Can an acoustic observatory contribute to the conservation of threatened species?

Observatories are designed to collect data for a range of uses. The Australian Acoustic Observatory (A2O) was established to collect environmental sound, including audible species calls, from 344 recorders at 86 sites around Australia. We examine the potential of the A2O to monitor near threatened, threatened, endangered and critically endangered species, based on their vocal behaviour, geographic distributions in relation to the sites of the A2O and on some knowledge of habitat use. Using IUCN and EPBC lists of threatened and endangered species, we extracted species that vocalized in the audible range, and using conservative estimates of their geographic ranges, determined whether there was a possibility of hearing them at these sites. We found that it may be possible to detect up to 171 threatened species at sites established for the A2O, and that individual sites have the potential to detect up to 40 threatened species. All 86 sites occurred in locations where threatened species could possibly be detected, and the list of detectable species included birds, amphibians, and mammals. We have incidentally detected one mammal and four bird species in the data during other work. Threatening processes to which potentially detectable species were exposed included all but two IUCN threat categories. We concluded that with applications of technology to search the audio data from the A2O, it could serve as an important tool for monitoring threatened species

Determinants of tenancy sustainment following homelessness: A Systematic Review

Background: Tenancy sustainment—the maintenance of a tenancy to avoid a premature end of tenure—is fundamental to homelessness prevention. Understanding what enables a successful tenancy is essential to inform interventions to support people leave homelessness. Objective: To conduct a systematic review to identify determinants associated with tenancy sustainment following homelessness. Search methods: A detailed search of 12 electronic databases, as well as grey literature sources, was conducted in 2015 and updated in 2016. The study protocol is registered with PROSPERO (CRD42015019361). Selection criteria: All study designs with a population of homeless or formerly homeless individuals, in which tenancy sustainment was the primary outcome were included. Abstract and full text review was carried out independently by two reviewers. The methodological quality of articles was assessed using QualSyst, a validated quality appraisal tool. Data collection and analysis: A data extraction form was developed for the review and was completed by two reviewers to ensure accuracy. The heterogeneity of included studies indicated that a narrative overview of the results was most appropriate. Main results: Forty three articles reporting 38 studies were included. The determinants were categorized at four levels: individual, interpersonal, community and structural. Participation in specific programs, for example Housing First, receiving social support and being older were identified as the possible determinants of tenancy sustainment. Author’s conclusions: This systematic review is the first, to our knowledge, to focus solely on tenancy sustainment as a primary outcome. A range of determinants associated with tenancy sustainment was identified but it was difficult to draw strong conclusions due to the heterogeneity of the studies. Despite being a fundamental concept in homelessness research, tenancy sustainment is poorly defined and conceptualised. A deeper understanding of tenancy sustainment will inform the development and evaluation of interventions that support people to leave homelessness and maintain tenancies. Public health implications: Housing stability is central to preventing homelessness and addressing the numerous public health concerns that can co-occur with homelessness. Our review highlights that a standardized approach to measuring housing stability and more high quality intervention studies are essential in future research

Alternatives to Robinson and Redford's method of assessing overharvest from incomplete demographic data

Conservation biologists often must make decisions about the sustainability of harvest rates based on minimal demographic information. To assist them Robinson anti Redford (1991) formulated a method to estimate maximum rates of production which could be used to detect overharvesting based on only age at first reproduction, fecundity, and maximum longevity. By assuming constant adult survival we reduced the Euler equation to a simple form that allows calculation of population growth from the same minimal demographic data, brit that can incorporate empirical prereproductive and adult survival rates if available. With this formula, we computed growth rates rising various explicit survival schedules, and we compared these rates and those from Robinson and Redford's (1991) method to rates calculated from 19 relatively complete mammalian life tables gleaned from the literature. When we applied our method (assuming 1% survival to maximum longevity) and that of Robinson and Redford (1991) to the same minimal demographic data, we found that our growth rates were closer to those from complete life tables. We therefore reexamined the data of Fa et al (1995) and Fitzgibbon et al. (1995), who analyzed overharvesting of several populations of commercially exploited African mammals based on Robinson and Redford's (1991) methods Our reanalysis indicates that several additional populations may be overharvested. Our analysis also suggests that data on survival to age at first reproduction improves estimates of population growth rates more than data on age-specific adult survival. Regardless of the method, approximate growth rates based on incomplete life tables can be used to detect when populations are overharvested, brit one should not conclude that harvest rates are sustainable when they are less than approximate production rates because simplifying assumptions often lend to overestimates

Drink driving among Aboriginal and Torres Strait Islander Australians: what has been done and where to next?

The Australian Government will set the direction for addressing road safety over the next decade with its 2021–2030 National Road Safety Strategy. This road map will detail objectives and goals agreed upon by all Australian states and territories. Similar to previous national strategies, Aboriginal and Torres Strait Islander (Indigenous) Australians are a high priority population. Indigenous Australians are over-represented in serious injury and fatal road crashes, with alcohol a leading factor. Therapeutic and educational programs are a major strategy among the suite of measures designed to reduce and prevent drink driving in Australia. The release of this new strategy provides a timely opportunity to reflect on what is known about drink driving among Indigenous Australians and to consider the suitability of existing therapeutic and educational drink driving programs for Indigenous Australian contexts. Here, we summarise factors that contribute to drink driving in this population and identify outstanding knowledge gaps. Then, we present an overview of drink driving programs available for Indigenous Australians along with suggestions for why tailored programs are needed to suit local contexts. The response to address drink driving among Indigenous Australians has been fragmented Australia-wide. A coordinated national response, with ongoing monitoring and evaluation, would improve policy effectiveness and inform more efficient allocation of resources. Together this information can help create suitable and effective drink driving programs for Indigenous drivers and communities Australia-wide

Immune-mediated changes in actinic keratosis following topical treatment with imiquimod 5% cream

BACKGROUND: The objective of this study was to identify the molecular processes responsible for the anti-lesional activity of imiquimod in subjects with actinic keratosis using global gene expression profiling. METHODS: A double-blind, placebo-controlled, randomized study was conducted to evaluate gene expression changes in actinic keratosis treated with imiquimod 5% cream. Male subjects (N = 17) with ≥ 5 actinic keratosis on the scalp applied placebo cream or imiquimod 3 times a week on nonconsecutive days for 4 weeks. To elucidate the molecular processes involved in actinic keratosis lesion regression by imiquimod, gene expression analysis using oligonucleotide arrays and real time reverse transcriptase polymerase chain reaction were performed on shave biopsies of lesions taken before and after treatment. RESULTS: Imiquimod modulated the expression of a large number of genes important in both the innate and adaptive immune response, including increased expression of interferon-inducible genes with known antiviral, anti-proliferative and immune modulatory activity, as well as various Toll-like receptors. In addition, imiquimod increased the expression of genes associated with activation of macrophages, dendritic cells, cytotoxic T cells, and natural killer cells, as well as activation of apoptotic pathways. CONCLUSION: Data suggest that topical application of imiquimod stimulates cells in the skin to secrete cytokines and chemokines that lead to inflammatory cell influx into the lesions and subsequent apoptotic and immune cell-mediated destruction of lesions

Subjective Sleep Quality Deteriorates Before Development of Painful Temporomandibular Disorder

There is good evidence that poor sleep quality increases risk of painful temporomandibular disorder (TMD). However little is known about the course of sleep quality in the months preceding TMD onset, and whether the relationship is mediated by heightened sensitivity to pain. The Pittsburgh Sleep Quality Index was administered at enrollment into the OPPERA prospective cohort study. Thereafter the Sleep Quality Numeric Rating Scale was administered every three months to 2,453 participants. Sensitivity to experimental pressure pain and pinprick pain stimuli was measured at baseline and repeated during follow-up of incident TMD cases (n=220) and matched TMD-free controls (n=193). Subjective sleep quality deteriorated progressively, but only in those who subsequently developed TMD. A Cox proportional hazards model showed that risk of TMD was greater among participants whose sleep quality worsened during follow-up (adjusted hazard ratio=1.73, 95% confidence limits: 1.29, 2.32). This association was independent of baseline measures of sleep quality, psychological stress, somatic awareness, comorbid conditions, non-pain facial symptoms and demographics. Poor baseline sleep quality was not significantly associated with baseline pain sensitivity or with subsequent change in pain sensitivity. Furthermore the relationship between sleep quality and TMD incidence was not mediated via baseline pain sensitivity nor change in pain sensitivity

Identification of clusters of individuals relevant to temporomandibular disorders and other chronic pain conditions: the OPPERA study

The classification of most chronic pain disorders gives emphasis to anatomical location of the pain to distinguish one disorder from the other (eg, back pain vs temporomandibular disorder [TMD]) or to define subtypes (eg, TMD myalgia vs arthralgia). However, anatomical criteria overlook etiology, potentially hampering treatment decisions. This study identified clusters of individuals using a comprehensive array of biopsychosocial measures. Data were collected from a case–control study of 1031 chronic TMD cases and 3247 TMD-free controls. Three subgroups were identified using supervised cluster analysis (referred to as the adaptive, pain-sensitive, and global symptoms clusters). Compared with the adaptive cluster, participants in the pain-sensitive cluster showed heightened sensitivity to experimental pain, and participants in the global symptoms cluster showed both greater pain sensitivity and greater psychological distress. Cluster membership was strongly associated with chronic TMD: 91.5% of TMD cases belonged to the pain-sensitive and global symptoms clusters, whereas 41.2% of controls belonged to the adaptive cluster. Temporomandibular disorder cases in the pain-sensitive and global symptoms clusters also showed greater pain intensity, jaw functional limitation, and more comorbid pain conditions. Similar results were obtained when the same methodology was applied to a smaller case–control study consisting of 199 chronic TMD cases and 201 TMD-free controls. During a median 3-year follow-up period of TMD-free individuals, participants in the global symptoms cluster had greater risk of developing first-onset TMD (hazard ratio = 2.8) compared with participants in the other 2 clusters. Cross-cohort predictive modeling was used to demonstrate the reliability of the clusters

Epistatic interactions between mutations of TACI (TNFRSF13B) and TCF3 result in a severe primary immunodeficiency disorder and systemic lupus erythematosus

Common variable immunodeficiency disorders (CVID) are a group of primary immunodeficiencies where monogenetic causes account for only a fraction of cases. On this evidence, CVID is potentially polygenic and epistatic although there are, as yet, no examples to support this hypothesis. We have identified a non-consanguineous family, who carry the C104R (c.310T>C) mutation of the Transmembrane Activator Calcium-modulator and cyclophilin ligand Interactor (TACI, TNFRSF13B) gene. Variants in TNFRSF13B/TACI are identified in up to 10% of CVID patients, and are associated with, but not solely causative of CVID. The proband is heterozygous for the TNFRSF13B/TACI C104R mutation and meets the Ameratunga et al. diagnostic criteria for CVID and the American College of Rheumatology criteria for systemic lupus erythematosus (SLE). Her son has type 1 diabetes, arthritis, reduced IgG levels and IgA deficiency, but has not inherited the TNFRSF13B/TACI mutation. Her brother, homozygous for the TNFRSF13B/TACI mutation, is in good health despite profound hypogammaglobulinemia and mild cytopenias. We hypothesised that a second unidentified mutation contributed to the symptomatic phenotype of the proband and her son. Whole-exome sequencing of the family revealed a de novo nonsense mutation (T168fsX191) in the Transcription Factor 3 (TCF3) gene encoding the E2A transcription factors, present only in the proband and her son. We demonstrate mutations of TNFRSF13B/TACI impair immunoglobulin isotype switching and antibody production predominantly via T-cell-independent signalling, while mutations of TCF3 impair both T-cell-dependent and -independent pathways of B-cell activation and differentiation. We conclude that epistatic interactions between mutations of the TNFRSF13B/TACI and TCF3 signalling networks lead to the severe CVID-like disorder and SLE in the proband.We thank AMRF, A+ Trust, IDFNZ, ASCIA and the Australian National Health and Medical Research Council (NHMRC, Program Grant 1054925, Project Grant 1127198 and Independent Research Institutes Infrastructure Support Scheme Grant 361646) for grant support. We also received support from Bloody Long Way (BLW) the Victorian State Government Operational Infrastructure scheme and Walter and Eliza Hall Institute (WEHI) Innovation Grant. CAS is supported by NHMRC postgraduate scholarship 1075666

Effect of comorbid migraine on propranolol efficacy for painful TMD in a randomized controlled trial

Introduction The migraine-preventive drug propranolol is efficacious in reducing pain from temporomandibular disorder, suggesting potential modifying or mediating effects of comorbid migraine. Methods In this randomized controlled trial, myofascial temporomandibular disorder patients were treated with propranolol or placebo for 9 weeks. The primary endpoint was change in a facial pain index derived from daily symptom diaries. Linear and logistic regression models tested for a migraine × treatment-group interaction in reducing facial pain index. Counterfactual models explored changes in headache impact and heart rate as mediators of propranolol's efficacy. Results Propranolol's efficacy in reducing facial pain index was greater among the 104 migraineurs than the 95 non-migraineurs: For example, for the binary ≥ 30% reduction in facial pain index, odds ratios were 3.3 (95% confidence limits: 1.4, 8.1) versus 1.3 (0.5, 3.2), respectively, although the interaction was statistically non-significant (p = 0.139). Cumulative response curves confirmed greater efficacy for migraineurs than non-migraineurs (differences in area under the curve 26% and 6%, respectively; p = 0.081). While 9% of the treatment effect was mediated by reduced headache impact, 46% was mediated by reduced heart rate. Conclusions Propranolol was more efficacious in reducing temporomandibular disorder pain among migraineurs than non-migraineurs, with more of the effect mediated by reduced heart rate than by reduced headache impact. Study identification and registration SOPPRANO; NCT02437383; https://clinicaltrials.gov/ct2/show/NCT0243738