Que mulher é essa?: identidade, política e saúde no movimento de travestis e transexuais

O objeto desta dissertação é explorar os discursos militantes relativos à diferenciação entre as identidades coletivas de travestis e transexuais no âmbito do movimento de travestis e transexuais brasileiro e sua repercussão nas demandas e proposições de políticas públicas de saúde, mais especificamente no que tange às transformações corporais. Realizei entrevistas semi-estruturadas com ativistas reconhecidas como lideranças desse movimento, tendo como principais eixos: trajetória militante, diferenciação entre travestis e transexuais, organização do movimento, agenda política, transformações corporais e demandas relativas à saúde. Além disso, realizei etnografias em encontros gerais do movimento LGBT, assim como nos específicos de travestis e transexuais, com destaque para o XVI e XVII Encontro Nacional de Travestis e Transexuais (ENTLAIDS), realizados no Rio de Janeiro em 2009 e em Aracaju em 2010; a V Conferência Regional para América Latina e Caribe da ILGA (International Lesbian and Gay Association), realizada em Curitiba em 2009; e a I Marcha Nacional Contra a Homofobia, realizada em 19 de maio de 2010 em Brasília. A partir dos resultados das entrevistas e das etnografias, busco construir um histórico do movimento de travestis e transexuais no Brasil, no qual é possível localizar a emergência das categorias identitárias e seus conflitos. Assim, minha investigação passa pela análise da relação com categorias estigmatizantes como a prostituição e, especialmente, das capacidades de incorporação ou de apropriação de discursos médicos e psiquiátricos na construção de identidades, o que inclui a influência de fatores de classe e de acesso a serviços de saúde especializados, notoriamente o processo transexualizador no SUS. A análise das principais demandas do movimento me levou a uma relação entre políticas de reconhecimento e processos de purificação. Por fim, busco compreender o processo de construção de uma carreira militante no movimento de travestis e transexuais.

O gênero encarnado: modificações corporais e riscos à saúde de mulheres trans

Este estudo discute as transformações corporais realizadas por mulheres trans a partir das suas narrativas, coletadas através de entrevistas semi-estruturadas e complementadas pela observação participante realizada em seus diferentes espaços de sociabilidade. Agrega também análise documental e pesquisa bibliográfica, com o objetivo de contextualizar e localizar histórica e socialmente o objeto da pesquisa. Fizeram parte deste estudo: travestis, mulheres transexuais, bombadeiras, cirurgiões plásticos e a equipe de saúde do ambulatório trans de um hospital universitário da cidade do Rio de Janeiro.O processo de investigação desdobrou-se em três diferentes níveis: análise dos discursos contidos nos dispositivos legais, políticas de saúde voltadas para as pessoas trans, materiais informativos, técnicos e educativos; análise das narrativas de travestis e mulheres transexuais em seus itinerários de reconstrução corporal; e análise de saberes e práticas de bombadeiras, cirurgiões plásticos e profissionais de saúde, suas concepções sobre a relação corpo e gênero e sua percepção de risco e cuidados com a saúde. Os dados coletados foram sistematizados e interpretados à luz da análise de conteúdo temática, privilegiando as narrativas dos sujeitos sobre suas experiências, saberes e práticas, comparando-os aos resultados da revisão de literatura e ao previsto nos dispositivos legais que normatizam o direito das mulheres trans à saúde.Os resultados demonstram que as mulheres trans investigadas começam a estranhar seus corpos, gostos e desejos ainda na infância e que dois fatos parecem indispensáveis para a decisão em modificar o corpo: a emergência e aceitação da identidade trans e o acesso à informação sobre técnicas, substâncias e pessoas que podem ajudá-las a fazer um corpo de mulher. As minhas interlocutoras demonstraram conhecer os riscos do uso do silicone industrial e hormônios na construção clandestina do corpo, mas também me fizeram constatar que é a situação financeira de cada uma que define as formas seguras ou não de modificação corporal. O conjunto de normativas, através das leis, resoluções e portarias que, de certa forma, anunciam uma política de saúde para as mulheres trans, entende de forma diferenciada e reducionista as identidades trans, localizando travestis e transexuais em diferentes alternativas de cuidado à saúde, muitas vezes, centrando as travestis nas estratégias de prevenção das DST-AIDS e as mulheres transexuais no acesso à cirurgia de transgenitalização, sem que seja proposto, ou melhor, efetivados serviços e práticas de modificação corporal no SUS. Essa conformação das políticas, sistemas e serviços de saúde, acaba por recrudescer a recorrência das mulheres trans aos serviços das bombadeiras, fato que aumenta os riscos à saúde dessas pessoas. Mesmo para as mulheres transexuais cadastradas no processo transexualizador, o foco do atendimento é a construção da genitália, ficando a modificação corporal (implante de próteses mamária e/ou glúteos, depilação a laser, lipoescultura, rinoplastia e feminização da face) para quando possível. Estas mulheres esperam que o sistema de saúde compreenda sua necessidade de modificação corporal não como uma questão meramente de estética, mas como uma questão de saúde pública.

La función de la piel y de las modificaciones corporales en la constitución del Yo

En la teoría de las relaciones objetales y en particular en la teoría de Esther Bick, la piel cumple una función definitiva dentro del proceso de constitución del Yo: con la noción de piel-como-continente se enfatiza la función de este órgano en permitir al infante integrar las partes de su personalidad. Para desarrollar esta función, resulta indispensable introyectar la función contenedora de la madre, pues de no realizarse tal introyección, el individuo deberá desarrollar métodos sustitutivos para contenerse. De acuerdo con la teoría de Bick, estos métodos tomarían la forma de una segunda piel. Este artículo analiza las modificaciones corporales y su posible relación con las manifestaciones de segunda piel en la adultez.

O dispositivo analítico no hospital na clínica com transexuais: entre o ser e o sujeito

Pós-graduação em Psicologia - FCLAS

Corpos tatuados : experiências sensíveis em realidade aumentada móvel

Tese (doutorado)—Universidade de Brasília, Instituto de Artes, Programa de Pós-Graduação em Artes, 2015.

Reactive Oxygen Species and Reactive Nitrogen Species in Epigenetic Modifications

For the normal homeostasis of a cell, there must be a balance between radical oxygen species/radical nitrogen species (ROS/RNS) production and the neutralization of these species by antioxidant scavenging. In times of stress, this balance is not maintained, and the result is oxidative stress. This stress can affect many pathways in the body and result in pathological consequences. Recent evidence suggests that ROS/RNS can affect the epigenetic regulation of genes by affecting the function of histone and DNA modifying enzymes, thus affecting phenotypic changes within the cellular environment. In the following chapter, we provide a broad overview of how oxidative stress induced by ROS/RNS can affect epigenetics, and using lung disease as our model we link the connection between these processes.

Synthetic Modifications of Estrogens and Androgens

Estrogens the female sex hormones have numerous biological actions. Estradiol is the most abundant estrogen in women before menopause. It influences the development, maturation and function of the female reproductive tract. It also plays a role in mammary cancer. Accordingly determinations of estradiol level in body fluids assist in the evaluation of ovarian function and diagnosis for malignancies. Estriol is the primary estrogen in pregnant women and secreted from the fetoplacental unit. Measurement of estriol in maternal body fluids is the basis of fetoplacental monitoring test. Concentration of estrogens in body fluids is determined by immunoassay. Accuracy of this measurement depends on the availability of a specific antibody. As estrogens are not antigenic, their derivatives (haptens) are coupled with a carrier and this hapten-protein conjugate is used to generate antibodies. Specificity of the generated antibody largely depends on the structure of hapten. Therefore the synthesis of a hapten with a right structure is crucial for the accurate measurement of a steroid. We have synthesised new haptens for estradiol and estriol by adding an alkyl or alkoxy side chain at the C-7 of estrane skeleton. The side chains carry a terminal amino group, which can be used for conjugation with a carrier molecule. Estrogens and their biosynthetic precursor androgens both exist as fatty acid esters. They are known to act as hormone storage but their physiological role is not completely known yet. Our collaborator is studying their effect in cardiovascular diseases. We synthesised fatty acid ester derivatives of several steroids in high yield by a very rapid procedure (in 1 min) under microwave irradiation in an ionic liquid (IL). An expedient regioselective hydrolysis at C-3 of estradiol diesters is also reported. 8-Isoestrogens are compounds of pharmaceutical interests, their synthesis, structure, conformation and biological activity studies are ongoing. 7-Hydroxy-8-isoestradiol and 7-alkyl ether of it were synthesised as well. During this study we have developed a selective O-debenzylation method. A mild route for selective removal of benzylic protection on phenol in presence of benzyl protected alcohol was explored.

The effects of an acute bout of whole-body vibration on pulse wave velocity in individuals with SCI

Cardiovascular disease is a leading cause of mortality in the spinal cord injured (SCI) population. Reduced arterial compliance is a cardiovascular risk factor and whole body vibration (WBV) has be en shown to improve arterial compliance in able-bodied individuals. The study investigated the effect of an acute session ofWBV on arterial compliance as measured by pulse wave velocity (PWV). On separate days, arm, leg and aortic PWV were measured pre- and post- a 45 minute session of passive stance (PS) and WBV. The WBV was intermittent with a set frequency of 45Hz and amplitude of O.6mm. There was no condition by time effect when comparing PWV after WBV and PS. Following WBV, aortic (928.6±127.7 vs. 901.1±96.6cm/sec), leg (1035.2±113.8 vs.l099.8±114.2cm/sec) and arm PWV (1118.9±119.8 vs. 1181.1±124.4cm/s) did not change. As such, WBV did not reduce arterial compliance, however future research with protocol modifications is recommended.

Effect of increased milk intake combined with endurance exercise training on body composition, blood-lipids and inflammatory markers in overweight young males

Consuming low-fat milk (LFM) after resistance training leads to improvements in body composition. Habitual aerobic exercise and dairy intake are relatively easy lifestyle modifications that could benefit a population at risk for becoming obese. Thus, the purpose of this study was to investigate combining increased LFM intake with endurance exercise on body composition, blood-lipid profile and metabolic markers. 40 young males were randomized into four groups: one ingesting 750mL LFM immediately post-exercise, the other 6hrs post-exercise; and two isocaloric carbohydrate groups ingesting at the two different times. Participants completed a 12 week endurance-training program (cycling 1 hour/day at ~60%VO2peak, 5 days/week). 23 participants completed the study. Increases in lean mass (p < 0.05), and decreases in anti-inflammatory marker adiponectin (p < 0.05) were seen in all groups. No other significant changes were observed. Future analyses should focus on longer duration exercise and include a larger sample.

Regulation of BAP1 tumor suppressor complex by post-translational modifications

Le régulateur transcriptionnel BAP1 est une déubiquitinase nucléaire (DUB) dont le substrat est l’histone H2A modifiée par monoubiquitination au niveau des residus lysines 118 et 119 (K118/K119). Depuis les dernières années, BAP1 emerge comme un gene suppresseur de tumeur majeur. En effet, BAP1 est inactivé dans un plethore de maladies humaines héréditaires et sporadiques. Cependant, malgré l’accumulation significative des connaissances concernant l’occurrence, la pénétrance et l’impact des défauts de BAP1 sur le développement de cancers, ses mécanismes d’action et de régulation restent très peu compris. Cette étude est dédiée à la caractérisation moléculaire et fonctionnelle du complexe multi-protéique de BAP1 et se présente parmi les premiers travaux décrivant sa régulation par des modifications post-traductionnelles. D’abord, nous avons défini la composition du corps du complexe BAP1 ainsi que ses principaux partenaires d’interaction. Ensuite, nous nous sommes spécifiquement intéressés a investiguer d’avantage deux principaux aspects de la régulation de BAP1. Nous avons d’abord décrit l’inter-régulation entre deux composantes majeures du complexe BAP1, soit HCF-1 et OGT. D’une manière très intéressante, nous avons trouvé que le cofacteur HCF-1 est un important régulateur des niveaux protéiques d’OGT. En retour, OGT est requise pour la maturation protéolytique de HCF-1 en promouvant sa protéolyse par O-GlcNAcylation, un processus de régulation très important pour le bon fonctionnement de HCF-1. D’autre part, nous avons découvert un mécanisme unique de régulation de BAP1 médiée par l’ubiquitine ligase atypique UBE2O. en effet, UBE2O se caractérise par le fait qu’il s’agit aussi bien d’une ubiquitine conjuratrice et d’une ubiquitine ligase. UBE2O, multi-monoubiquitine BAP1 au niveau de son domaine NLS et promeut son exclusion du noyau, le séquestrant ainsi dans le cytoplasme. De façon importante, nos travaux ont permis de mettre de l’emphase sur le rôle de l’activité auto-catalytique de chacune de ces enzymes, soit l’activité d’auto-déubiquitination de BAP1 qui est requise pour la maintenance de sa localisation nucléaire ainsi que l’activité d’auto-ubiquitination d’UBE2O impliquée dans son transport nucléo-cytoplasmique. De manière significative, nous avons trouvé que des défauts au niveau de l’auto-déubiquitination de BAP1 due à des mutations associées à certains cancers indiquent l’importance d’une propre regulation de cette déubiquitinase pour les processus associés à la suppression de tumeurs.

Pseudechis australis Venomics: Adaptation for a Defense against Microbial Pathogens and Recruitment of Body Transferrin

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

A new species of the neotropical catfish genus Trichomycterus (Siluriformes : Trichomycteridae) representing a new body shape for the family

Trichomycterus crassicaudatus is described as a new species from the Rio Iguacu basin in southern Brazil. The new species has an exceptionally deep posterior region of the body (caudal peduncle depth 22.8-25.4% SL), resulting in an overall shape which distinguishes it at once from all other members of the Trichomycteridae. The caudal fin of the species is broad-based and forked, a shape also distinguishing it from all other species in the family. A number of autapomorphic modifications of T. crassicaudatus are associated with the deepening of the caudal region, including an elongation of the hemal and neural spines of the vertebrae at the middle of the caudal peduncle. Phylogenetic relationships of the new species are yet unresolved, but it shares a similar color pattern and a thickening of caudal-fin procurrent rays with T. stawiarski, a poorly-known species also from the Rio Iguacu basin. Coloration and body shape also include similarities with T. lewi from Venezuela.

Changes in food intake, metabolic parameters and insulin resistance are induced by an isoenergetic, medium-chain fatty acid diet and are associated with modifications in insulin signalling in isolated rat pancreatic islets

LLong-chain fatty acids are capable of inducing alterations in the homoeostasis of glucose-stimulated insulin secretion (GSIS), but the effect of medium-chain fatty acids (MCFA) is poorly elucidated. In the present study, we fed a normoenergetic MCFA diet to male rats from the age of 1 month to the age of 4 months in order to analyse the effect of MCFA on body growth, insulin sensitivity and GSIS. The 45% MCFA substitution of whole fatty acids in the normoenergetic diet impaired whole body growth and resulted in increased body adiposity and hyperinsulinaemia, and reduced insulin-mediated glucose uptake in skeletal muscle. In addition, the isolated pancreatic islets from the MCFA-fed rats showed impaired GSIS and reduced protein kinase Ba (AKT1) protein expression and extracellular signal-related kinase isoforms 1 and 2 (ERK(1/2)) phosphorylation, which were accompanied by increased cellular death. Furthermore, there was a mildly increased cholinergic sensitivity to GSIS. We discuss these findings in further detail, and advocate that they might have a role in the mechanistic pathway leading to the compensatory hyperinsulinaemic status found in this animal model.

LPS-induced modifications in spontaneous network activity causes neuronal apoptosis in neonatal cerebral cortex

During the perinatal period the developing brain is most vulnerable to inflammation. Prenatal infection or exposure to inflammatory factors can have a profound impact on fetal neurodevelopment with long-term neurological deficits, such as cognitive impairment, learning deficits, perinatal brain damage and cerebral palsy. Inflammation in the brain is characterized by activation of resident immune cells, especially microglia and astrocytes whose activation is associated with a variety of neurodegenerative disorders like Alzheimer´s disease and Multiple sclerosis. These cell types express, release and respond to pro-inflammatory mediators such as cytokines, which are critically involved in the immune response to infection. It has been demonstrated recently that cytokines also directly influence neuronal function. Glial cells are capable of releaseing the pro-inflammatory cytokines MIP-2, which is involved in cell death, and tumor necrosis factor alpha (TNFalpha), which enhances excitatory synaptic function by increasing the surface expression of AMPA receptors. Thus constitutively released TNFalpha homeostatically regulates the balance between neuronal excitation and inhibition in an activity-dependent manner. Since TNFalpha is also involved in neuronal cell death, the interplay between neuronal activity MIP-2 and TNFalpha may control the process of cell death and cell survival in developing neuronal networks. An increasing body of evidence suggests that neuronal activity is important in the regulation of neuronal survival during early development, e.g. programmed cell death (apoptosis) is augmented when neuronal activity is blocked. In our study we were interested on the impact of inflammation on neuronal activity and cell survival during early cortical development. To address this question, we investigated the impact of inflammation on neuronal activity and cell survival during early cortical development in vivo and in vitro. Inflammation was experimentally induced by application of the endotoxin lipopolysaccharide (LPS), which initiates a rapid and well-characterized immune response. I studied the consequences of inflammation on spontaneous neuronal network activity and cell death by combining electrophysiological recordings with multi-electrode arrays and quantitative analyses of apoptosis. In addition, I used a cytokine array and antibodies directed against specific cytokines allowing the identification of the pro-inflammatory factors, which are critically involved in these processes. In this study I demonstrated a direct link between inflammation-induced modifications in neuronal network activity and the control of cell survival in a developing neuronal network for the first time. Our in vivo and in vitro recordings showed a fast LPS-induced reduction in occurrence of spontaneous oscillatory activity. It is indicated that LPS-induced inflammation causes fast release of proinflammatory factors which modify neuronal network activity. My experiments with specific antibodies demonstrate that TNFalpha and to a lesser extent MIP-2 seem to be the key mediators causing activity-dependent neuronal cell death in developing brain. These data may be of important clinical relevance, since spontaneous synchronized activity is also a hallmark of the developing human brain and inflammation-induced alterations in this early network activity may have a critical impact on the survival of immature neurons.

Age-related functional and structural retinal modifications in the Igf1−/− null mouse

Background. Mutations in the gene encoding human insulin-like growth factor-I (IGF-I) cause syndromic neurosensorial deafness. To understand the precise role of IGF-I in retinal physiology, we have studied the morphology and electrophysiology of the retina of the Igf1−/− mice in comparison with that of the Igf1+/− and Igf1+/+ animals during aging. Methods. Serological concentrations of IGF-I, glycemia and body weight were determined in Igf1+/+, Igf1+/− and Igf1−/− mice at different times up to 360 days of age. We have analyzed hearing by recording the auditory brainstem responses (ABR), the retinal function by electroretinographic (ERG) responses and the retinal morphology by immunohistochemical labeling on retinal preparations at different ages. Results. IGF-I levels are gradually reduced with aging in the mouse. Deaf Igf1−/− mice had an almost flat scotopic ERG response and a photopic ERG response of very small amplitude at postnatal age 360 days (P360). At the same age, Igf1+/− mice still showed both scotopic and photopic ERG responses, but a significant decrease in the ERG wave amplitudes was observed when compared with those of Igf1+/+ mice. Immunohistochemical analysis showed that P360 Igf1−/− mice suffered important structural modifications in the first synapse of the retinal pathway, that affected mainly the postsynaptic processes from horizontal and bipolar cells. A decrease in bassoon and synaptophysin staining in both rod and cone synaptic terminals suggested a reduced photoreceptor output to the inner retina. Retinal morphology of the P360 Igf1+/− mice showed only small alterations in the horizontal and bipolar cell processes, when compared with Igf1+/+ mice of matched age. Conclusions. In the mouse, IGF-I deficit causes an age-related visual loss, besides a congenital deafness. The present results support the use of the Igf1−/− mouse as a new model for the study of human syndromic deaf-blindness.