Structural Levels of Mental Illness Stigma and Discrimination

Most of the models that currently describe processes related to mental illness stigma are based on individual-level psychological paradigms. In this article, using a sociological paradigm, we apply the concepts of structural discrimination to broaden our understanding of stigmatizing processes directed at people with mental illness. Structural, or institutional, discrimination includes the policies of private and governmental institutions that intentionally restrict the opportunities of people with mental illness. It also includes major institutions' policies that are not intended to discriminate but whose consequences nevertheless hinder the options of people with mental illness. After more fully defining intentional and unintentional forms of structural discrimination, we provide current examples of each. Then we discuss the implications of structural models for advancing our understanding of mental illness stigma, including the methodological challenges posed by this paradigm

Motorcycle Safety Research Project: Interim Summary Report Research Deliverable 1: Investigate and Develop a Pre-Learner Motorcycle Licensing Package

Motorcycle trauma is a serious road safety issue in Queensland and throughout Australia. In 2009, Queensland Transport (later Transport and Main Roads or TMR) appointed CARRS-Q to provide a three-year program of Road Safety Research Services for Motorcycle Rider Safety. Funding for this research originated from the Motor Accident Insurance Commission. This program of research was undertaken to produce knowledge to assist TMR to improve motorcycle safety by further strengthening the licensing and training system to make learner riders safer by developing a pre-learner package (Deliverable 1 which is the focus of this report), and by evaluating the Q-Ride CAP program to ensure that it is maximally effective and contributes to the best possible training for new riders (Deliverable 2), which is the focus of this report. Deliverable 3 of the program identified potential new licensing components that will reduce the incidence of risky riding and improve higher-order cognitive skills in new riders. While fatality and injury rates for learner car drivers are typically lower than for those with intermediate licences, this pattern is not found for learner motorcycle riders. Learner riders cannot be supervised as effectively as learner car drivers and errors are more likely to result in injury for learner riders than learner drivers. It is therefore imperative to improve safety for learner riders. Deliverable 1 examines the potential for improving the motorcycle learner and licence scheme by introducing a pre-learner motorcycle licensing and training scheme within Queensland. The tasks undertaken for Deliverable 1 were a literature review, analysis of learner motorcyclist crash and licensing data, and the development of a potential pre-learner motorcycle rider program

Lyplal1 is dispensable for normal fat deposition in mice.

Genome-wide association studies (GWAS) have detected association between variants in or near the Lysophospholipase-like 1 (LYPLAL1) locus and metabolic traits, including central obesity, fatty liver and waist-to-hip ratio. LYPLAL1 is also known to be upregulated in the adipose tissue of obese patients. However, the physiological role of LYPLAL1 is not understood. To investigate the function of Lyplal1 in vivo we investigated the phenotype of the Lyplal1tm1a(KOMP)Wtsi homozygous mouse. Body composition was unaltered in Lyplal1 knockout mice as assessed by dual-energy X-ray absorptiometry (DEXA) scanning, both on normal chow and on a high-fat diet. Adipose tissue distribution between visceral and subcutaneous fat depots was unaltered, with no change in adipocyte cell size. The response to both insulin and glucose dosing was normal in Lyplal1tm1a(KOMP)Wtsi homozygous mice, with normal fasting blood glucose concentrations. RNAseq analysis of liver, muscle and adipose tissue confirmed that Lyplal1 expression was ablated with minimal additional changes in gene expression. These results suggest that Lyplal1 is dispensable for normal mouse metabolic physiology and that despite having been maintained through evolution Lyplal1 is not an essential gene, suggesting possible functional redundancy. Further studies will be required to clarify its physiological role

Association between Physical Activity and Sport Participation on Hemoglobin A1c among Children and Adolescents with Type 1 Diabetes

Purpose: To determine associations between physical activity (PA) and sport participation on HbA1c levels in children with type 1 diabetes (T1D). Method: Pediatric patients with T1D were invited to complete a PA and sport participation survey. Data were linked to their medical records for demographic characteristics, diabetes treatment and monitoring plans, and HbA1c levels. Results: Participants consisted of 71 females and 81 males, were 13 +- 3 years old with an average HbA1c level of 8.75 +- 1.81. Children accumulating 60 min of activity 3 days or more a week had significantly lower HbA1c compared to those who accumulated less than 3 days (p \u3c 0.01) of 60 min of activity. However, there was no significant difference in HbA1c values based on sport participation groups. A multiple linear regression model indicated that PA, race, age, duration of diagnosis, and CGM use all significantly predicted HbA1c (p \u3c 0.05). Conclusion: This study demonstrated the significant relationship between daily PA and HbA1c. Those in this sample presented with lower HbA1c values even if accumulating less than the recommended number of days of activity. Further, it was shown that sport participation alone may not be adequate enough to impact HbA1c in a similar manner

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression

Changes in gene expression during tumorigenesis are often considered the consequence of de novo mutations occurring in the tumour. An alternative possibility is that the transcriptional response of oncogenic transcription factors evolves during tumorigenesis. Here we show that aberrant E2f activity, following inactivation of the Rb gene family in a mouse model of liver cancer, initially activates a robust gene expression programme associated with the cell cycle. Slowly accumulating E2f1 progressively recruits a Pontin/Reptin complex to open the chromatin conformation at E2f target genes and amplifies the E2f transcriptional response. This mechanism enhances the E2f-mediated transactivation of cell cycle genes and initiates the activation of low binding affinity E2f target genes that regulate non-cell-cycle functions, such as the Warburg effect. These data indicate that both the physiological and the oncogenic activities of E2f result in distinct transcriptional responses, which could be exploited to target E2f oncogenic activity for therapy

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression

Changes in gene expression during tumorigenesis are often considered the consequence of de novo mutations occurring in the tumour. An alternative possibility is that the transcriptional response of oncogenic transcription factors evolves during tumorigenesis. Here we show that aberrant E2f activity, following inactivation of the Rb gene family in a mouse model of liver cancer, initially activates a robust gene expression programme associated with the cell cycle. Slowly accumulating E2f1 progressively recruits a Pontin/Reptin complex to open the chromatin conformation at E2f target genes and amplifies the E2f transcriptional response. This mechanism enhances the E2f-mediated transactivation of cell cycle genes and initiates the activation of low binding affinity E2f target genes that regulate non-cell-cycle functions, such as the Warburg effect. These data indicate that both the physiological and the oncogenic activities of E2f result in distinct transcriptional responses, which could be exploited to target E2f oncogenic activity for therapy

A Search for Correlation of Ultra-High Energy Cosmic Rays with IRAS-PSCz and 2MASS-6dF Galaxies

We study the arrival directions of 69 ultra-high energy cosmic rays (UHECRs) observed at the Pierre Auger Observatory (PAO) with energies exceeding 55 EeV. We investigate whether the UHECRs exhibit the anisotropy signal expected if the primary particles are protons that originate in galaxies in the local universe, or in sources correlated with these galaxies. We cross-correlate the UHECR arrival directions with the positions of IRAS-PSCz and 2MASS-6dF galaxies taking into account particle energy losses during propagation. This is the first time that the 6dF survey is used in a search for the sources of UHECRs and the first time that the PSCz survey is used with the full 69 PAO events. The observed cross-correlation signal is larger for the PAO UHECRs than for 94% (98%) of realisations from an isotropic distribution when cross-correlated with the PSCz (6dF). On the other hand the observed cross-correlation signal is lower than that expected from 85% of realisations, had the UHECRs originated in galaxies in either survey. The observed cross-correlation signal does exceed that expected by 50% of the realisations if the UHECRs are randomly deflected by intervening magnetic fields by 5 degrees or more. We propose a new method of analysing the expected anisotropy signal, by dividing the predicted UHECR source distribution into equal predicted flux radial shells, which can help localise and constrain the properties of UHECR sources. We find that the 69 PAO events are consistent with isotropy in the nearest of three shells we define, whereas there is weak evidence for correlation with the predicted source distribution in the two more distant shells in which the galaxy distribution is less anisotropic.Comment: 23 pages, version published in JCA

Strain-specific metabolic responses to long-term caloric restriction in female ILSXISS recombinant inbred mice

The role that genetic background may play in the responsiveness of organisms to interventions such as caloric restriction (CR) is underappreciated but potentially important. We investigated genetic background on a suite of metabolic parameters in female recombinant inbred ILSXISS mouse strains previously reported to show divergent lifespan responses to 40% CR (TejJ89-lifespan extension; TejJ48-lifespan unaffected; TejJ114-lifespan shortening). Body mass was reduced across all strains following 10 months of 40% CR, although this loss (relative to ad libitum controls) was greater in TejJ114 relative to the other strains. Gonadal white adipose tissue (gWAT) mass was similarly reduced across all strains following 40% CR, but brown adipose tissue (BAT) mass increased only in strains TejJ89 and TejJ48. Surprisingly, glucose tolerance was improved by CR only in TejJ114, while strains TejJ89 and TejJ114 were relatively hyperinsulinemic following CR relative to their AL controls. We subsequently undertook an unbiased metabolomic approach in gWAT and BAT tissue from strains TejJ89 and TejJ114 mice under AL and 40% CR. gWAT from TejJ89 showed a significant reduction in several long chain unsaturated fatty acids following 40% CR, but gWAT from TejJ114 appeared relatively unresponsive to CR, with far fewer metabolites changing. Phosphatidylethanoloamine lipids within the BAT were typically elevated in TejJ89 following CR, while some phosphatidylglycerol lipids were decreased. However, BAT from strain TejJ114 again appeared unresponsive to CR. These data highlight strain-specific metabolic differences exist in ILSXISS mice following CR. We suggest that precisely how different fat depots respond dynamically to CR may be an important factor in the variable longevity under CR observed in these mice

Net positive outcomes for nature

Much research and policy effort is being expended on seeking ways to conserve living nature while enabling the economic and social development needed to increase global equity and end poverty. We propose that this will only be possible if the language of policy shifts away from setting conservation targets that focus on avoiding losses and towards developing processes that consider net outcomes for biodiversity

Super-resolution fluorescence microscopy reveals clustering behaviour of Chlamydia pneumoniae’s major outer membrane protein

Chlamydiapneumoniaeis a Gram-negative bacterium responsible for a number of humanrespiratory diseases and linked to some chronic inflammatory diseases. The major outer membraneprotein (MOMP) ofChlamydiais a conserved immunologically dominant protein located in the outermembrane, which, together with its surface exposure and abundance, has led to MOMP being themain focus for vaccine and antimicrobial studies in recent decades. MOMP has a major role in thechlamydial outer membrane complex through the formation of intermolecular disulphide bonds,although the exact interactions formed are currently unknown. Here, it is proposed that due to thelarge number of cysteines available for disulphide bonding, interactions occur between cysteine-richpockets as opposed to individual residues. Such pockets were identified using a MOMP homologymodel with a supporting low-resolution (~4 Å) crystal structure. The localisation of MOMP in theE. colimembrane was assessed using direct stochastic optical reconstruction microscopy (dSTORM),which showed a decrease in membrane clustering with cysteine-rich regions containing two mutations.These results indicate that disulphide bond formation was not disrupted by single mutants locatedin the cysteine-dense regions and was instead compensated by neighbouring cysteines within thepocket in support of this cysteine-rich pocket hypothesis