Submitted by Hellen Luz (hellencrisluz@gmail.com) on 2017-07-13T17:22:19Z No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Dissertacao_PedacosPoteBonecos.PDF: 2961764 bytes, checksum: 65e457ee11a8dc7e6290cd75813cf11f (MD5) / Approved for entry into archive by Irvana Coutinho (irvana@ufpa.br) on 2017-07-17T13:59:37Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Dissertacao_PedacosPoteBonecos.PDF: 2961764 bytes, checksum: 65e457ee11a8dc7e6290cd75813cf11f (MD5) / Made available in DSpace on 2017-07-17T13:59:37Z (GMT). No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Dissertacao_PedacosPoteBonecos.PDF: 2961764 bytes, checksum: 65e457ee11a8dc7e6290cd75813cf11f (MD5) Previous issue date: 2014-09-04 / A região de Maracá, Município de Mazagão, no Amapá, reúne em seu território um enorme potencial arqueológico, no qual se destacam contextos com urnas funerárias de características antropomorfas e zoomorfas em sítios de áreas fechadas, em ambientes de caverna. Essa dissertação é uma etnografia sobre as representações que moradores da vila de Laranjal de Maracá, localizada no entorno de vários desses sítios, possuem sobre esses vestígios, bem como sobre as pesquisas desses materiais. Além disso, aborda questões sobre práticas de encantaria e também imaginários sobre os lugares praticados pelos moradores dessa vila. Para tanto, utilizou como técnicas a observação participante, entrevistas e análises bibliográficas, buscando refletir a partir da Arqueologia Pública sobre as diferentes formas de impacto da cultura material. / The Maracá region, in the municipality of Mazagão, state of Amapá, holds a vast archaeological potential, in which contexts of secondary burial in urns with anthropomorfic and zoomorfic characteristics—found in caves and shelters—feature prominently. The present dissertation is an ethnography about the representations that inhabitants of Vila de Laranjal de Maracá—located in the surroundings of several such sites—share of the archaeological traces found, as well as of the research carried out on these materials. Besides that, this study also tackles issues on practices of encantaria (Enchant Cult) and on the imaginary related to places described by the inhabitants. To accomplish that, participant observation, interviews, and bibliographic analysis were used in the attempt to reflect—based on the principles of Public Archaeology—on the different forms of impact of material culture.

Les travaux épidémiologiques et expérimentaux effectués à ce jour sur le cancer du sein ont montré que les oestrogènes - comme l’eostradiole (E2) - et leur récépteur (ER) - un facteur de transcription les liants - sont fortement impliqués dans au moins 70% des cas de cancer du sein. Cette implication est d’autant plus visible que les patients, suite à une thérapie anti-oestrogénique, ont tendance à développer une résistance endocrinienne au traitement. Pendant longtemps, l’ER a été étudié en tant que facteur indépendant liant directement une séquence ADN spécifique sur le génome. Aujourd’hui le paradigme a profondément changé. Il est bien connu que ER s’associe avec de nombreux autres facteurs de transcription et protéines régulant la chromatine afin de réguler l’expression des gènes. Cependant, nos connaissances concernant la fonction de modifications épigénétiques suite à l’activation de ER - notamment la méthylation de l’ADN et l’acétylation des histones - sont encore limitées. Dans cette étude, j’ai mis en place un protocole de culture cellulaire adapté à l’étude de la privation et à la re-stimulation d’E2 stricto sensu. Dans un premier temps, ce protocole a été évalué à l’aide de la toute dernière technologie de puce permettant la lecture du méthylome et couvrant la liste complète des éléments amplificateurs. Dans un deuxième temps, j’ai mesuré le transcriptome et les profiles d’acétylation de l’histone H3 (H3K27ac) afin de déterminer la capacité de ER à réguler l’expression des gènes J’ai découvert que, suite à la privation de E2, les niveaux de méthylation de l’ADN et de H3K27ac changent et que ces changements s’accentuent avec le temps, en particulier au niveau des éléments amplificateurs. Une analyse d’enrichissement des facteurs de transcription et des séquences de liaison spécifiques a révélé que les facteurs de transcriptions des familles AP-1 et FOX sont des intermédiaires favorisants la liaison de ER aux éléments amplificateurs. Finalement, la re-stimulation des cellules par de l’E2 a montré que la majorité des changements épigénétiques observé sont réversibles mais que certains éléments amplificateurs restent hyperméthylés et déacétylés. Ceci pourrait indiquer que les traitements anti-oestrogéniques sont efficaces mais pourrait également indiquer un marqueur de résistance endocrinienne. Cette étude apporte des informations nouvelles quant aux effets de l’inhibition et l’activation de ER sur la méthylation de l’ADN et l’acétylation de l’histone H3 à l’échelle du génome et renforce l’importance du rôle d’autres facteurs au niveau des amplificateurs / Previous epidemiological and experimental studies have strongly implicated estrogens in breast cancer risk and Estrogen Receptor (ER), the transcription factor to which estrogen binds, is considered as the major molecular driver of around 70% breast cancers. The importance of the deregulated estrogen signalling is further highlighted by increasing evidence that current chemopreventive and therapeutic strategies that target hormonally responsive breast cancers frequently result in the development of resistance to anti-estrogens and metastatic progression, highlighting the need for understanding the molecular underlying mechanisms. While until recently, ER was believed to act as a stand-alone transcription factor, which can directly bind its motifs in DNA, it is now accepted that ER activity is a complex and dynamic process that requires highly concerted actions of a dozen transcriptional cofactors and various chromatin regulators at DNA. Recent studies focused on characterising ER-associated cofactors and their role in opening the chromatin provided a remarkable insight into transcriptional regulation mediated by ER. However DNA methylation and histone acetylation are poorly understood in the context of ER’s dynamic binding. In this thesis, I combined a cell culture protocol adapted for studying estradiol (E2) deprivation and re-stimulation in stricto sensu in ER-positive breast cancer cells with the latest methylation array, that allowed a genome-wide interrogation of DNA methylation (including a comprehensive panel of enhancers). I further investigated histone acetylation (ChIP-seq) and transcriptome (RNA-seq) after E2 deprivation and re-stimulation to better characterise the ability of ER to coordinate gene regulation. I found that E2 deprivation and re-stimulation result in time-dependent DNA methylation changes and in histone acetylation across diverse genomic regions, many of which overlap with enhancers. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER tethering mainly through two partner TF families, AP-1 and FOX, in the proximity of enhancers that are differentially methylated and acetylated. This is the first study that comprehensively characterized DNA methylation at enhancers in response to inhibition and activation of ER signalling. The transcriptome and genome occupancy data further reinforced the notion that ER activity may orchestrate a broad transcriptional programme through regulating a limited panel of critical enhancers. Finally, the E2 re-stimulation experiments revealed that although the majority of the observed epigenetic changes induced by E2 deprivation could be largely reversed when the cells were re-stimulated we show that DNA hypermethylation and H3K27 acetylation at enhancers as well as several gene expression changes are selectively retained. The partial reversibility can be interpreted as a sign of treatment efficiency but also as a mechanism by which ER activity may contribute to endocrine resistance. This study provides entirely new information that constitutes a major advance in our understanding of the events by which ER and its cofactors mediate changes in DNA methylation and chromatin states at enhancers. These findings should open new avenues for studying role of the deregulated estrogen signalling in the mechanism underlying the “roots” of endocrine resistance that commonly develops in response to anti-estrogen therapy

We have used a series of observations of HD119419, performed in 2012 and 2013at the European Southern Observatory 3.6-m telescope in La Silla, Chile. These are high resolutionspectropolarimetric observations with coverage in all four Stokes parameters. We performed a chemical abundance analysis of HD119419, in the absence of any being published previously for this star. We used a LLmodels stellar atmosphere code with effective temperature11500 K and surface gravity log g = 4.0, together with the spectrum synthesis code synmast. Abundances were adjusted until the synthetic spectra matched the mean observed spectra as well as possible, and these abundances were assumed to be representative of the photosphere of HD119419. We found good estimates for some Fe-peak elements and rare-earth elements. The abundance estimates were used to compute least-squares deconvolution Stokes spectra, from which we calculated how the longitudinal magnetic field and net linear polarization varies with rotational phase for HD119419. We calculated an improved rotational period for HD119419 using our longitudinal magnetic field measurements together with previous measurements from the literature, determining it to be 2.60059(1) days. We found that the Stokes QUV are unusually strong for the rare-earth elements in HD119419, considering their weaker Stokes I profiles compared to the Fe-peak elements in particular.

No description available.

No description available.

Les sites apuriniques/apyrimidiniques (AP) sont des sites de l’ADN hautement mutagène. Les dommages au niveau de ces sites peuvent survenir spontanément ou être induits par une variété d’agents. Chez l’humain, les sites AP sont réparés principalement par APE1, une enzyme de réparation de l’ADN qui fait partie de la voie de réparation par excision de base (BER). APE1 est une enzyme multifonctionnelle; c’est une AP endonucléase, 3’-diestérase et un facteur redox impliqué dans l’activation des facteurs de transcription. Récemment, il a été démontré qu’APE1 interagit avec l’enzyme glycolytique GAPDH. Cette interaction induit l’activation d’APE1 par réduction. En outre, la délétion du gène GAPDH sensibilise les cellules aux agents endommageant l’ADN, induit une augmentation de formation spontanée des sites AP et réduit la prolifération cellulaire. A partir de toutes ces données, il était donc intéressant d’étudier l’effet de la délétion de GAPDH sur la progression du cycle cellulaire, sur la distribution cellulaire d’APE1 et d’identifier la cystéine(s) d’APE1 cible(s) de la réduction par GAPDH. Nos travaux de recherche ont montré que la déficience en GAPDH cause un arrêt du cycle cellulaire en phase G1. Cet arrêt est probablement dû à l’accumulation des dommages engendrant un retard au cours duquel la cellule pourra réparer son ADN. De plus, nous avons observé des foci nucléaires dans les cellules déficientes en GAPDH qui peuvent représenter des agrégats d’APE1 sous sa forme oxydée ou bien des focis de la protéine inactive au niveau des lésions d’ADN. Nous avons utilisé la mutagénèse dirigée pour créer des mutants (Cys en Ala) des sept cystéines d’APE1 qui ont été cloné dans un vecteur d’expression dans les cellules de mammifères. Nous émettons l’hypothèse qu’au moins un mutant ou plus va être résistant à l’inactivation par oxydation puisque l’alanine ne peut pas s’engager dans la formation des ponts disulfures. Par conséquent, on anticipe que l’expression de ce mutant dans les cellules déficientes en GAPDH pourrait restaurer une distribution cellulaire normale de APE1, libérerait les cellules de l’arrêt en phase G1 et diminuerait la sensibilité aux agents endommageant l’ADN. En conclusion, il semble que GAPDH, en préservant l’activité d’APE1, joue un nouveau rôle pour maintenir l’intégrité génomique des cellules aussi bien dans les conditions normales qu’en réponse au stress oxydatif. / Apurinic/apyrimidinic (AP) sites are highly mutagenic DNA lesions occurring either spontaneously or by the action of DNA damaging agents. In human cells, AP sites are processed by the major DNA repair enzyme APE1 through the base excision repair (BER) pathway. APE1 is a multifunctional protein that has AP endonuclease/3’-diesterase activities in addition to its role as a redox factor in activating many transcription factor. Recently, it has been shown that APE1 interacts with the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), an interaction that results in the activation of APE1 by reduction. Interestingly, depletion of GAPDH sensitized the cells to DNA damaging agents and induced an increase in spontaneous AP sites frequency. Moreover, cells knocked-down for GAPDH showed defects in proliferation. Here we set up to investigate the effects of GAPDH knockdown on cell cycle progression, APE1 subcellular localization and to identify the cysteine residue(s) of APE1, target(s) of GAPDH reduction. Our studies showed that GAPDH deficient cells arrested in G1 phase of the cell cycle. The defect in cell cycle progression is most probably due to accumulation of DNA damage which activates checkpoints leading to a delay in the cell cycle to allow DNA repair. Furthermore, in GAPDH deficient cells, APE1 formed nuclear foci-like structures that could represent aggregates of the oxidized form of APE1 or inactive APE1 foci on DNA lesions. Using site-directed mutagenesis, we created seven APE1 cysteine to alanine mutants which were cloned into a mammalian expression vector. We expect that at least one of these mutants is likely to resist the inactivation by oxidation as it cannot engage in disulfide bridge formation. Therefore, the expression of this mutant(s) in GAPDH knockdown cells is expected to restore a normal APE1 cellular distribution, rescue the cell cycle defects, and render the cells less sensitive to DNA damaging agents. In conclusion, our results show a new role of GAPDH in maintaining genomic stability under oxidative stress by maintaining APE1 in its functional state.

Le complexe transcriptionnel AP-1 est une famille ubiquitaire de facteurs de transcription dimériques. Ses composants les mieux étudiés sont les membres des familles multigéniques Fos et Jun. Les mécanismes transcriptionnels gouvernés par ce complexe sont encore mal caractérisés, en raison du grand nombre de dimères AP-1 possibles, de l’abondance et de l’activité finement régulées de ses constituants qui dépendent des contextes cellulaires et physiopathologiques. De plus, les limitations techniques ont longtemps donné l'impression que AP-1 régule l’expression de ses gènes cibles en se fixant principalement à proximité de leurs promoteurs. Fra-1 est la protéine de la famille Fos la plus souvent impliquée dans les cancers épithéliaux. En particulier, elle est surexprimée dans les cancers du sein triple négatifs (TNBCs) où elle contribue à la tumorigenèse et à l'agressivité tumorale par des effets pléiotropes. Dans ce contexte, l’objectif de mes travaux de thèse était d’aboutir à une meilleure compréhension des actions transcriptionnelles de Fra-1 au niveau du génome dans une lignée cellulaire TNBC de référence, la lignée MDA-MB-231. Pour ce faire, j'ai combiné des données transcriptomiques avec des données de ChIP-seq et de NG-Capture C (technique à haute résolution et à haut débit dérivée du 3C). J'ai également inclus dans ces études le membre Fra-2, de la famille Fos, qui présente la même spécificité de fixation à l’ADN et est également exprimé dans les TNBCs, bien qu'à un niveau beaucoup plus bas, où il contribue aussi au phénotype tumoral. En accord avec leurs effets pléiotropes, Fra-1 et Fra-2 activent ou répriment, soit individuellement soit de façon redondante ou complémentaire, l’expression de nombreux gènes associés à une large gamme de processus biologiques. Il est intéressant de noter que la régulation des gènes cibles est rarement due à la liaison de Fra-1 et/ou Fra-2 au niveau des régions promotrices de ces gènes mais fait intervenir leur liaison sur des enhancers distaux. Mes résultats de NG-Capture C suggèrent la présence d’interactions chromatiniennes à longue distance enhancer/promoteur, ainsi que des réseaux d’enhancers. Ces réseaux contiennent des enhancers liés par Fra-1 et d’autres indépendants de celui-ci. Aucune preuve d’un rôle de Fra-1 dans le contrôle des interactions chromatiniennes au niveau de ces réseaux n'a été trouvée en utilisant un panel de 35 gènes régulés par ce facteur. En parallèle, j'ai abordé les mécanismes de la répression transcriptionnelle médiée par Fra-1, mécanismes très rarement étudiés dans la littérature, en utilisant deux gènes modèles, TGFB2 et SMAD6. Ces études ont mis en évidence des mécanismes différents mis en jeu par Fra-1 pour la répression de ces deux gènes, ce qui montre la complexité des mécanismes de la régulation transcriptionnelle médiée par Fra-1. / The AP-1 transcription complex is a ubiquitous family of dimeric transcription factors. Its best-studied components are the members of the Fos and Jun multigene families. The mechanisms whereby AP-1 exerts its transcriptional actions are still ill-understood due to the wide number of possible AP-1 dimers and the exquisitely regulated abundance and activity of its constituents, that all depend on the cell types and physiopathological contexts. Moreover, technical limitations have long given the impression that AP-1 mostly operates in the vicinity of gene promoters. Fra-1 is the Fos family protein that is most often implicated in epithelial cancers. In particular, it is overexpressed in triple negative breast cancers (TNBCs) where it contributes to tumorigenesis and tumor aggressiveness through pleiotropic effects. Based on this, the aim of my thesis was to gain a more comprehensive view of Fra-1 transcriptional actions at the genome-wide level in the MDA-MB-231 reference TNBC cell line, . To this aim, I have combined transcriptomic data with ChIP-seq and NG-Capture C (high resolution, high throughput 3C-derived technique) data. I have also included in my studies its Fos family kin Fra-2, as it displays the same DNA binding specificity and is also expressed in TNBCs, albeit at a much lower level, where it also contributes to the tumor phenotype. Consistently with their pleiotropic effects, Fra-1 and Fra-2 were found to up- or down-regulate either individually, together or redundantly many genes associated with a wide range of biological processes. Interestingly, the regulation of target genes is rarely due to Fra-1 and Fra-2 binding at gene promoters, but involves their binding to distal enhancers. My NG-Capture C results imply the presence of long-range chromatin interactions in Fra-1 modes of action, as well as enhancer hubs containing Fra-1- and non-Fra-1-binding enhancers. No evidence for a role for Fra-1 in the control of chromatin looping was however found using a panel of 35 Fra-1-regulated genes. Moreover, I have addressed the mechanisms of transcriptional repression mediated by Fra-1, as these have practically never been studied, using two model genes, TGFB2 and SMAD6. These studies underlined different mechanisms employed by Fra-1 for the repression of these genes, embodying the complexity of Fra-1 transcriptional regulation mechanisms.

Made available in DSpace on 2014-12-17T13:54:46Z (GMT). No. of bitstreams: 1 LuizAN.pdf: 1830713 bytes, checksum: 33c7ccb755be0994c00e84eb15cb1205 (MD5) Previous issue date: 2009-07-01 / This work considers a ethnography boarding on the Ap?niekra J?-Timbira group of Central Brazil - leaving of a proposal of agreement of the group in perspectives of historical situations, analyzing its social organization from situational approaches. Taking the ethnography as main tool of production of data, the focus of the research takes dimension, when in the course of the ethnography situation, they come out, from certain events, social dramas that if ramify in crises, conflicts, faccionalismo. I analyze the mechanisms elaborated for the group to neutralize these dramas , such as the constitution of a tribal court , composites for native mediators and external mediators, dynamics ritual processes and politicians. / Este trabalho prop?e uma abordagem etnogr?fica sobre os Ap?niekra grupo J?- Timbira do Brasil Central - partindo de uma proposta de entendimento do grupo em perspectivas de situa??es hist?ricas, analisando sua organiza??o social a partir de enfoques situacionais. Tomando a etnografia como ferramenta principal de produ??o de dados, o foco da pesquisa toma dimens?o, quando no curso da situa??o etnogr?fica, eclodem, a partir de certos eventos, dramas sociais que se ramificam em crises, conflitos, faccionalismo. Analiso os mecanismos elaborados pelo grupo para neutralizar esses dramas , tais como a constitui??o de um tribunal tribal , compostos por mediadores nativos e mediadores externos, dinamizando processos rituais e pol?ticos. Palavras- have: Ap?niekra, Timbira, situa??o social, drama social, processo ritual.

Made available in DSpace on 2015-03-03T15:19:19Z (GMT). No. of bitstreams: 1 AndreaLO.pdf: 448824 bytes, checksum: 4a360d0db40a607834f5c380870bc7f5 (MD5) Previous issue date: 2009-02-27 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / The genome of all organisms is subject to injuries that can be caused by endogenous and environmental factors. If these lesions are not corrected, it can be fixed generating a mutation which can be lethal to the organisms. In order to prevent this, there are different DNA repair mechanisms. These mechanisms are well known in bacteria, yeast, human, but not in plants. Two plant models Oriza sativa and Arabidopsis thaliana had the genome sequenced and due to this some DNA repair genes have been characterized. The aim of this work is to characterized two sugarcane cDNAs that had homology to AP endonuclease: scARP1 and scARP3. In silico has been done with these two sequences and other from plants. It has been observed domain conservation on these sequences, but the cystein at 65 position that is a characteristic from the redox domain in APE1 protein was not so conservated in plants. Phylogenetic relationship showed two branches, one branch with dicots and monocots sequence and the other branch with only monocots sequences. Another approach in order to characterized these two cDNAs was to construct overexpression cassettes (sense and antisense orientation) using the 35S promoter. After that, these cassettes were transferred to the binary vector pPZP211. Furthermore, previously in the laboratory was obtained a plant from nicotiana tabacum containing the overexpression cassette in anti-sense orientation. It has been observed that this plant had a slow development and problems in setting seeds. After some manual crossing, some seeds were obtained (T2) and it was analyzed the T2 segregation. The third approach used in this work was to clone the promoter region from these two cDNAs by PCR walking. The sequences obtained were analyzed using the program PLANTCARE. It was observed in these sequences some motives that may be related to oxidative stress response / O genoma de todos os organismos est? sujeitos a les?es que podem ser causados por fatores end?genos e ambientais. Uma vez no genoma, as les?es podem levar a forma??o e ac?mulo de muta??es, as quais podem ser prejudiciais ao desenvolvimento do organismo. As vias de reparo de DNA s?o um mecanismo que permite o organismo detectar e corrigir essas les?es ou minimizar seus efeitos. V?rias vias de reparo de DNA s?o conhecidas e bem caracterizadas em animais e microorganismos. Em plantas, as vias de reparo ainda n?o s?o bem caracterizadas, mas muitas pesquisas t?m revelado a participa??o de todas as vias conhecidas no reparo do genoma das plantas, sendo os modelos mais estudados Arabidopsis thaliana e Oriza sativa. A via de reparo de interesse deste trabalho ? a via de BER, a qual apresenta v?rias prote?nas atuando no reparo do DNA. Por?m, a classe de prote?nas da via BER focadas s?o as AP endonucleases, respons?veis pela hidr?lise do s?tio AP. Este trabalho teve como objetivo caracterizar dois cDNAs de cana-de-a??car: scARP1 e scARP3, hom?logos a AP endonucleases de A.thaliana e identificados num trabalho de data-mining do projeto SUCEST. Para tanto, foram constru?dos cassetes de super-express?o, contendo o cDNA scARP1 sob o controle do promotor forte 35S. Al?m disso, anteriormente no laborat?rio foi obtido uma planta de icotiana tabacum contendo o cassete de super-express?o (35S+scARP1) em orienta??o anti-senso. Foi analisado o desenvolvimento desta planta, e foram obtidas tamb?m algumas sementes (T2) desta planta. Estas sementes foram germinadas e analisadas quanto ? presen?a do cassete de super-express?o e desenvolvimento. Al?m disso, para estes dois genes foram clonados as regi?es promotoras por PCR walking. Os fragmentos obtidos foram clonados, sequenciados e, analisados por meio do programa PLANTCARE. Os motivos encontrados nessas regi?es dos genes de cana-de-a??car foram comparados com potenciais regi?es promotoras das plantas de Arabidopis, O. sativa e S. bicolor. Estas an?lises mostraram a presen?a de diferentes motivos relacionados ? respostas ao estresse oxidativo

Devido ao compromisso com a melhoria do meio ambiente, aliado às crescentes exigências dos órgãos ambientais, e a necessidade de identificar a contribuição de cada atividade/processo desenvolvido em institutos de pesquisas, quanto ao impacto destes à qualidade do ar, este trabalho teve a finalidade de desenvolver um modelo de inventário e aplicar uma metodologia de cálculo, que permita estimar a emissão de poluentes atmosféricos, decorrentes das atividades dos centros de pesquisa e desenvolvimento do Instituto de Pesquisas Energéticas e Nucleares (IPEN/CNEN-SP). O estudo foi motivado pela ausência de metodologias de cálculo de emissões atmosféricas específicas para fontes fixas como capelas químicas de exaustão e da necessidade em atender as condicionantes estabelecidas no licenciamento ambiental da instituição. Para a elaboração dos cálculos foram adotados os fatores de emissão e a equação descrita na AP-42 da EPA- Environmental Protection Agency. Foram utilizadas como abordagens de cálculo de emissões: a) Mensuração direta (por meio do inventário de emissões atmosféricas); e b) Estimativa de emissões (utilizando estimativa da taxa de emissão calculada a partir do fator de emissão apropriado). O estudo foi detalhadamente realizado tendo como base inicial o inventário e o modelo de estimativa de emissão atmosférica das fontes fixas aplicado no Centro de Química e Meio Ambiente (CQMA). Cabe ressaltar que o monitoramento online da qualidade do ar no campus é realizado em estação fixa, parceria IPEN CETESB, na estação CETESB Cid. Universitária IPEN - USP. O estudo possibilitou estabelecer, de forma efetiva, o Programa de Monitoramento e Controle de Emissões Atmosféricas (PMEA IPEN), podendo servir de modelo para outras instituições de Pesquisa, Desenvolvimento & Inovação. Como produto final obteve-se um inventário de emissões atmosféricas de fontes fixas da instituição, a taxa de emissão de poluentes, bem como a concentração de poluentes emitidos. A estimativa das emissões não ultrapassou os limites dispostos na legislação em âmbito nacional e estadual. / Atmospheric Emission Factors and Significance Analysis applied to the Air Quality Management in the IPEN / CNEN-SP Campus due to the commitment to improve the environment, combined with the increasing demands of environmental agencies, and the need to identify the contribution of each activity / process developed in research institutes, as well as the impact of these on the air quality, this work aims to develop an inventory model and apply a methodology of calculation for measuring the emission of atmospheric pollutants, arising from the activities of the research and development centers of the Nuclear and Energy Research Institute (IPEN / CNEN-SP). The study was motivated by the absence of atmospheric emission calculation methodologies specific to stationary sources, such as fume hoods. For preparation of the calculations, the emission factors and the equation described in the AP-42 EPA- Environmental Protection Agency were adopted. The emission calculation methods used were: a) Direct measurement (through the inventory of air emissions); and b) Emissions estimate (using the emission rate estimate calculated from the appropriate emission factor). The study was carried out in detail, based on the inventory and model of atmospheric emission of fixed sources applied at the Chemistry and Environment Center (CQMA). It should be noted that online monitoring of air quality on campus is carried out at a fixed station, IPEN CETESB partnership, at CETESB Cid station. University - IPEN - USP. The study has made it possible to establish, in an effective way, the Atmospheric Emission Monitoring and Control Program (PMEA - IPEN), which could serve as a model for other Research, Development and Innovation institutions. The final product was an inventory of atmospheric emissions from fixed sources of the institution, the emission rate of pollutants, as well as the concentration of pollutants emitted. The estimation of the emissions did not exceed the limits established in the national legislation and state level.