Growth rates between individually tagged Atlantic halibut, from a single batch of farm produced eggs, on-grown in sea cages and pump ashore tanks for three years were significantly different. The tank reared fish 405g - 5992g showed a 29% premium in growth (final weight) compared to the cage reared fish 444g -4640g. Females in both systems reached a greater size (7352g tanks, 5836g cages) than males. Males that matured early (3819g tanks, 2877g cages) had a lower mean end weight than males maturing a year later (4326g tanks, 3086g cages). Early maturing males had the largest initial size. Seasonal variations in growth were observed for all groups. Major divergences in growth between males and females only became apparent when the males first matured at around 1.5 - 2 kg. No female maturation was observed during the trial. Halibut growth was determined to be positively allometric with growth of males being more linear then females. Condition factor increased with time whilst there was a decrease in Specific Growth Rate (SGR) from approximately 0.5%day⁻¹ to 0.1%day⁻¹ throughout the trial. Concentrations of plasma cortisol, osmolality, chloride and glucose measured through the trial provided no evidence of chronic stress at either site. Acute confinement stress (2, 12 and 30 minutes) was shown to elicit both primary and secondary stress responses in accordance with other marine teleosts. Increases in plasma cortisol, osmolality, CI⁻, Na⁺ and glucose were observed, reaching maximum concentrations within 80 minutes, although there was no effect on plasma K⁺. The duration of the confinement appeared to have no effect on the magnitude of the response. Following repeat confinements (4 days later) there was no evidence of either habituation or a cumulative effect in terms of cortisol or glucose whereas the effects on osmoregulatory function (Na⁺, CI⁻ and osmolality) appeared to be longer lasting. The results provided the first information regarding the stress response of the Atlantic halibut and enabled a better interpretation of the vales measured in the fish reared in tanks and cages (chapter 1). In vitro cortisol production (% above basal secretion), measured by radioimmunoassay, from perifused interrenal tissue of the Atlantic halibut was significantly stimulated by porcine adrenocorticotrophic hormone (ACTH) (0.01-1.0 μM) and [Asn¹, Val⁵] angiotensin II (All) (0.1-lO μm). No significant increase in cortisol production resulted from physiological levels of potassium (K⁺) although non-physiological levels (lOmMKl) did elicit a mild response in comparison to the effects of ACTH and All. Maximum steroid production was in response to 0.01μM ACTH (1351% above basal secretion) and 1.0μM All (397% above basal secretion). With increased concentrations above these levels of both ACTH and All there was a reduction in the degree of cortisol stimulation. The results show that the interrenal tissue of the Atlantic halibut responds in accordance to that of other teleosts to classical steroidogenic peptides.

Osteoarthritis is a degenerative joint disease characterized by progressive erosion of the articular cartilage. Epidemiological studies have established a relationship between osteoarthritis and menopause suggesting that estrogen may be important in the development of cartilage regeneration therapies. The overall goal of this research project was to advance the field of cartilage tissue regeneration by investigating the role of 17 ß -estradiol (E2), an active estrogen metabolite, on the chondrocyte phenotype. The central hypothesis was that E2 plays an important and sex-specific role in regulating chondrogenesis. Specific Aim-1 focused on establishing and characterizing a primary human articular chondrocyte (HAC) cell source, and then examining the response of the cells in culture to E2. It was demonstrated that the response of HACs to E2 treatment was sex-specific despite both male and females cells expressing estrogen receptors. Female HACs showed changes in proliferation, matrix production, and differentiation while male cells did not. In addition, the female response was regulated through a rapid membrane signaling pathway mediated by protein kinase C. Specific Aim-2 involved establishing an ovariectomized animal model to investigate the effects of E2 on orthopaedic tissue implants. Human demineralized bone matrix (DBM) was implanted intramuscularly into female nude mice and rats. Ovariectomy was shown to reduce the ability of DBM to induce the formation of cartilage and bone tissue. Moreover, the inductive properties of DBM were reestablished with subcutaneous E2 supplementation. Specific Aim-3 entailed developing and characterizing a microencapsulation method for in vitro culture and in vivo delivery of chondrocytes to study the effects of E2 on chondrogenesis. Rat growth plate chondrocytes and HACs were microencapsulated in alginate using an extrusion method in conjunction with high electrostatic potential. Chondrocytes maintained their phenotype in alginate suspension but were unable to form cartilage tissue when implanted into our animal model. Further optimization of the system is required before the role of E2 on chondrogenesis of tissue engineered constructs can be determined. In summary, our results suggest that the successful production of tissue engineered therapies will likely depend on understanding and manipulating the actions of sex hormones in both the in vitro and in vivo environment.

Many organisms are sexually dimorphic for ecologically and socially important traits. One of the major foci of biology is to understand the evolution of such sexually dimorphic traits. Here I present my work on the evolution of a dimorphic trait, female-limited Batesian mimicry, in Papilio swallowtail butterflies. I begin by developing a character state path network to study the diversity of mimicry types and directionality of trait change during the evolution of female-limited mimicry. My phylogenetic analysis showed that female-limited mimicry has evolved independently in several groups of swallowtails, mainly via single-step character changes from monomorphic non-mimetic ancestors to female-limited mimetic descendents. Mimetic polymorphism has evolved in tandem with female-limited mimicry, the two being tightly correlated among mimetic species. Most traditional explanations of female-limited mimicry and mimetic polymorphism invoke sexual selection. In reviewing these hypotheses, I show that their key assumptions and predictions remain untested, and that sexual selection cannot maintain female polymorphism under some conditions. Sexual selection hypotheses are also unable to explain community ecological aspects of mimicry rings. Hence, I developed a novel model of female-limited mimicry based on sex-specific, frequency- and density-dependent advantages of mimicry. This model shows that both-sex mimicry, female-limited mimicry and mimetic polymorphism are favored along a gradient of relative mimic frequency. My ecological data from south Indian mimicry rings support a key prediction of this model. Finally, I employ the patterns of female-limited mimicry among swallowtail butterflies to highlight the contrast between Darwin’s sexual selection model and Wallace’s natural selection model of sexual dimorphism. I show that most of the sexual dimorphism in swallowtail wing color patterns is a product of natural selection for protective female coloration, predominantly in the form of female-limited mimicry. Thus, swallowtails support Wallace’s model of sexual dimorphism, underlining the importance of natural selection. / text

Gender is a pervasive and regulating social institution that is operationalized in mainstream Western culture as a natural extension of the ontological difference perceived to exist between the binarily sexed bodies of male and female. Feminist theory has widely established, however, that gender is done - i.e., gender is not a naturally occurring phenomenon, but is an ongoing construction engaged and replicated by individual actors and which, while compulsory, is nevertheless optional. Within this canon is a small number of feminist theorists, notably Judith Lorber, Judith Bulter, and Nancy Tuana, who argue that the constructive manifestations of gender performativity (that is, doing of gender) are not limited to the social sphere. They argue the role of gender in the construction of the material body, asserting that doing gender has a constructive role in physical embodiment: what we do influences, and in fact creates, what our bodies are. This study engages feminist theory on the production of the body through a qualitative exploration of the lived experience of gendered bodily change, as described in the first-hand narratives of trans-identified individuals. I predict that the analysis of the narratives in the sample will show that in comparison to cisgender individuals, trans individuals possess a heightened awareness of the performative nature of gender, and that trans individuals consciously engage performativity in order to conform to the normative expectations associated with the desired gender role. I further predict that trans individuals experience sexually dimorphic bodily change to be a direct result of changes to their gender identity. The interview analysis findings provide mixed support for the first hypothesis, demonstrating that while trans individuals in the sample do demonstrate a heightened awareness of the ways in which gender is performed, the respondents’ insights came largely from their experiences in their compulsorily cisgender, pre-transition lives, rather than their current gender embodiments. The concept of performativity and its perceived implication of artificiality clashed with the respondents’ sense of their gendered actions as an expression of an authentic self, and my analysis thus addresses performativity as a necessarily polemic concept located between the subjectivity of the individual narratives and the theoretical position that gender is done. The findings provide a substantial level of support for the second hypothesis that trans individuals understand experienced bodily change to be a direct result of changes in gender identity. This study’s exploration of trans experiences of lived bodily change contributes a narrative perspective to the ongoing discussion in feminist theory which surrounds the role of gender in the production of the material body.

Submitted by Celso Magalhaes (celsomagalhaes@ufrrj.br) on 2017-05-03T14:02:59Z No. of bitstreams: 1 2014 - Natalia Soares Carvalho de Souza.pdf: 1833535 bytes, checksum: 4574c94ab4a477d9f8d0ddf31d6b4069 (MD5) / Made available in DSpace on 2017-05-03T14:03:00Z (GMT). No. of bitstreams: 1 2014 - Natalia Soares Carvalho de Souza.pdf: 1833535 bytes, checksum: 4574c94ab4a477d9f8d0ddf31d6b4069 (MD5) Previous issue date: 2014-08-26 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior - CAPES / Premenopausal women are less prone to develop cardiovascular diseases than men and this advantage do not persist in postmenopausal women. Thus herein we aimed to investigate the gender difference and the estrogen influence in cardiac function, fluid balance and thyroid status, in Wistar rats subjected to experimental model of myocardial infarction (MI). In the first step, adult male (n = 18) and female (n = 21) rats underwent experimental MI (MIm and MIf,) or sham-operation (ShamM and ShamF) respectively. One and four weeks post-MI rats were placed in metabolic cages, subjected to echocardiography (ECHO), electrocardiography and then euthanized for blood sample collection and tissue collection (heart, lung and liver). In the second step female rats were ovariectomized (n = 24) or continued intact (n = 21), two weeks later they were subjected to MI (MIOVX and MIINT, respectively) or sham operation (ShamOVX and ShamINT). Four weeks post-MI, they were subjected to the same evaluations of the first step, not only the electrocardiography. In the third step, female rats were subjected to ovariectomy and treated with estrogen (E2) (n = 13) or vehicle (n = 22). Two weeks later they underwent experimental MI (MIOVX+E2 and MIOVX+Veh). Four weeks post-MI they were subjected to the same evaluations of the second step. Male infarcted rats developed cardiac dysfunction (shortening fraction, SF, reduction, ~ 70%) and fluid homeostasis changes (sodium intake increasing, ~ 146% and urinary volume reduction, ~55%) earlier than female, in the first week post-MI while female presented these changes (SF reduction, ~28% and sodium intake increasing, ~143%) only in the fourth week and attenuated compared to male. MIM showed reduction in LF/HF ratio (~70%), one week post-MI. And only male rats presented hypothyroidism after MI (T4 ~52% and T3 ~38%, reduction). We also verified reduction in SF (~55%), increasing in LA/Ao ratio (~75%) and changes in fluid balance (sodium intake reduction, ~67% and urinary volume reduction, ~40%) more pronounced in MIOVX than in MIINT. MIOVX group reduced thyroid hormone levels after MI (T3 ~35%). MIOVX+Veh showed more pronounced reduction in SF (~55%) and increasing in LA/Ao ratio (~75%) than the MIOVX+E2 group. The sodium intake reduced in MIOVX+Veh (~67%) and in the urinary volume we verified significant reduction in ShamOVX+Veh and MIOVX+Veh groups compared to ShamOVX+E2 and MIOVX+E2 groups (P < 0.05). Serum T3 reduced significantly (~35%) only in MIOVX+Veh group. The pathophysiological development of heart failure post-MI was attenuated in female compared to male. And female rats subjected to MI presented fluid balance more favorable and related to the less pronounced development of heart failure. Estrogen seems to influence positively the cardiac function and attenuate the dysfunction that occur post-MI. The euthyroid status in female intact do not seems to be determinant to the less pronounced development of heart failure / Sabe-se que mulheres na pr?-menopausa apresentam menor preval?ncia de doen?as cardiovasculares do que homens e, esta diferen?a desaparece ap?s a menopausa. Sendo assim, o presente estudo buscou avaliar o dimorfismo sexual e a influ?ncia do estr?geno nas altera??es da fun??o card?aca, do equil?brio hidroeletrol?tico e do status tireoidiano de ratos Wistar submetidos ao infarto do mioc?rdio (IM) experimental. Na primeira etapa ratos wistar machos (n = 18) e f?meas (n = 21) foram submetidos ao infarto experimental (INF.M e INF.F) ou ? falsa cirurgia (Sham.M e Sham.F). Na primeira e quarta semana p?s-IM foram colocados em gaiolas metab?licas e submetidos ? ecodopplercardiografia (ECO) e eletrocardiografia (an?lise espectral), seguido de eutan?sia para coleta de sangue (dosagem s?rica de horm?nios tireoidianos) e de tecidos (cora??o, pulm?o e f?gado, para biometria). Na segunda etapa, f?meas foram ovariectomizadas (n = 24) ou mantidas intactas (n = 21) e ap?s duas semanas submetidas ao infarto do mioc?rdio (INFOVX e INFINT) ou ? falsa cirurgia (ShamOVX e ShamINT). Quatro semanas ap?s p?s-IM, as mesmas avalia??es da etapa anterior foram realizadas exceto a eletrocardiogr?fica. Na terceira etapa, foi realizada ovariectomia e reposi??o com estr?geno (E2) ( n = 13) ou ve?culo (n = 22). Ap?s duas semanas foi realizada a cirurgia de indu??o ao infarto (INFOVX+E2 e INFOVX+Veic) e a falsa cirurgia (ShamOVX+E2 e ShamOVX+Veic). Decorridas quatro semanas foram feitas as mesmas avalia??es da segunda etapa. O grupo INFM desenvolveu disfun??o card?aca (fra??o de encurtamento, FEnc%, ~70% de redu??o) e altera??es na regula??o hidroeletrol?tica (aumento do apetite por s?dio, ~146% e redu??o do volume urin?rio, ~55%), uma semana p?s-IM e, portanto, mais cedo que as f?meas, que apresentaram altera??es na fun??o card?aca (FEnc%, ~28% de redu??o) e regula??o hidroeletrol?tica (aumento do apetite por s?dio, ~143%) na quarta semana p?s-IM. O grupo INFM apresentou redu??o na rela??o LF/HF (~70%), uma semana p?s-IM. E, apenas os ratos machos desenvolveram hipotireoidismo ap?s o infarto. Tamb?m foi observada redu??o da FEnc% (~55%), aumento da rela??o ?trio esquerdo/ aorta (AE/Ao, ~75%) e altera??es na regula??o hidroeletrol?tica (redu??o do apetite por s?dio, ~67% e do volume urin?rio, ~40%) mais pronunciadas em INFOVX do que em INFINT. O grupo INFOVX tamb?m apresentou redu??o dos n?veis s?ricos de T3 (~35%) p?s-IM. O grupo INFOVX+Vei mostrou redu??o da FEnc% (~55%) e aumento na rela??o AE/Ao (~75%) mais pronunciadas que o grupo INFOVX+E2. INFOVX+Vei reduziu o apetite por s?dio (~67%) e, no volume urin?rio, foi observada redu??o significativa nos grupos ShamOVX+Vei e INFOVX+Vei em rela??o aos grupos ShamOVX+E2 e INFOVX+E2 (P<0,05). O T3 s?rico reduziu significativamente (~35%) apenas no grupo INFOVX+Vei. Houve diferen?a no desenvolvimento fisiopatol?gico da insufici?ncia card?aca (IC) p?s- IM entre machos e f?meas, sendo mais brando nas f?meas. E f?meas infartadas apresentaram uma regula??o hidroeletrol?tica mais favor?vel e compat?vel com o desenvolvimento menos acentuado da IC. O estr?geno influenciou positivamente a regula??o hidroeletrolitica de f?meas infartadas, o que favoreceu a fun??o card?aca e atenuou desta forma, a disfun??o que ocorre ap?s o infarto. A manuten??o do status eutire?ideo n?o pareceu ser determinante para o desenvolvimento menos pronunciado da IC