussed. The total electron yield in an SEM is shown to be a function of dopant concentration which can potentially be used for quantitative dopant profiling. Etch-and-regrowth is a commonly employed strategy to generate the desired patterned p-n and p-i junctions. The devices involving etch-and-regrowth have poor performance characteristics like high leakage currents, and lower breakdown voltages. This is due to damage induced by the dry etching process, and the nature of the regrowth interface, which is important to understand in order to address the key issue of leakage currents in etched and regrown devices. Electron holography is used for electrostatic potential profiling across the regrowth interfaces to identify the charges introduced by the etching process. SIMS is used to identify the impurities introduced at the interfaces due to etch-and-regrowth process. / Dissertation/Thesis / Doctoral Dissertation Materials Science and Engineering 2019