Citizen or consumer? Contrasting Australia and Europe’s data protection policies

© 2019, Alexander von Humboldt Institute for Internet and Society. All rights reserved. This paper examines how data access and transfer rights are conceptualised in the European Union and Australia. The study discusses the planned introduction of a Consumer Data Right (CDR) to Australia and contrasts it to comparable developments in European law. We then assess the broader reform moments around data (which these various data access and transfer rights form a part of), that have occurred in each jurisdiction. The paper shows that Europe has placed an increasing value on protecting the fundamental rights of citizens, whereas Australia has taken a more neoliberal approach to data, only granting individuals rights in the context of the market

Mitochondrial dynamics in Caenorhabditis elegans programmed cell death

As multicellular organisms appeared in evolution, about 1.5 billion years ago, a process called programmed cell death or apoptosis evolved. Genetic studies of physiological cell death in the nematode Caenorhabditis elegans have elucidated a molecular model of the central cell death machinery consisting of the genes egl-1, ced-9, -4 and -3. Remarkably, considering C. elegans evolutionarily separated from mammals millions of years ago, this pathway appears to be highly conserved from the nematode to humans. However, unlike in mammals, even though egl-1, ced-4 and -9 appear to localize to the mitochondrion in vivo there has been very little evidence to date that mitochondria play any role in the induction of C. elegans physiological cell death. This investigation demonstrates that mitochondria fragment upon induction of cell death and that this mitochondrial morphological change is not seen in egl-1 and ced-9 mutants but in ced-4 and -3 mutants. This genetic analysis suggests that mitochondrial division is an active process that occurs before caspase activation. Furthermore, the mitochondrial fragmentation event is both required and sufficient for physiological cell death in C. elegans. In conclusion, this work supports an important role of mitochondria in the execution of programmed cell death, suggesting that the evolutionary conservation from worm to man is stronger than previously assumed

Structural basis for recruitment of mitochondrial fission complexes by Fis1

Mitochondrial fission controls mitochondrial shape and physiology, including mitochondrial remodeling in apoptosis. During assembly of the yeast mitochondrial fission complex, the outer membrane protein Fis1 recruits the dynamin-related GTPase Dnm1 to mitochondria. Fis1 contains a tetratricopeptide repeat (TPR) domain and interacts with Dnm1 via the molecular adaptors Mdv1 and Caf4. By using crystallographic analysis of adaptor-Fis1 complexes, we show that these adaptors use two helices to bind to both the concave and convex surfaces of the Fis1 TPR domain. Fis1 therefore contains two interaction interfaces, a binding mode that, to our knowledge, has not been observed previously for TPR domains. Genetic and biochemical studies indicate that both binding interfaces are important for binding of Mdv1 and Caf4 to Fis1 and for mitochondrial fission activity in vivo. Our results reveal how Fis1 recruits the mitochondrial fission complex and will facilitate efforts to manipulate mitochondrial fission

MARGINALISED WOMEN AND TIME SCARCITY: A MIXED METHOD STUDY ON ‘ON DEMAND WORK APPS’

On-demand work applications (ODWA), a form of digital platforms, are the primary enablers of short-term or ‘gig’ work economy. In this paper, we study these platforms in their role as enablers of women belonging to low socio-economic sections. These women act as the primary unpaid workers while being expected to make economic contribution. Hence, they suffer from classic case of time scarcity. Gig economy enabled by these ODWAs have made this possible to some extent. We employ the theoretical lens of affordance theory to delineate the affordances that are provided by the various features of ODWA and their impact on these women. We do a mixed method study employing inter-views of gig workers supplemented with survey of 927 workers of one of the largest ODWA in India. Our analysis points to the sense of identity and individuality that these platforms provide. We also find that the presence of a digital platform between the customer and these women lowers the societal boundaries that have been the biggest challenge in their inclusion. Our research is, hence, significant from both information systems and inclusion research perspective as it contributes to the theoretical understanding of the impact of digital platforms on breaking societal structures

Design of graphite and the Polyhedral Compilation Package

Graphite is the loop transformation framework that was introduced in GCC 4.4. This paper gives a detailed description of the design and future directions of this infrastructure. Graphite uses the polyhedral model as the internal representation (GPOLY). The plan is to create a polyhedral compilation package (PCP) that will provide loop optimization and analysis capabilities to GCC. This package will be separated from GIMPLE via an interface language that is restricted to express only what GPOLY can represent. The interface language is a set of data structures that encodes the control flow and memory accesses of a code region. A syntax for the language is also defined to facilitate debugging and testing

Proteolytic Processing of OPA1 Links Mitochondrial Dysfunction to Alterations in Mitochondrial Morphology

Many muscular and neurological disorders are associated with mitochondrial dysfunction and are often accompanied by changes in mitochondrial morphology. Mutations in the gene encoding OPA1, a protein required for fusion of mitochondria, are associated with hereditary autosomal dominant optic atrophy type I. Here we show that mitochondrial fragmentation correlates with processing of large isoforms of OPA1 in cybrid cells from a patient with myoclonus epilepsy and ragged-red fibers syndrome and in mouse embryonic fibroblasts harboring an error-prone mitochondrial mtDNA polymerase {gamma}. Furthermore, processed OPA1 was observed in heart tissue derived from heart-specific TFAM knock-out mice suffering from mitochondrial cardiomyopathy and in skeletal muscles from patients suffering from mitochondrial myopathies such as myopathy encephalopathy lactic acidosis and stroke-like episodes. Dissipation of the mitochondrial membrane potential leads to fast induction of proteolytic processing of OPA1 and concomitant fragmentation of mitochondria. Recovery of mitochondrial fusion depended on protein synthesis and was accompanied by resynthesis of large isoforms of OPA1. Fragmentation of mitochondria was prevented by overexpressing OPA1. Taken together, our data indicate that proteolytic processing of OPA1 has a key role in inducing fragmentation of energetically compromised mitochondria. We present the hypothesis that this pathway regulates mitochondrial morphology and serves as an early response to prevent fusion of dysfunctional mitochondria with the functional mitochondrial network

Pleural Effusion in a Peritoneal Dialysis Patient

A 34-year-old female presented with end-stage renal disease (ESRD) treated by peritoneal dialysis (CAPD) complained of a dry cough. Chest X-ray and chest computed tomography (CT) scan revealed massive right hydrothorax. Because the glucose concentration of pleural fluid was markedly high compared with that of serum, we performed isotope and contrast peritoneography. We used CT for localizing it. MRI was also trying to show transdiaphragmatic leakage in peritoneoflural fistula. Temporary discontinuation of CAPD, tetracycline instillation into the pleural space and surgical patch grafting of the diaphragmatic leak have all been described. A novel method may be video-assisted talc pleurodesis

Mitochondrial Dysfunction in Astrocytes Impairs the Generation of Reactive Astrocytes and Enhances Neuronal Cell Death in the Cortex Upon Photothrombotic Lesion

Mitochondria are key organelles in regulating the metabolic state of a cell. In the brain, mitochondrial oxidative metabolism is the prevailing mechanism for neurons to generate ATP. While it is firmly established that neuronal function is highly dependent on mitochondrial metabolism, it is less well-understood how astrocytes function rely on mitochondria. In this study, we investigate if astrocytes require a functional mitochondrial electron transport chain (ETC) and oxidative phosphorylation (oxPhos) under physiological and injury conditions. By immunohistochemistry we show that astrocytes expressed components of the ETC and oxPhos complexes in vivo. Genetic inhibition of mitochondrial transcription by conditional deletion of mitochondrial transcription factor A (Tfam) led to dysfunctional ETC and oxPhos activity, as indicated by aberrant mitochondrial swelling in astrocytes. Mitochondrial dysfunction did not impair survival of astrocytes, but caused a reactive gliosis in the cortex under physiological conditions. Photochemically initiated thrombosis induced ischemic stroke led to formation of hyperfused mitochondrial networks in reactive astrocytes of the perilesional area. Importantly, mitochondrial dysfunction significantly reduced the generation of new astrocytes and increased neuronal cell death in the perilesional area. These results indicate that astrocytes require a functional ETC and oxPhos machinery for proliferation and neuroprotection under injury conditions