Conflicts of law and the mutual recognition of same-sex unions in the EU

My thesis uses legal arguments to demonstrate a requirement for recognition of same-sex marriages and registered partnerships between EU Member States. I draw on the US experience, where arguments for recognition of marriages void in some states previously arose in relation to interracial marriages. I show how there the issue of recognition today depends on conflicts of law and its interface with US constitutional freedoms against discrimination. I introduce the themes of the importance of domicile, the role of the public policy exception, vested rights, and relevant US constitutional freedoms. Recognition in the EU also depends on managing the tension between private international law and freedoms guaranteed by higher norms, in this case the EU Treaties and the European Convention on Human Rights. I set out the inconsistencies between various private international law systems and the problems this creates. Other difficulties are caused by the use of nationality as a connecting factor to determine personal capacity, and the overuse of the public policy exception. I argue that EU Law can constrain the use of conflicts law or public policy by any Member State where these are used to deny effect to same-sex unions validly formed elsewhere. I address the fact that family law falls only partly within Union competence, that existing EU Directives have had limited success at achieving full equality and that powers to implement new measures have not been used to their full potential. However, Treaty provisions outlawing discrimination on grounds of nationality can be interpreted so as to require recognition in many cases. Treaty citizenship rights can also be interpreted favourably to mandate recognition, once private international law is itself recognised as an obstacle to free movement. Finally, evolving interpretations of the European Convention on Human Rights may also support claims for cross-border recognition of existing relationships.

Estrogens, brain and behavior: studies in fundamental neurobiology and observations related to women's health

Mechanisms and consequences of the effects of estrogen on the brain have been studied both at the fundamental level and with therapeutic applications in mind. Estrogenic hormones binding in particular neurons in a limbic-hypothalamic system and their effects on the electrophysiology and molecular biology of medial hypothalamic neurons were central in establishing the first circuit for a mammalian behavior, the female-typical mating behavior, lordosis. Notably, the ability of estradiol to facilitate transcription from six genes whose products are important for lordosis behavior proved that hormones can turn on genes in specific neurons at specific times, with sensible behavioral consequences. The use of a gene knockout for estrogen receptor alpha (ERalpha) revealed that homozygous mutant females simply would not do lordosis behavior and instead were extremely aggressive, thus identifying a specific gene as essential for a mammalian social behavior. In dramatic contrast, ERbeta knockout females can exhibit normal lordosis behavior. With the understanding, in considerable mechanistic detail, of how the behavior is produced, now we are also studying brain mechanisms for the biologically adaptive influences which constrain reproductive behavior. With respect to cold temperatures and other environmental or metabolic circumstances which are not consistent with successful reproduction, we are interested in thyroid hormone effects in the brain. Competitive relations between two types of transcription factors - thyroid hormone receptors and estrogen receptors have the potential of subserving the blocking effects of inappropriate environmental circumstances on female reproductive behaviors. TRs can compete with ERalpha both for DNA binding to consensus and physiological EREs and for nuclear coactivators. In the presence of both TRs and ERs, in transfection studies, thyroid hormone coadministration can reduce estrogen-stimulated transcription. These competitive relations apparently have behavioral consequences, as thyroid hormones will reduce lordosis, and a TRbeta gene knockout will increase it. In sum, we not only know several genes that participate in the selective control of this sex behavior, but also, for two genes, we know the causal routes. Estrogenic hormones are also the foci of widespread attention for their potential therapeutic effects improving, for example, certain aspects of mood and cognition. The former has an efficient animal analog, demonstrated by the positive effects of estrogen in the Porsolt forced swim test. The latter almost certainly depends upon trophic actions of estrogen on several fundamental features of nerve cell survival and growth. The hypothesis is raised that the synaptic effects of estrogens are secondary to the trophic actions of this type of hormone in the nucleus and nerve cell body.

Molecular mechanisms of crosstalk between thyroid hormones and estrogens

Purpose of review Novel analyses of the relations between thyroid hormone receptor signaling and estrogen receptor—dependent mechanisms are timely for two sets of reasons. Clinically, both affect mood and foster neuronal growth and regeneration. Mechanistically, they overlap at the levels of DNA recognition elements, coactivators, and signal transduction systems. Crosstalk between thyroid hormone receptors and estrogen receptors is possibly important to integrate external signals to transcription within neurons. Recent findings It has been shown that reproductive functions, including behaviors, driven by estrogens can be antagonized by thyroid hormones, and it has been argued that such crosstalk is biologically adaptive to ensure optimal reproduction. Transcriptional facilitation during transient transfunction studies show that the interactions between thyroid receptor isoforms and estrogen receptor isoforms depend on cell type and promoter context. Overall, this pattern of interactions assures multiple and flexible means of transcriptional regulation. Surprisingly, in some brain areas, thyroid hormone actions can synergize with estrogenic effects, particularly when nongenomic modes of action are considered, such as kinase activation, which, as has been reported, affect later estrogen receptor—induced genomic events. Summary In summary, recent work with nerve cells has contributed to a paradigm shift in how the molecular and behavioral effects of hormones which act through nuclear receptors are viewed.

Distinct behavioral phenotypes in male mice lacking the thyroid hormone receptor alpha1 or beta isoforms

Thyroid hormones influence both neuronal development and anxiety via the thyroid hormone receptors (TRs). The TRs are encoded by two different genes, TRalpha and TRbeta. The loss of TRalpha1 is implicated in increased anxiety in males, possibly via a hippocampal increase in GABAergic activity. We compared both social behaviors and two underlying and related non-social behaviors, state anxiety and responses to acoustic and tactile startle in the gonadally intact TRalpha1 knockout (alpha1KO) and TRbeta (betaKO) male mice to their wild-type counterparts. For the first time, we show an opposing effect of the two TR isoforms, TRalpha1 and TRbeta, in the regulation of state anxiety, with alpha1 knockout animals (alpha1KO) showing higher levels of anxiety and betaKO males showing less anxiety compared to respective wild-type mice. At odds with the increased anxiety in non-social environments, alpha1KO males also show lower levels of responsiveness to acoustic and tactile startle stimuli. Consistent with the data that T4 is inhibitory to lordosis in female mice, we show subtly increased sex behavior in alpha1KO male mice. These behaviors support the idea that TRalpha1 could be inhibitory to ERalpha driven transcription that ultimately impacts ERalpha driven behaviors such as lordosis. The behavioral phenotypes point to novel roles for the TRs, particularly in non-social behaviors such as state anxiety and startle.

Thyroid hormones regulate anxiety in the male mouse

Thyroid hormone levels are implicated in mood disorders in the adult human but the mechanisms remain unclear partly because, in rodent models, more attention has been paid to the consequences of perinatal hypo and hyperthyroidism. Thyroid hormones act via the thyroid hormone receptor (TR) alpha and beta isoforms, both of which are expressed in the limbic system. TR's modulate gene expression via both unliganded and liganded actions. Though the thyroid hormone receptor (TR) knockouts and a transgenic TRalpha1 knock-in mouse have provided us valuable insight into behavioral phenotypes such as anxiety and depression, it is not clear if this is because of the loss of unliganded actions or liganded actions of the receptor or due to locomotor deficits. We used a hypothyroid mouse model and supplementation with tri-iodothyronine (T3) or thyroxine (T4) to investigate the consequences of dysthyroid hormone levels on behaviors that denote anxiety. Our data from the open field and the light-dark transition tests suggest that adult onset hypothyroidism in male mice produces a mild anxiogenic effect that is possibly due to unliganded receptor actions. T3 or T4 supplementation reverses this phenotype and euthyroid animals show anxiety that is intermediate between the hypothyroid and thyroid hormone supplemented groups. In addition, T3 but not T4 supplemented animals have lower spine density in the CA1 region of the hippocampus and in the central amygdala suggesting that T3-mediated rescue of the hypothyroid state might be due to lower neuronal excitability in the limbic circuit.

Stigma and risky behaviors among male clients of sex workers in the UK in 2001

This paper builds on existing theoretical work on sex markets (Della Giusta, Di Tommaso, and Strøm, 2009a). Using data from the British Sexual Attitudes Survey, we aim to replicate the analysis of the demand for paid sex previously conducted for the US (Della Giusta, Di Tommaso, Shima and Strøm, 2009b). We want to test formally the effect of attitudes, risky behaviors and personal characteristics on the demand for paid sex. Findings from empirical studies of clients suggest that personal characteristics (personal and family background, self-perception, perceptions of women, sexual preferences etc), economic factors (education, income, work) as well as attitudes towards risk (both health hazard and risk of being caught where sex work is illegal), and attitude towards relationships and sex are all likely to affect demand. Previous theoretical work has argued that stigma plays a fundamental role in determining both demand and risk, and that in particular due to the presence of stigma the demand for sex and for paid sex are not, as has been argued elsewhere, perfect substitutes. We use data from the British Sexual Attitudes Survey of 2001 to test these hypotheses. We find a positive effect of education (proxy for income), negative effects of professional status (proxies for stigma associated with buying sex), positive and significant effects of all risky behavior variables and no significant effects of variables which measure the relative degree of conservatism in morals. We conclude with some policy implications.