We describe a general framework in which we can precisely compare the structures of quantum-like theories which may initially be formulated in quite different mathematical terms. We then use this framework to compare two theories: quantum mechanics restricted to qubit stabiliser states and operations, and Spekkens's toy theory. We discover that viewed within our framework these theories are very similar, but differ in one key aspect -a four element group we term the phase group which emerges naturally within our framework. In the case of the stabiliser theory this group is Z4 while for Spekkens's toy theory the group is Z2 × Z2. We further show that the structure of this group is intimately involved in a key physical difference between the theories: whether or not they can be modelled by a local hidden variable theory. This is done by establishing a connection between the phase group, and an abstract notion of GHZ state correlations. We go on to formulate precisely how the stabiliser theory and toy theory are 'similar' by defining a notion of 'mutually unbiased qubit theory', noting that all such theories have four element phase groups. Since Z4 and Z2 × Z2 are the only such groups we conclude that the GHZ correlations in this type of theory can only take two forms, exactly those appearing in the stabiliser theory and in Spekkens's toy theory. The results point at a classification of local/non-local behaviours by finite Abelian groups, extending beyond qubits to finitary theories whose observables are all mutually unbiased.

In this article, we focus on data trust and data privacy, and how attitudes may be changing during the COVID-19 period. On balance, it appears that Australians are more trusting of organizations with regards to data privacy and less concerned about their own personal information and data than they were prior to the spread of COVID-19. The major determinant of this change in trust with regards to data was changes in general confidence in government institutions. Despite this improvement in trust with regards to data privacy, trust levels are still low.

Genetic approaches for the diagnosis and treatment of inherited muscle diseases have advanced rapidly in recent years. Many of the advances have occurred in the treatment of Duchenne muscular dystrophy (DMD), a muscle wasting disease where affected boys are typically wheelchair bound by age 12 years and generally die in their twenties from respiratory failure or cardiomyopathy. Dystrophin is a 421 kD protein which links F-actin to the extracellular matrix via the dystrophin-associated protein complex (DAPC) at the muscle membrane. In the absence of dystrophin, the DAPC is lost, making the muscle membrane more susceptible to contraction-induced injury. The identification of the gene causing DMD in 1986 resulted in improved diagnosis of the disease and the identification of hotspots for mutation. There is currently no effective treatment. However, there are several promising genetic therapeutic approaches at the preclinical stage or in clinical trials including read-through of stop codons, exon skipping, delivery of dystrophin minigenes and the modulation of expression of the dystrophin related protein, utrophin. In spite of significant progress, the problem of targeting all muscles, including diaphragm and heart at sufficiently high levels, remains a challenge. Any therapy also needs to consider the immune response and some treatments are mutation specific and therefore limited to a subgroup of patients. This short review provides a summary of the current status of DMD therapy with a particular focus on those genetic strategies that have been taken to the clinic.

Although recent regulatory approval of splice-switching oligonucleotides (SSOs) for the treatment of neuromuscular disease such as Duchenne muscular dystrophy has been an advance for the splice-switching field, current SSO chemistries have shown limited clinical benefit due to poor pharmacology. To overcome limitations of existing technologies, we engineered chimeric stereopure oligonucleotides with phosphorothioate (PS) and phosphoryl guanidine-containing (PN) backbones. We demonstrate that these chimeric stereopure oligonucleotides have markedly improved pharmacology and efficacy compared with PS-modified oligonucleotides, preventing premature death and improving median survival from 49 days to at least 280 days in a dystrophic mouse model with an aggressive phenotype. These data demonstrate that chemical optimization alone can profoundly impact oligonucleotide pharmacology and highlight the potential for continued innovation around the oligonucleotide backbone. More specifically, we conclude that chimeric stereopure oligonucleotides are a promising splice-switching modality with potential for the treatment of neuromuscular and other genetic diseases impacting difficult to reach tissues such as the skeletal muscle and heart.