The regulation of research by funding bodies : an emerging ethical issue for the alcohol and other drug sector?

The degree to which funding bodies can and do control the content and dissemination of research products raises important issues which need to be openly debated by the alcohol and other drug (AOD) sector. Current policies relating to censorship and other means of controlling research topics or output are explored alongside an examination of how some institutions, particularly some academic journals, deal with such issues. We argue that regulation of research by funding bodies clearly contravenes the scientific ideal of freedom of information and open access to knowledge. Using international ethical guidelines, we also demonstrate that regulation raises concerns in relation to the ethical concept of beneficence. A number of examples specific to harm reduction strategies are presented in order to demonstrate how censorship might conceivably increase the harms associated with drug use. The commentary closes with recommendations concerning the establishment the prevalence of censorship and other forms of control over research in the AOD sector, and the role that ethics committees, journal editorial boards and professional societies might play in resisting the imposition of unacceptable conditions on publication of findings.

Regulation of fat oxidative genes in human skeletal muscle

The ability of skeletal muscle to adapt fat oxidation rates is important for human health. Lipid metabolism requires the involvement of many proteins encoded by their corresponding genes. This thesis demonstrates that manipulating plasma free fatty acid levels alters the expression of selected genes involved in regulating fatty acid metabolism.

Regulation of GLUT4 expression in human skeletal muscle

Increasing the number of glucose transporters in muscle ameliorates many of the symptoms associated with type 2 diabetes. This thesis identifies mechanisms regulating glucose transporter gene expression, and therefore glucose transporter number, in human skeletal muscle and provides potential targets for the treatment and management of type 2 diabetes.

Societal constructions of the psycho-legal notion of mental impairment in Victoria

This thesis explored the factors relevant to decision-making when the defence of mental impairment is raised in Victoria. Findings indicate that disorder type, crime outcome, and the relationship between victim and offender were significantly associated with verdict decisions, while offender gender did not play a significant role in responsibility decisions. The portfolio discusses the role of co-morbid psychopathology in the assessment and treatment of veterans with chronic PTSD by presenting four case histories.

Arsenic induced regulation of base excision repair in human cells

Short term exposure to low levels of arsenic in human cells increased the cells' capacity to repair its DNA. In turn, cells became resistant to the toxic effects of UV radiation. However prolonged increases in principal repair proteins may actually lead to cancerous effects by destabilizing DNA repair.

Natriuretic peptide regulation of the kidney and urinary bladder in the cane toad, Bufo marinus

The natriuretic peptide system of mammals is important in the control of blood volume but its function in non-mammalian animals is unclear. This study identified a functional natriuretic peptide system in an amphibian and showed that the hormones are involved in the control of fluid balance.

Central regulation of energy balance in Psammomys obesus

This body of work focussed on the central regulation of energy balance in a polygenic animal model of obesity and type II diabetes, the Israeli Sand Rat. These studies investigated the role of a number of hypothalamic neuropeptides in the development of obesity, and highlighted the complex nature of this disease.

Risk and the regulation of youth(ful) identities in an age of manufactured uncertainty

Examines the benefits and dangers of allowing experts to intervene in the lives of youth, and their families, on the basis of assessing them as being at-risk.  Highlights the dangers of expert promises to prevent risk by intervening in people's lives on the basis of what is perceived to be normal or good.

Regulation of skeletal muscle oxidative capacity and insulin signaling by the Mitochondrial Rhomboid Protease PARL

Type 2 diabetes mellitus (T2DM) and aging are characterized by insulin resistance and impaired mitochondrial energetics. In lower organisms, remodeling by the protease pcp1 (PARL ortholog) maintains the function and lifecycle of mitochondria. We examined whether variation in PARL protein content is associated with mitochondrial abnormalities and insulin resistance. PARL mRNA and mitochondrial mass were both reduced in elderly subjects and in subjects with T2DM. Muscle knockdown of PARL in mice resulted in malformed mitochondrial cristae, lower mitochondrial content, decreased PGC1α protein levels, and impaired insulin signaling. Suppression of PARL protein in healthy myotubes lowered mitochondrial mass and insulin-stimulated glycogen synthesis and increased reactive oxygen species production. We propose that lower PARL expression may contribute to the mitochondrial abnormalities seen in aging and T2DM.

The role and regulation of MAFbx/atrogin-1 and MuRF1 in skeletal muscle atrophy

Skeletal muscle atrophy occurs in many chronic diseases and disuse conditions. Its severity reduces patient recovery, independence and quality of life. The discovery of two muscle-specific E3 ubiquitin ligases, MAFbx/ atrogin-1 and Muscle RING Finger-1 (MuRF1), promoted an expectation of these molecules as targets for therapeutic development. While numerous studies have determined the conditions in which MAFbx/atrogin-1 and MuRF1 mRNA levels are regulated, few studies have investigated their functional role in skeletal muscle. Recently, studies identifying new target substrates for MAFbx/atrogin-1 and
MuRF1, outside of their response to the initiation of muscle atrophy, suggest that there is more to these proteins than
previously appreciated. This review will highlight our present knowledge of MAFbx/atrogin-1 and MuRF1 in skeletal muscle atrophy, the impact of potential therapeutics and their known regulators and substrates. Finally, we will comment on new approaches that may expand our knowledge of these two molecules in their control of skeletal muscle function.