#LetThemStay: : Visual Representations of Protests and Community Mobilization for Asylum Seekers in Australia

This article is distributed under a Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Users may reproduce, disseminate, display, or adapt this article for non-commercial purposes, provided the author is properly cited. See https:/creativecommons.org/licenses/by-nc/4.0/.The indefinite mandatory detention on the mainland and in offshore processing centers of asylum seekers applying for protection in Australia is particularly controversial due to the government’s notoriously harsh policy. In response, large-scale public protests have been staged across the country in recent years to register popular dissent and convey concerns to decision-makers. However, dominant media representations of protests have historically been largely negative, often cast as ineffectual at best, and at worst, violent clashes that alienate the broader population from the cause in question. This paper outlines a visual analysis of media representations of protests that took place in February 2016 against the proposed deportation of 267 asylum seekers from the Australian mainland as part of the #LetThemStay campaign. Through the analysis of four photographs from a range of media outlets, we found that depicting peaceful protests methods and community mobilization complicated dominant understandings of protests and protesters. Indeed, #LetThemStay demonstrated the political power of compassionate solidarity between participants afforded the privilege of safe residency and citizenship, and those forcibly absent who are denied such rights. As such, the paper highlights the impact of peaceful protesting, while also recognizing its limitations in changing Australia’s punitive asylum seeker policies.Peer reviewedFinal Published versio

Potent dual inhibitors of Plasmodium falciparum M1 and M17 aminopeptidases through optimization of S1 pocket interactions

Malaria remains a global health problem, and though international efforts for treatment and eradication have made some headway, the emergence of drug-resistant parasites threatens this progress. Antimalarial therapeutics acting via novel mechanisms are urgently required. P. falciparum M1 and M17 are neutral aminopeptidases which are essential for parasite growth and development. Previous work in our group has identified inhibitors capable of dual inhibition of PfA-M1 and PfA-M17, and revealed further regions within the protease S1 pockets that could be exploited in the development of ligands with improved inhibitory activity. Herein, we report the structure-based design and synthesis of novel hydroxamic acid analogues that are capable of potent inhibition of both PfA-M1 and PfA-M17. Furthermore, the developed compounds potently inhibit Pf growth in culture, including the multi-drug resistant strain Dd2. The ongoing development of dual PfA-M1/PfA-M17 inhibitors continues to be an attractive strategy for the design of novel antimalarial therapeutics

Dysregulated mitophagy and mitochondrial organization in optic atrophy due to OPA1 mutations

Objective: To investigate mitophagy in 5 patients with severe dominantly inherited optic atrophy (DOA), caused by depletion of OPA1 (a protein that is essential for mitochondrial fusion), compared with healthy controls. Methods: Patients with severe DOA (DOA plus) had peripheral neuropathy, cognitive regression, and epilepsy in addition to loss of vision. We quantified mitophagy in dermal fibroblasts, using 2 high throughput imaging systems, by visualizing colocalization of mitochondrial fragments with engulfing autophagosomes. Results: Fibroblasts from 3 biallelic OPA1(2/2) patients with severe DOA had increased mitochondrial fragmentation and mitochondrial DNA (mtDNA)–depleted cells due to decreased levels of OPA1 protein. Similarly, in siRNA-treated control fibroblasts, profound OPA1 knockdown caused mitochondrial fragmentation, loss of mtDNA, impaired mitochondrial function, and mitochondrial mislocalization. Compared to controls, basal mitophagy (abundance of autophagosomes colocalizing with mitochondria) was increased in (1) biallelic patients, (2) monoallelic patients with DOA plus, and (3) OPA1 siRNA–treated control cultures. Mitophagic flux was also increased. Genetic knockdown of the mitophagy protein ATG7 confirmed this by eliminating differences between patient and control fibroblasts. Conclusions: We demonstrated increased mitophagy and excessive mitochondrial fragmentation in primary human cultures associated with DOA plus due to biallelic OPA1 mutations. We previously found that increased mitophagy (mitochondrial recycling) was associated with visual loss in another mitochondrial optic neuropathy, Leber hereditary optic neuropathy (LHON). Combined with our LHON findings, this implicates excessive mitochondrial fragmentation, dysregulated mitophagy, and impaired response to energetic stress in the pathogenesis of mitochondrial optic neuropathies, potentially linked with mitochondrial mislocalization and mtDNA depletion

Positional identification of variants of Adamts16 linked to inherited hypertension

A previously reported blood pressure (BP) quantitative trait locus on rat Chromosome 1 was isolated in a short congenic segment spanning 804.6 kb. The 804.6 kb region contained only two genes, LOC306664 and LOC306665. LOC306664 is predicted to translate into A Disintegrin-like and Metalloproteinase with Thrombospondin Motifs-16 (Adamts16). LOC306665 is a novel gene. All predicted exons of both LOC306664 and LOC306665 were sequenced. Non-synonymous variants were identified in only one of these genes, LOC306664. These variants were naturally existing polymorphisms among inbred, outbred and wild rats. The full-length rat transcript of Adamts16 was detected in multiple tissues. Similar to ADAMTS16 in humans, expression of Adamts16 was prominent in the kidney. Renal transcriptome analysis suggested that a network of genes related to BP was differential between congenic and S rats. These genes were also differentially expressed between kidney cell lines with or without knock-down of Adamts16. Adamts16 is conserved between rats and humans. It is a candidate gene within the homologous region on human Chromosome 5, which is linked to systolic and diastolic BP in the Quebec Family Study. Multiple variants, including an Ala to Pro variant in codon 90 (rs2086310) of human ADAMTS16, were associated with human resting systolic BP (SBP). Replication study in GenNet confirmed the association of two variants of ADAMTS16 with SBP, including rs2086310. Overall, our report represents a high resolution positional cloning and translational study for Adamts16 as a candidate gene controlling BP

Hominin home ranges and habitat variability: exploring modern African analogues using remote sensing

The palaeoanthropological literature contains numerous examples of putative home range sizes associated with various hominin species. However, the resolution of the palaeoenvironmental record seldom allows the quantitative analysis of the effects of different range sizes on access to different habitat types and resources. Here we develop a novel approach of using remote sensing data of modern African vegetation as an analogue for past hominin habitats, and examine the effects of different range sizes on the access to habitat types. We show that when the location of the ranges are chosen randomly then the number of habitat types within a range is surprisingly scale invariant – that is increasing range size makes only a very modest difference to the number of habitat types within an estimated hominin home range. However, when transects are placed perpendicular to a water body (such as a lake or river bank) it is apparent that the greatest number of habitats are seen near water bodies, and decline with distance. This suggests additional advantages to living by freshwater other than the obvious one associated with access to drinking water, and may indicate that the finding of hominins in fluvial and lacustrine deposits is not simply a taphonomic issue

Parasite of the Month: Plasmodium vivax

Plasmodium vivax is a eukaryotic human pathogen and the most frequent and widely distributed cause of the recurring disease malaria. P. vivax is one of five species of malaria parasites that commonly infect humans. Although less virulent than Plasmodium falciparum, P. vivax malaria infections can lead to severe disease and death. The disease is transmitted to humans by female anopheline mosquitoes during acquisition of a blood meal. An obligate liver stage of development precedes blood stage replication which accounts for all disease-associated morbidity and mortality and chloroquine is still used to treat the disease. Approximately 2.5 billion people are at risk of infection with P. vivax, and it is found mainly in Asia and Latin America where it accounts for 65% of malaria cases. In Africa, the widespread lack of the Duffy antigen in the population has constrained transmission. A dormant liver stage form, known as the hypnozoite can reactivate and causes disease relapses and the majority of blood stage infections are caused by relapse. The hypnozoite is thus a challenge for malaria eradication campaigns and primaquine and tafenoquine are the only drugs known to target the hypnozoite. However, these therapies are inadequate since primaquine cannot be administered to pregnant women and people with commonly occurring glucose-6-phosphate dehydrogenase deficiency and tafenoquine cannot be administered to children. There is no effective P. vivax vaccine

Parasite of the Month: Plasmodium vivax

Plasmodium vivax is the most widely distributed of several plasmodial species that cause malaria, a disease associated with blood stage parasite replication. About 2.5 billion people are at risk of P. vivax infection, living mainly in Southeast Asia and the Americas, where P. vivax accounts for approximately 72% of malaria cases. In Africa, widespread lack of the Duffy antigen constrains transmission. The dormant liver form of the parasite, the hypnozoite, which can reactivate long after the primary infection and give rise to a relapsing blood stage infection, complicates eradication. In fact, hypnozoites are the origin of the majority of active blood stage infections. Primaquine and tafenoquine are the only drugs that prevent relapse; however, neither can be used during pregnancy or by people with glucose-6-phosphate dehydrogenase deficiency; and tafenoquine is not yet approved in children. Thus, this species of malaria-causing parasite is a unique challenge for eradication campaigns

Sternoclavicular septic arthritis: review of 180 cases

Septic arthritis can be a devastating condition that leads to further morbidity and potential mortality if not identified early in its course. Emergency providers must keep septic arthritis high on their differential of any joint-related pain in the pediatric population. We present a case of an eight-year-old female who initially presented with the chief complaint of chest pain and was subsequently diagnosed with septic arthritis of the left sternoclavicular joint in the emergency department