The quest for universality: reflections on the Universal Draft Declaration on Bioethics and Human Rights

This essay focuses on two underlying presumptions that impinge on the effort of UNESCO to engender universal agreement on a set of bioethical norms: the conception of universality that pervades much of the document, and its disregard of structural inequalities that significantly impact health. Drawing on other UN system documents and recent feminist bioethics scholarship, we argue that the formulation of universal principles should not rely solely on shared ethical values, as the draft document affirms, but also on differences in ethical values that obtain across cultures. UNESCO's earlier work on gender mainstreaming illustrates the necessity of thinking from multiple perspectives in generating universal norms. The declaration asserts the 'fundamental equality of all human beings in dignity and rights'(1) and insists that 'the highest attainable standard of health is one of the fundamental rights of every human being without distinction of race, religion, political belief, economic or social condition'(2) yet it does not explicitly recognize disparities of power and wealth that deny equal dignity and rights to many. Without attention to structural (as opposed to merely accidental) inequities, UNESCO's invocation of rights is so abstract as to be incompatible with its avowed intention.     

Contribution of intra- and interhost dynamics to norovirus evolution

Norovirus (NoV) is an emerging RNA virus that has been associated with global epidemics of gastroenteritis. Each global epidemic arises with the emergence of novel antigenic variants. While the majority of NoV infections are mild and self-limiting, in the young, elderly, and immunocompromised, severe and prolonged illness can result. As yet, there is no vaccine or therapeutic treatment to prevent or control infection. In order to design effective control strategies, it is important to understand the mechanisms and source of the new antigenic variants. In this study, we used next-generation sequencing (NGS) technology to investigate genetic diversification in three contexts: the impact of a NoV transmission event on viral diversity and the contribution to diversity of intrahost evolution over both a short period of time (10 days), in accordance with a typical acute NoV infection, and a prolonged period of time (288 days), as observed for NoV chronic infections of immunocompromised individuals. Investigations of the transmission event revealed that minor variants at frequencies as low as 0.01% were successfully transmitted, indicating that transmission is an important source of diversity at the interhost level of NoV evolution. Our results also suggest that chronically infected immunocompromised subjects represent a potential reservoir for the emergence of new viral variants. In contrast, in a typical acute NoV infection, the viral population was highly homogenous and relatively stable. These results indicate that the evolution of NoV occurs through multiple mechanisms.     

Generating adaptive behaviour within a memory-prediction framework

The Memory-Prediction Framework (MPF) and its Hierarchical-Temporal Memory implementation (HTM) have been widely applied to unsupervised learning problems, for both classification and prediction. To date, there has been no attempt to incorporate MPF/HTM in reinforcement learning or other adaptive systems; that is, to use knowledge embodied within the hierarchy to control a system, or to generate behaviour for an agent. This problem is interesting because the human neocortex is believed to play a vital role in the generation of behaviour, and the MPF is a model of the human neocortex.We propose some simple and biologically-plausible enhancements to the Memory-Prediction Framework. These cause it to explore and interact with an external world, while trying to maximize a continuous, time-varying reward function. All behaviour is generated and controlled within the MPF hierarchy. The hierarchy develops from a random initial configuration by interaction with the world and reinforcement learning only. Among other demonstrations, we show that a 2-node hierarchy can learn to successfully play "rocks, paper, scissors" against a predictable opponent.     

Discovery of the Corallivorous Polyclad Flatworm, Amakusaplana acroporae, on the Great Barrier Reef, Australia - the First Report from the Wild

The role of corallivory is becoming increasingly recognised as an important factor in coral health at a time when coral reefs around the world face a number of other stressors. The polyclad flatworm, Amakusaplana acroporae, is a voracious predator of Indo-Pacific acroporid corals in captivity, and its inadvertent introduction into aquaria has lead to the death of entire coral colonies. While this flatworm has been a pest to the coral aquaculture community for over a decade, it has only been found in aquaria and has never been described from the wild. Understanding its biology and ecology in its natural environment is crucial for identifying viable biological controls for more successful rearing of Acropora colonies in aquaria, and for our understanding of what biotic interactions are important to coral growth and fitness on reefs. Using morphological, histological and molecular techniques we determine that a polyclad found on Acropora valida from Lizard Island, Australia is A. acroporae. The presence of extracellular Symbiodinium in the gut and parenchyma and spirocysts in the gut indicates that it is a corallivore in the wild. The examination of a size-range of individuals shows maturation of the sexual apparatus and increases in the number of eyes with increased body length. Conservative estimates of abundance show that A. acroporae occurred on 7 of the 10 coral colonies collected, with an average of 2.6±0.65 (mean ±SE) animals per colony. This represents the first report of A. acroporae in the wild, and sets the stage for future studies of A. acroporae ecology and life history in its natural habitat.     

Host and viral factors in the immunopathogenesis of primary hepatitis C virus infection

Individuals infected with hepatitis C virus (HCV) have two possible outcomes of infection, clearance or persistent infection. The focus of this review is the host mechanisms that facilitate clearance. The interaction between HCV viral components and the immune system ultimately determines the balance between the virus and host. Strong evidence points to the aspects of cellular immune response as the key determinants of outcome. The recent discovery of viral evasion strategies targeting innate immunity suggests that the interferon-alpha/beta induction pathways are also critical. A growing body of evidence has implicated polymorphisms in both innate and adaptive immune response genes as determinants of viral clearance in individuals infected with HCV.