The Swedish old-age care will in the near future face an extensive need to recruit enrolled nurses by virtues of the demographical development. The generation born in the 1940s will soon retire, and at the same time the rest of the population is growing older. One thing that becomes more important in how to draw more people to the old-age care, is to understand how the ones who allready work there experience their own worksituation. The purpose of this study was to find out how enrolled nurses from two different generations experienced their own occupational role and make similarities and differences between the two generations experiences visible. The topics of interest in our study are the respondents own thoughts about their education, their worksituation today, what they think of the future and how they believe others regard their work. To fulfill the purpose of our study we used qualitative interviews. We have performed interviews with three enrolled nurses between 50 and 57 years of age and four enrolled nurses between 20 and 25 years of age. The result was then analyzed with the help of Ingleharts theory “The silent revolution” and the concept of generations. The results showed that there were differences between the two generations. We can´t either on the basis of the small selection of respondents in our study draw any general conclusions. But some differences that show is that the older generation in a larger extent identify with their own occupational role. We also experience that the older are more satisfied with their work situation. They see possibilities to develop in their profession, which the younger don´t. The younger make demands on more possibilities and are more restless then the older generation. From the result we can also see that eatch generation is relative homogeneous. When their is differences between the generations their is often similarites within the own generation. One thing that both generations have in common and that shows clear in the interviews are the importens of empathy and good treatment.

In eukaryotic cells, genomic DNA exists as chromatin in association with histone octamers called nucleosomes, and various other chromatin proteins. Chromatin structure varies along the chromosome and this influences the state of gene expression. Based on such variations in structure and gene expression, chromatin can be broadly classified into euchromatin (transcriptionally active) and heterochromatin (silent or transcriptionally repressed). In the budding yeast, Saccharomyces cerevisiae, there are four canonical transcriptionally silent regions, namely, the HMR, the HML (cryptic mating loci), the telomeres and the RDN1. Silencing at the HM loci and the telomeres is very well characterized. The repressive structure at the HMR spans around 3.5 Kb and extends between the two silencers E and I. It is well established that silencing in HMR is due to a specialized chromatin organization brought about by Orc1p, Rap1p, Abf1p and Sir proteins. Following recruitment, the Sir proteins spread along the DNA to form a repressive chromatin domain believed to arise from the deacetylation of amino-terminal tails of histones H3 and H4 by Sir2p (an NAD dependent deacetylase) and the interaction of Sir3p and Sir4p with the histones. The bi-directional spreading of silencing at HMR is restricted by barrier or boundary elements that flank the silencers. A tRNAThr gene in the right boundary of HMR acts as a strong barrier. Mutations in the promoter of this tRNA gene (tDNA) or in RNA polymerase III subunits/ transcription factors weaken the barrier activity of this tDNA. The barrier activity of this tDNA is also dependent on histone acetyltransferases like Sas2p and Gcn5p. Silencing in HML is uniformly high between the silencers E and I and falls sharply outside I. Recently, barriers to HML silencing have been discovered. A 0.71Kb sequence near E, which maps to the upstream activating sequence of YCL069W, acts as a robust barrier to spread of HML silencing. This is effectively the left boundary of silent HML. The right boundary maps to the promoter of CHA1 gene though silencing is believed to terminate at HML-I. An unusual form of silencing occurs at the RDN1, which contains 100-150 copies of tandemly repeated rRNA genes. Some RNA polymerase II transcribed genes integrated within the array are silenced by a Sir2p dependent mechanism whereas genes driven by RNA polymerases III and I are transcriptionally active. Though all the three forms of silencing (RDN1, HM and telomere) require Sir2p, RDN1 silencing differs from the others in its relative strength and factors responsible for repression. Several trans-acting factors required for RDN1 silencing are known. However, it is still unclear as to what limits the spread of RDN1 heterochromatin into neighbouring essential genes. RDN1 silencing spreads unidirectionally in its left hand side sequence. However, the zone of RDN1 heterochromatin does not engulf the essential gene, ACS2, which is present ~3 kb away from NTS1. This implies that there is a mechanism by which rDNA heterochromatin is contained. There could be several ways by which this is accomplished. Firstly, the cell could be critically maintaining the levels of Sir2p, the protein required for silencing at all the four silenced loci, such that silencing in the left flank of RDN1 does not spread beyond 300 bp of NTS1 (Buck et al, 2002). There is a ~2.5 kb gene free intervening sequence between NTS1 of the rDNA array and the Ty1 LTR, in which interval Sir2p level could fall below the threshold mark required for causing repression. In fact Buck et al. have demonstrated that Sir2p is bound to upto 1.5 kb from the NTS1 in the left flank but there is no accompanying silencing of the mURA3 reporter in these regions (1200L and 2000L), suggesting that the level of Sir2p at these sequences could be lower than the threshold required for initiation of silencing. Secondly, there could be cis-acting boundary elements or barriers as in the case of HMR, which prevents the propagation of RDN1 silencing. The third option is that termination of RNA polymerase I transcription at the terminator sites automatically halts the spread of rDNA silencing since Buck et al. have demonstrated that progression of rDNA heterochromatin is dependent on RNA pol I transcription. This however, does not seem to be the case as deletion of both the terminator sites within NTS1 does not lengthen the zone of silencing. Finally, there could be an euchromatin organizing center further from the array, which creates an “open” chromatin configuration required to confront the Sir2p mediated condensed chromatin. The balance of these two opposing activities, much like that at the telomeres, could set up a molecular boundary for containing rDNA silent chromatin. We have attempted to identify whether there are any sequences in the unique left flank of RDN1 that can act as a heterochromatin barrier. Towards that end we tested four overlapping fragments from NTS1 of RDN1 to the promoter of ACS2 for boundary activity in a quantitative mating assay. We have found that of all the four fragments tested, only a 0.427 kb tRNAGln-Ty1 LTR fragment, which is present 2.4 Kb from the NTS1 acts as a robust barrier in this assay. Further mapping revealed that the barrier activity of this sequence resides in the tRNAGln gene and that its activity is orientation-independent. tDNAs are transcribed by RNA polymerase III from internal promoters termed Box A and Box B. It has been shown for the HMR-tRNAThr that the transcriptional potential of the tDNA is crucial for its barrier function. Mutations in genes encoding various subunits of the RNA polymerase III complex, or transitions in the conserved bases within Box B known to disrupt transcription complex assembly and subsequent transcription, abrogate the barrier activity of HMR-tRNAThr. Similarly, loss of transcriptional ability of the tRNAAla in the centromere of S. pombe also abolishes its barrier activity, enforcing the fact that RNA polymerase III transcription is a decisive factor for a tDNA barrier. Contrary to the above observations, we report that barrier activity of tRNAGln is very negligibly dependent on RNA polymerase III mediated transcription. Mating assays done with the RNA pol III mutants and promoter point mutants, G18C and C55G in boxes A and B respectively, underline the fact that for this tDNA barrier, RNA pol III driven transcription is dispensable. We also show by RT-PCR analysis that in the C55G tRNAGln mutant there is loss of transcription as expected, whereas other wild type copies of tRNAGln are transcribed. Studies with another tDNA barrier, TRT2-tRNAThr, yielded similar results, again emphasizing the point that transcription through the tDNA, which leads to nucleosome displacement and therefore barrier activity, may not be applicable for all tDNA barriers. Acetylation of amino terminal tails of histones is known to influence the epigenetic state of chromatin. Addition of acetyl moiety to histones H3 and H4 initiates a cascade of events, which involves recruitment of a host of other chromatin modifiers to the target sequence, and ultimately culminates in the formation of an euchromatin-favouring environment. As reported for the HMR right boundary, we find that barrier activity of tRNAGln depends on two histone acetyl transferase complexes, SAS-I (comprised of Sas2p, Sas4p and Sas5p) and SAGA (contains Gcn5p HAT). Contrary to the HMR boundary, the barrier activity of tRNAGln is independent of two other nucleoplasmic HATs, NuA3 (Sas3p being the HAT) and NuA4 (Esa1p is the HAT). Barrier function of TRT2-tRNAThr also depends on HATs. Therefore it appears that requirement of HATs for boundary activity is a conserved theme, albeit with differential effects at different barrier sequences. We next attempted to determine the function of tRNAGln in its natural location on chromosome XII. As mentioned earlier, RDN1 silencing spreads upto ~0.3 kb in its left flanking sequence. However, Sir2p occupancy has been observed till 1.5 kb although there is no silencing of reporter genes observed beyond 0.3 kb of NTS1. This lead us to speculate that there could be a boundary sequence in the left flank that stops silencing, or a euchromatin-organizing element, which counters the propagation of silencing by a long-range effect. Since over expression of Sir2p extends the domain of silencing from 0.3 kb to 2.0 kb and the tRNAGln is present at 2.3 kb from NTS1, it was a good candidate for a heterochromatin barrier/ euchromatiniser. However, deletion of tRNAGln does not affect the zone of RDN1 silencing as is evident from our cell viability assays (which is a measure of the expression of the essential gene ACS2 situated further to the left of tRNAGln). Deletion of SAS2 and GCN5, factors that are required for barrier activity of tRNAGln in mating assays, also have no effect on the extent of spreading of RDN1 silencing in normal or Sir2p over expression conditions. Together, these observations imply that in situ, tRNAGln does not act as a barrier or an element with long-range euchromatin inducing properties. It still remains unclear as to what contains RDN1 silencing. It is possible that the cell critically monitors the level of Sir2p in order to maintain boundaries of silencing at the rDNA locus. Telomeres also nucleate the formation of silenced domain which spreads along the subtelomeric region upto ~ 2Kb. The key players in the formation of telomeric heterochromation are the Sir proteins, Sir2p, Sir3p and Sir4p, Rap1p, yKu complex and ORC. Protein-protein interactions between the telosome and the subtelomeric repeat bound silencing proteins create a domain of core heterochromatin that spreads in the adjacent sequences. While Sir2p deacetylates H4K16, Sir3p interacts with the hypoacetylated histone tails and helps in the spreading of the repressive chromatin structure. As a result telomere proximal genes are silent whereas the ones further away are expressed. There is a gradient of acetylation of histone H4, with the hypoacetylated histones at the telomeric ends and the hyperacetylated ones distant from the telomere. Recently it has been shown that this gradient is maintained by the concerted and antagonistic actions of Sir2p and Sas2p. In a sas2Δ strain Sir3p spreads to ~15 kb in the subtelomeric regions and there is increase in the levels of hypoacetylated histones. Though the molecular mechanism by which telomeric silencing is restrained is beginning to be understood, it remains unanswered whether there are any cis-acting sequences, capable of recruiting euchromatin-inducing factors such as Sas2p, near the telomeres. We have identified a RNA polymerase II driven gene, AAD3, in the subtelomeric region of chromosome III that has robust anti-silencing activity. Deletion mapping revealed that only 0.381 kb in the 5′ portion of the gene (excluding the promoter) is sufficient for barrier activity and that this property is orientation-independent (henceforth referred to as TEL-B). The barrier acivity of TEL-B depends strongly on Sas2p and Esa1p but not on Gcn5p and Sas3p, and is independent of cohesin. Previous investigations have shown that acetylation of H4K16 by Sas2p at subtelomeric regions of chromosome VI leads to deposition of HTZ1 in the nucleosome and its subsequent acetylation by Esa1p of NuA4. All these events together are required to contain the onslaught of telomeric core heterochromatin on neighbouring active regions. Since barrier activity of TEL-B depends on Sas2p and Esa1p, it is possible that TEL-B has the potential to act as a bona fide barrier in situ in its endogenous context. Our hypothesis is further cemented by the observation that there is a physical association between Sas2p, the molecule at the top of the entire cascade of events, with TEL-B by yeast one hybrid analysis. Further experiments will shed light on the role of this sequence in its natural location. In summary, I have identified and characterized two different barrier sequences in S. cerevisiae. Not many barriers are known in budding yeast and there is extensive ongoing research dedicated to understand the mechanism(s) of barrier function. In chapter I of my thesis I present a review of current literature regarding silencing barriers in yeast and other systems. In chapter II I have outlined a detailed characterization of a tDNA barrier element, tRNAGln, present near the silenced rDNA array on chromosome XII. My work addresses the various models for barrier activity and their applicability to the tRNAGln barrier. I have also attempted to understand the role of this tDNA in its natural location on the chromosome with respect to limitation of RDN1 silencing. In chapter III I have described an intensive study of a RNA polymerase II transcribed gene, AAD3, present near the right telomere of chromosome III, which acts as a robust barrier to silencing. I have attempted to answer which mechanism(s) is/are operational at this sequence so as to endow it with barrier potential. My studies with the two barrier elements highlight novel trans-acting factors required for barrier function, differential and selective requirements of certain factors for different barriers, and provide a mechanistic view of the boundary activity of these sequences.

The work in this thesis concerns mechanisms of excitability of neurons. Specifically, it deals with how neurons respond to input, and how their response is controlled by ion channels and other active components of the neuron. I have studied excitability in two systems of the nervous system, the hippocampus which is responsible for memory and spatial navigation, and the peripheral C–fibre which is responsible for sensing and conducting sensory information to the spinal cord. Within the work, I have studied the role of excitability mechanisms in normal function and in pathological conditions. For hippocampus the normal function includes changes in excitability linked to learning and memory. However, it also is intimately linked to pathological increases in excitability observed in epilepsy. In C–fibres, excitability controls sensitivity to responses to stimuli. When this response becomes enhanced, this can lead to pain. I have used computational modelling as a tool for studying hyperexcitability in neurons in the central nervous system in order to address mechanisms of epileptogenesis. Epilepsy is a brain disorder in which a subject has repeated seizures (convulsions) over time. Seizures are characterized by increased and highly synchronized neural activity. Therefore, mechanisms that regulate synchronized neural activity are crucial for the understanding of epileptogenesis. Such mechanisms must differentiate between synchronized and semi synchronized synaptic input. The candidate I propose for such a mechanism is the fast outward current generated by the A-type potassium channel (KA). Additionally, I have studied the propagation of action potentials in peripheral axons, denoted C–fibres. These C–fibres mediate information about harmful peripheral stimuli from limbs and organs to the central nervous system and are thereby linked to pathological pain. If a C–fibre is activated repeatedly, the excitability is altered and the mechanisms for this alteration are unknown. By computational modelling, I have proposed mechanisms which can explain this alteration in excitability. In summary, in my work I have studied roles of particular ion channels in excitability related to functions in the nervous system. Using computational modelling, I have been able to relate specific properties of ion channels to functions of the nervous system such as sensing and learning, and in particular studied the implications of mechanisms of excitability changes in diseases. / <p>QC 20102423</p>

Many studies have suggested a relationship between sex steroids and negative mental and mood changes in women. Allopregnanolone, a potent endogenous ligand of the GABA-A receptor and a metabolite of progesterone, is one of the most accused neuroactive steroids. Variations in the levels of neuroactive steroids that influence the activity of the GABA-A receptor cause a vulnerability to mental and emotional pathology. In women, there are physiological conditions in which allopregnanolone production increases acutely (e.g. stress) or chronically (e.g. menstrual cycle, pregnancy), thus exposing the GABA-A receptor to high allopregnanolone concentrations. In such conditions, tolerance to allopregnanolone probably develops. We have evaluated the 3β-hydroxy pregnane steroid UC1011 as a functional antagonist to allopregnanolone-induced negative effects in rats. In vivo, we used the Morris Water Maze (MWM) test of learning and, in vitro, we studied chloride ion uptake into cortical and hippocampal membrane preparations. The steroid UC1011 reduces the allopregnanolone-induced learning impairment in the MWM and the increase in chloride ion uptake induced by allopregnanolone. To detect whether chronic tolerance develops to an allopregnanolone-induced condition, male rats were pretreated with allopregnanolone injections for three or seven days. These rats were then tested in the Morris Water Maze for five days and compared with relevant controls. Rats with seven days’ allopregnanolone pretreatment experienced improved performance compared with the acutely allopregnanolone-exposed group, reflecting chronic tolerance development. To study the GABA-A receptor changes in acute allopregnanolone tolerance, we used the silent second (SS) anaesthesia threshold method. At acute tolerance, 90 minutes of anaesthesia, the abundance of the GABA-A receptor α4 subunit and the expression of the α4 subunit mRNA in the thalamus ventral-posteriomedial (VPM) nucleus were reduced. There was also a significant negative correlation between the increase in the allopregnanolone dose needed to maintain anaesthesia and the α4 mRNA in the VPM nucleus. We also investigated whether allopregnanolone tolerance was still present one or two days after the end of the anaesthesia-induced acute tolerance. Tolerance persisted to one day, but not two days, after the treatment and the α4 subunit mRNA expression in the VPM nucleus was negatively related to the allopregnanolone doses needed after one day. In conclusion, the current thesis shows that the substance UC1011 can reduce the allopregnanolone-induced negative effects in the water maze test. Chronic allopregnanolone tolerance can develop to the effects of allopregnanolone. Allopregnanolone tolerance persists one day after the induction of acute allopregnanolone tolerance. The GABA-A receptor α4 subunit in the thalamus might be involved in the development and persistence of acute tolerance to allopregnanolone.

Zugl.: Freiburg (Breisgau), Universiẗat, Diss., 2007.

Univ., Diss./2004--Frankfurt am Main, 2003.

Entre 1916 et 1928, un certain nombre de films muets américains expérimentent les formes complexes d’un assemblage ostensiblement articulé entre un ou des récits situés dans le passé (historique, antique ou biblique) et un récit situé à l’époque moderne. Nous avons appelé cet assemblage le « Spectacle des Siècles », suivant la formule publicitaire rencontrée sur l’affiche d’un de ces films, Noah’s Ark (M. Curtiz, 1928). Les films du Spectacle des Siècles ne se confondent pas avec les films historiques ou bibliques également mis en scène dans le cinéma muet, et qui supposent une action unique et une diégèse centrée autour de la période reconstituée. Les films étudiés font dialoguer passés et présents en relatant une multiplicité d’époques, de décors, d’actions et de personnages. Cette recherche se propose de mettre en lumière outre la variété des contenus, les diverses solutions d’assemblage élaborées par ces films pour aboutir à l’harmonie d’une œuvre cohérente. Les formes originales imaginées par les cinéastes font apparaître les multiples passages, transferts et métamorphoses de ces parallèles entre le passé et le présent, l’ancien et le nouveau. Elles interrogent ce que les films ont à dire sur leur siècle, en instaurant un présent démultiplié et orienté vers de nouvelles promesses. Ainsi les films du Spectacle des Siècles donnent à lire un moment de l’histoire du cinéma muet américain qui connut une brève période d’activité. / Between 1916 and 1928, some American silent films are in search of putting together one or several stories set in the past (historical, ancient, biblical) and one story set in the modern times, thus displaying complex cinematic forms conspicuously articulated. We called this assembling the « Spectacle of the Ages », according to the advertising formula encountered on the poster of one of these films, Noah’s Ark (M. Curtiz, 1928). The films of the Spectacle of the Ages are not to be confused with biblical or historical films – also produced in silent cinema – which assume a single action and a diegesis focused on the reenacted period. The films we are to sudy here confront the past with the present, by telling multiple ages, sets, actions and characters. Beyond the variety of these stories, this research aims to highlight the various assembling solutions created by the filmmakers to achieve a coherent and harmoniously shaped work of art. These cinematic forms show various passages, translations, metamorphosis of the parallels between the past and the present, the old and the new, thus revealing something of their Age and of a promising future. We perceive in the Spectacle of the Ages a short-lived moment in the history of American silent cinema.

Dans les années vingt, au moment de l’institutionnalisation du cinéma classique hollywoodien, discours critiques et pratiques publicitaires maintiennent actif un plaisir spectatoriel lié à la présence sensationnelle de réel dans le film. La notion de « réalisme » que ces discours utilisent est un concept fragmenté qui vise d’une part à asseoir la légitimité du cinéma sur le sérieux des arts réalistes, et d’autre part à mettre l’accent sur les liens que le film entretient avec la réalité, dans son tournage, sa fabrication en studio, ou les techniques de l’illusion réaliste. Ces discours révèlent donc tout ce qu’il y a de réel dans le travail de la fiction des films. Il y a donc derrière ces discours un projet réaliste de construction d’un regard spectatoriel anti-illusionniste et actif qui est invité à analyser le film comme une illusion artificielle. Ces discours sont étendus dans le quotidien des spectateurs par des pratiques publicitaires qui visent à créer un espace de réception ludique où réel et romanesque s’interpénètrent dans le ballyhoo aux accents forains, les décorations des entrées de salles de cinéma, et les prologues joués sur scène avant (ou pendant) le film. Ce regard réaliste que ces discours et pratiques développent nous permet d’analyser la réception des films muets hollywoodiens comme un moment ludique et participatif. En visant au réveil des sens et à l’acuité du regard chez le spectateur, ces discours et pratiques permettent de poser la question d’un réalisme hollywoodien dont l’objectif serait un jeu actif, conscient et critique avec l’illusion cinématographique. / In the 1920s, as Hollywood cinema is undergoing industrial institutionalization, critical and advertising discourses maintain active a spectatorial pleasure derived from the sensational presence of reality in fiction films. The notion of « realism » used in those discourses is a « cluster concept » aiming on the one hand to derive cinema’s legitimacy from the serious purpose of realistic arts, and on the other to emphasize the relationship between film and the reality of on location or studio shooting, of the manufacturing of films, and of the tricks behind the realistic illusion. Those discourses therefore reveal all that is real in how fiction works in films and support a realistic project to construct an active and non-illusionistic spectatorial gaze that is invited to analyze film as an artifical illusion. These discourses are extended to spectators’ daily life through advertising practices that aim to create a playful space of reception where reality and romance merge in circus-inspired ballyhoo, in lobby decorations, and in on-stage prologues before, or during, the film. This realistic gaze developped by such discourses and practices allows us to analyze the reception of Hollywood silent films as a playful and participative moment. Aiming to awaken spectators’ senses and sharpen their attention, such discourses and practices allow us to raise the question of a Hollywood realism that would aim to create an active, conscious and critical game with the filmic illusion.

Made available in DSpace on 2016-08-03T12:20:12Z (GMT). No. of bitstreams: 1 Capa.pdf: 28000 bytes, checksum: 2b84a6e2b692880021f4c072e4c38c20 (MD5) Previous issue date: 2004-08-30 / A proposta desta pesquisa é enfocar a história da Igreja Presbiteriana do Brasil no período de 1910 a 1966, a partir de uma análise histórica institucional, com vistas à compreensão do isolamento ecumênico da Igreja Presbiteriana do Brasil. A partir da análise de documentos pertencentes ao arquivo da Igreja Presbiteriana do Brasil, procurou-se proceder o levantamento da memória coletiva e individual dos grupos presbiterianos, conservador e liberal, na tentativa de revelar os acordos silenciosos ? acordos que se manifestam, de forma velada, no plano do discurso ? que expressam a subjetividade objetividade dos sujeitos envolvidos. Essa perspectiva de análise justifica a opção pelo tema "Os acordos silenciosos como fator determinante do isolamento ecumênico da Igreja Presbiteriana do Brasil (1910 1966)", uma vez que a pesquisa empreendida considera a espessura histórica, social, teórica e política de nosso objeto de estudo, necessária e fundamental para uma melhor compreensão desses acordos silenciosos. Nesse sentido, propomo-nos aproximar a realidade pensada da vivida, interpretar a polissemia de significados encontrados nos documentos e identificar a multiplicidade de pensamentos manifestos nos textos analisados, tomando o método histórico como procedimento de investigação. Os resultados deste trabalho acadêmico reforçam o papel ideológico da Igreja e sua doutrina como força psicológica e social que, ao lado do poder econômico, político e militar, forma o Poder Nacional, estabelece acordos internos e, quando alguém se declara contra esses acordos, as tensões já existentes, agravam-se. Na realização deste trabalho, pretende-se oferecer dados que propiciem a reflexão e o redimensionamento da leitura dos fatos ocorridos nesse período da história da Igreja Presbiteriana do Brasil, sem recairmos em posições reducionistas e lesivas para a autônoma e adequada interpretação da realidade analisada.(AU)

Ce travail étudie le rapport entre le langage narratif cinématographique et le discours musical contemporain. Le point de départ en a été l’étude des nouvelles créations contemporaines écrites pour accompagner certains films de l’époque du cinéma muet. Pour atteindre ces objectifs, nous sommes partis d’une vision théorique, pour arriver à l’analyse plus concrète qui nous a donné les consignes de base pour créer notre propre modèle d’analyse applicable à la composition. Ce modèle permet de préciser les concepts nous permettant d´aborder la relation entre le film et la musique selon deux axes, que nous appelons respectivement « points d’ancrage » (qui traitent des points d’articulation du discours cinématographique avec la musique) et « points de référence » (qui gèrent les éléments formels du discours cinématographique et musical). Dans la dernière partie de ce travail, nous appliquons notre modèle à la réalisation de quatre projets personnels, qui représentent une « conclusion artistique » des éléments analysés au cours de cette recherche. / This work studies the relationship between the film’s narrative language and the contemporary music speech. The starting point of this work is the study of the new contemporary scores, which were composed for silent films from the 1920’s onwards. To reach these goals, we started from a theoretical vision, to subsequently perform a practical analysis. This gave us the important points to create our analysis model to be used for music composition. This model allows us to clarify the relationship between the film and the music, based on two main axes: the “anchoring points” (giving us the articulation points between the music and the film) and the “reference points” (which deals with the formal elements of both film and music speech). In the last part of our work, we have applied our model to the composition of four personal projects, which were created as an artistic conclusion of our research.