Planning the post-political city: exploring public participation in the contemporary Australian city

This special section examines the possibility of meaningful debate and contestation over urban decisions and futures in politically constrained contexts. In doing so, it moves with the post-political times: critically examining the proliferation of deliber- ative mechanisms; identifying the informal assemblages of diverse actors taking on new roles in urban socio-spatial justice; and illuminating the spaces where informal and formal planning processes meet. These questions are particularly pertinent for understanding the processes shaping Australian cities and public participation today

\u2730-minute city\u27? Not in my backyard! Smart Cities Plan must let people have their say

The federal government\u27s Smart Cities Plan is framed around the 30-minute city . In this city, journeys will take no more than half an hour, regardless of your location. The recently released plan has significant implications for population, transport provision and land-use intensity in neighbourhoods - the places where people live and how they get around. The realisation of its goals will require ongoing densification of Australian suburbs

Redox-dependent Franck–Condon blockade and Avalanche Transport in a Graphene–Fullerene single-molecule transistor

We report transport measurements on a graphene–fullerene single-molecule transistor. The device architecture where a functionalized C60 binds to graphene nanoelectrodes results in strong electron–vibron coupling and weak vibron relaxation. Using a combined approach of transport spectroscopy, Raman spectroscopy, and DFT calculations, we demonstrate center-of-mass oscillations, redox-dependent Franck–Condon blockade, and a transport regime characterized by avalanche tunnelling in a single-molecule transistor

IL-1β reciprocally regulates chemokine and insulin secretion in pancreatic β-cells via NF-κB

© 2015 the American Physiological Society. Proinflammatory cytokines impact islet β-cell mass and function by altering the transcriptional activity within pancreatic β-cells, producing increases in intracellular nitric oxide abundance and the synthesis and secretion of immunomodulatory proteins such as chemokines. Herein, we report that IL-1β, a major mediator of inflammatory responses associated with diabetes development, coordinately and reciprocally regulates chemokine and insulin secretion. We discovered that NF-κB controls the increase in chemokine transcription and secretion as well as the decrease in both insulin secretion and proliferation in response to IL-1β. Nitric oxide production, which is markedly elevated in pancreatic β-cells exposed to IL-1β, is a negative regulator of both glucose-stimulated insulin secretion and glucose-induced increases in intracellular calcium levels. By contrast, the IL-1β-mediated production of the chemokines CCL2 and CCL20 was not influenced by either nitric oxide levels or glucose concentration. Instead, the synthesis and secretion of CCL2 and CCL20 in response to IL-1β were dependent on NF-κB transcriptional activity. We conclude that IL-1β-induced transcriptional reprogramming via NF-κB reciprocally regulates chemokine and insulin secretion while also negatively regulating β-cell proliferation. These findings are consistent with NF-κB as a major regulatory node controlling inflammation- associated alterations in islet β-cell function and mass

Depths and Thermal Habitat Used by Large versus Small Northern Pike in Three Minnesota Lakes

We monitored depths and temperatures used by large (>71‐cm) versus small Northern Pike Esox lucius in three north‐central Minnesota lakes with either acoustic telemetry or archival tags. Individual Northern Pike demonstrated flexibility in depths used within a season and between years. The fish had some tolerance for low levels of dissolved oxygen (<3 mg/L), but depth selection was generally constrained by low dissolved oxygen in summer and winter. The fish more fully exploited all available depths during winter and thermal turnover periods. During July and August, large Northern Pike tended to follow the thermocline into cooler water as upper water layers warmed. Selection ratios indicated that large Northern Pike preferred water temperatures of 16–21°C during August when temperatures up to 28°C were available. In two lakes providing dense overhead cover from water lilies in shallow water, small Northern Pike used warmer, shallower water compared with large fish during summer. In a third lake providing no such cover, small fish were more often in deeper, cooler water. For small Northern Pike, temperature seemed to be a secondary habitat consideration behind the presence of shallow vegetated cover. This study provided detailed temperature selection information that will be useful when considering temperature as an ecological resource for different sizes of Northern Pike.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141595/1/tafs1629.pd

Bioactivation of Trimethoprim to Protein-Reactive Metabolites in Human Liver Microsomes

ABSTRACT The formation of drug-protein adducts via metabolic activation and covalent binding may stimulate an immune response or may result in direct cell toxicity. Protein covalent binding is a potentially pivotal step in the development of idiosyncratic adverse drug reactions (IADRs). Trimethoprim (TMP)-sulfamethoxazole (SMX) is a combination antibiotic that commonly causes IADRs. Recent data suggest that the contribution of the TMP component of TMP-SMX to IADRs may be underappreciated. We previously demonstrated that TMP is bioactivated to chemically reactive intermediates that can be trapped in vitro by N-acetyl cysteine (NAC), and we have detected TMP-NAC adducts (i.e., mercapturic acids) in the urine of patients taking TMP-SMX. However, the occurrence and extent of TMP covalent binding to proteins was unknown

Geographically variable biotic interactions and implications for species ranges

The challenge Understanding how biotic interactions affect species' geographical ranges, biodiversity patterns and ecological responses to environmental change is one of the most pressing challenges in macroecology. Extensive efforts are underway to detect signals of biotic interactions in macroecological data. However, efforts are limited by bias in the taxa and spatial scale for which occurrence data are available and by difficulty in ascribing causality to co-occurrence patterns. Moreover, we are not necessarily looking in the right places; analyses are largely ad hoc, depending on availability of data, rather than focusing on regions, taxa, ecosystems or interaction types where biotic interactions might affect species' geographical ranges most strongly. Unpicking biotic interactions We suggest that macroecology would benefit from the recognition that abiotic conditions alter two key components of biotic interaction strength: frequency and intensity. We outline how and why variation in biotic interaction strength occurs, explore the implications for species' geographical ranges and discuss the challenges inherent in quantifying these effects. In addition, we explore the role of behavioural flexibility in mediating biotic interactions potentially to mitigate impacts of environmental change. New data We argue that macroecology should take advantage of "independent" data on the strength of biotic interactions measured by other disciplines, in order to capture a far wider array of taxa, locations and interaction types than are typically studied in macroecology. Data on biotic interactions are readily available from community, disease, microbial and parasite ecology, evolution, palaeontology, invasion biology and agriculture, but most are yet to be exploited within macroecology. Integrating biotic interaction strength data into macroecology Harmonization of data across interdisciplinary sources, taxa and interaction types could be achieved by breaking down interactions into elements that contribute to frequency and intensity. This would allow quantitative biotic interaction data to be incorporated directly into models of species distributions and macroecological patterns

Multiple mechanisms mediating carbon monoxide inhibition of the voltage-gated K+ channel Kv1.5

The voltage-gated K+ channel plays key roles in the vasculature and in atrial excitability, and contributes to apoptosis in various tissues. In this study, we have explored its regulation by carbon monoxide (CO), a product of the cytoprotective heme oxygenase enzymes, and a recognized toxin. CO inhibited recombinant Kv1.5 expressed in HEK293 cells in a concentration-dependent manner which involved multiple signalling pathways. CO inhibition was partially reversed by superoxide dismutase mimetics, and by suppression of mitochondrial reactive oxygen species. CO also elevated intracellular nitric oxide (NO) levels. Prevention of NO formation also partially reversed CO inhibition of Kv1.5, as did inhibition of soluble guanylyl cyclase. CO also elevated intracellular peroxynitrite levels, and a peroxynitrite scavenger markedly attenuated the ability of CO to inhibit Kv1.5. CO caused nitrosylation of Kv1.5, an effect which was also observed in C331A and C346A mutant forms of the channel, which had previously been suggested as nitrosylation sites within Kv1.5. Augmentation of Kv1.5 via exposure to hydrogen peroxide was fully reversed by CO. Native Kv1.5 recorded in HL-1 murine atrial cells was also inhibited by CO. Action potentials recorded in HL-1 cells were increased in amplitude and duration by CO, an effect mimicked and occluded by pharmacological inhibition of Kv1.5. Our data indicate that Kv1.5 is a target for modulation by CO via multiple mechanisms. This regulation has important implications for diverse cellular functions, including excitability, contractility and apoptosis

Rental Insights A COVID-19 Collection

This Collection offers insights from twenty of Australia’s leader academics and thinkers into the survey results of 15,000 Australian rental households. The Collection draws on data from The Australian Rental Housing Conditions Dataset funded by the Australian Research Council in partnership with six Australian universities as well an additional AHURI funded COVID-19 module

Salivary Defense Proteins: Their Network and Role in Innate and Acquired Oral Immunity

There are numerous defense proteins present in the saliva. Although some of these molecules are present in rather low concentrations, their effects are additive and/or synergistic, resulting in an efficient molecular defense network of the oral cavity. Moreover, local concentrations of these proteins near the mucosal surfaces (mucosal transudate), periodontal sulcus (gingival crevicular fluid) and oral wounds and ulcers (transudate) may be much greater, and in many cases reinforced by immune and/or inflammatory reactions of the oral mucosa. Some defense proteins, like salivary immunoglobulins and salivary chaperokine HSP70/HSPAs (70 kDa heat shock proteins), are involved in both innate and acquired immunity. Cationic peptides and other defense proteins like lysozyme, bactericidal/permeability increasing protein (BPI), BPI-like proteins, PLUNC (palate lung and nasal epithelial clone) proteins, salivary amylase, cystatins, prolin-rich proteins, mucins, peroxidases, statherin and others are primarily responsible for innate immunity. In this paper, this complex system and function of the salivary defense proteins will be reviewed