Dendritic spine head diameter is reduced in the prefrontal cortex of progranulin haploinsufficient mice.

Loss-of-function mutations in the progranulin (GRN) gene are an autosomal dominant cause of Frontotemporal Dementia (FTD). These mutations typically result in haploinsufficiency of the progranulin protein. Grn+/- mice provide a model for progranulin haploinsufficiency and develop FTD-like behavioral abnormalities by 9-10 months of age. In previous work, we demonstrated that Grn+/- mice develop a low dominance phenotype in the tube test that is associated with reduced dendritic arborization of layer II/III pyramidal neurons in the prelimbic region of the medial prefrontal cortex (mPFC), a region key for social dominance behavior in the tube test assay. In this study, we investigated whether progranulin haploinsufficiency induced changes in dendritic spine density and morphology. Individual layer II/III pyramidal neurons in the prelimbic mPFC of 9-10 month old wild-type or Grn+/- mice were targeted for iontophoretic microinjection of fluorescent dye, followed by high-resolution confocal microscopy and 3D reconstruction for morphometry analysis. Dendritic spine density in Grn+/- mice was comparable to wild-type littermates, but the apical dendrites in Grn+/- mice had a shift in the proportion of spine types, with fewer stubby spines and more thin spines. Additionally, apical dendrites of Grn+/- mice had longer spines and smaller thin spine head diameter in comparison to wild-type littermates. These changes in spine morphology may contribute to altered circuit-level activity and social dominance deficits in Grn+/- mice.

Mitochondrial damage and impaired mitophagy contribute to disease progression in SCA6.

Spinocerebellar ataxia type 6 (SCA6) is a neurodegenerative disease that manifests in midlife and progressively worsens with age. SCA6 is rare, and many patients are not diagnosed until long after disease onset. Whether disease-causing cellular alterations differ at different disease stages is currently unknown, but it is important to answer this question in order to identify appropriate therapeutic targets across disease duration. We used transcriptomics to identify changes in gene expression at disease onset in a well-established mouse model of SCA6 that recapitulates key disease features. We observed both up- and down-regulated genes with the major down-regulated gene ontology terms suggesting mitochondrial dysfunction. We explored mitochondrial function and structure and observed that changes in mitochondrial structure preceded changes in function, and that mitochondrial function was not significantly altered at disease onset but was impaired later during disease progression. We also detected elevated oxidative stress in cells at the same disease stage. In addition, we observed impairment in mitophagy that exacerbates mitochondrial dysfunction at late disease stages. In post-mortem SCA6 patient cerebellar tissue, we observed metabolic changes that are consistent with mitochondrial impairments, supporting our results from animal models being translatable to human disease. Our study reveals that mitochondrial dysfunction and impaired mitochondrial degradation likely contribute to disease progression in SCA6 and suggests that these could be promising targets for therapeutic interventions in particular for patients diagnosed after disease onset.

Endosomal dysfunction contributes to cerebellar deficits in spinocerebellar ataxia type 6.

Spinocerebellar ataxia type 6 (SCA6) is a rare disease that is characterized by cerebellar dysfunction. Patients have progressive motor coordination impairment, and postmortem brain tissue reveals degeneration of cerebellar Purkinje cells and a reduced level of cerebellar brain-derived neurotrophic factor (BDNF). However, the pathophysiological changes underlying SCA6 are not fully understood. We carried out RNA-sequencing of cerebellar vermis tissue in a mouse model of SCA6, which revealed widespread dysregulation of genes associated with the endo-lysosomal system. Since disruption to endosomes or lysosomes could contribute to cellular deficits, we examined the endo-lysosomal system in SCA6. We identified alterations in multiple endosomal compartments in the Purkinje cells of SCA6 mice. Early endosomes were enlarged, while the size of the late endosome compartment was reduced. We also found evidence for impaired trafficking of cargo to the lysosomes. As the proper functioning of the endo-lysosomal system is crucial for the sorting and trafficking of signaling molecules, we wondered whether these changes could contribute to previously identified deficits in signaling by BDNF and its receptor tropomyosin kinase B (TrkB) in SCA6. Indeed, we found that the enlarged early endosomes in SCA6 mice accumulated both BDNF and TrkB. Furthermore, TrkB recycling to the cell membrane in recycling endosomes was reduced, and the late endosome transport of BDNF for degradation was impaired. Therefore, mis-trafficking due to aberrant endo-lysosomal transport and function could contribute to SCA6 pathophysiology through alterations to BDNF-TrkB signaling, as well as mishandling of other signaling molecules. Deficits in early endosomes and BDNF localization were rescued by chronic administration of a TrkB agonist, 7,8-dihydroxyflavone, that we have previously shown restores motor coordination and cerebellar TrkB expression. The endo-lysosomal system is thus both a novel locus of pathophysiology in SCA6 and a promising therapeutic target.

Regulation of extracellular progranulin in medial prefrontal cortex.

Progranulin is a secreted pro-protein that has anti-inflammatory and neurotrophic effects and is necessary for maintaining lysosomal function. Mutations in progranulin (GRN) are a major cause of frontotemporal dementia. Most pathogenic GRN mutations cause progranulin haploinsufficiency, so boosting progranulin levels is a promising therapeutic strategy. Progranulin is constitutively secreted, then taken up and trafficked to lysosomes. Before being taken up from the extracellular space, progranulin interacts with receptors that may mediate anti-inflammatory and growth factor-like effects. Modifying progranulin trafficking is a viable approach to boosting progranulin, but progranulin secretion and uptake by cells in the brain is poorly understood and may involve distinct mechanisms from other parts of the body. Understanding the cell types and processes that regulate extracellular progranulin in the brain could provide insight into progranulin's mechanism of action and inform design of progranulin-boosting therapies. To address this question we used microdialysis to measure progranulin in interstitial fluid (ISF) of mouse medial prefrontal cortex (mPFC). Grn+/- mice had approximately 50% lower ISF progranulin than wild-type mice, matching the reduction of progranulin in cortical tissue. Fluorescent in situ hybridization and immunofluorescence confirmed that microglia and neurons are the major progranulin-expressing cell types in the mPFC. Studies of conditional microglial (Mg-KO) and neuronal (N-KO) Grn knockout mice revealed that loss of progranulin from either cell type results in approximately 50% reduction in ISF progranulin. LPS injection (i.p.) produced an acute increase in ISF progranulin in mPFC. Depolarizing cells with KCl increased ISF progranulin, but this response was not altered in N-KO mice, indicating progranulin secretion by non-neuronal cells. Increasing neuronal activity with picrotoxin did not increase ISF progranulin. These data indicate that microglia and neurons are the source of most ISF progranulin in mPFC, with microglia likely secreting more progranulin per cell than neurons. The acute increase in ISF progranulin after LPS treatment is consistent with a role for extracellular progranulin in regulating inflammation, and may have been driven by microglia or peripheral immune cells. Finally, these data indicate that mPFC neurons engage in constitutive progranulin secretion that is not acutely changed by neuronal activity.

Patients with sporadic FTLD exhibit similar increases in lysosomal proteins and storage material as patients with FTD due to GRN mutations.

Loss of function progranulin (GRN) mutations are a major autosomal dominant cause of frontotemporal dementia (FTD). Patients with FTD due to GRN mutations (FTD-GRN) develop frontotemporal lobar degeneration with TDP-43 pathology type A (FTLD-TDP type A) and exhibit elevated levels of lysosomal proteins and storage material in frontal cortex, perhaps indicating lysosomal dysfunction as a mechanism of disease. To investigate whether patients with sporadic FTLD exhibit similar signs of lysosomal dysfunction, we compared lysosomal protein levels, transcript levels, and storage material in patients with FTD-GRN or sporadic FTLD-TDP type A. We analyzed samples from frontal cortex, a degenerated brain region, and occipital cortex, a relatively spared brain region. In frontal cortex, patients with sporadic FTLD-TDP type A exhibited similar increases in lysosomal protein levels, transcript levels, and storage material as patients with FTD-GRN. In occipital cortex of both patient groups, most lysosomal measures did not differ from controls. Frontal cortex from a transgenic mouse model of TDP-opathy had similar increases in cathepsin D and lysosomal storage material, showing that TDP-opathy and neurodegeneration can drive these changes independently of progranulin. To investigate these changes in additional FTLD subtypes, we analyzed frontal cortical samples from patients with sporadic FTLD-TDP type C or Pick's disease, an FTLD-tau subtype. All sporadic FTLD groups had similar increases in cathepsin D activity, lysosomal membrane proteins, and storage material as FTD-GRN patients. However, patients with FTLD-TDP type C or Pick's disease did not have similar increases in lysosomal transcripts as patients with FTD-GRN or sporadic FTLD-TDP type A. Based on these data, accumulation of lysosomal proteins and storage material may be a common aspect of end-stage FTLD. However, the unique changes in gene expression in patients with FTD-GRN or sporadic FTLD-TDP type A may indicate distinct underlying lysosomal changes among FTLD subtypes.

Activation of TrkB-Akt signaling rescues deficits in a mouse model of SCA6.

Spinocerebellar ataxia type 6 (SCA6) is a neurodegenerative disease resulting in motor coordination deficits and cerebellar pathology. Expression of brain-derived neurotrophic factor (BDNF) is reduced in postmortem tissue from SCA6 patients. Here, we show that levels of cerebellar BDNF and its receptor, tropomyosin receptor kinase B (TrkB), are reduced at an early disease stage in a mouse model of SCA6 (SCA684Q/84Q). One month of exercise elevated cerebellar BDNF expression and improved ataxia and cerebellar Purkinje cell firing rate deficits. A TrkB agonist, 7,8-dihydroxyflavone (7,8-DHF), likewise improved motor coordination and Purkinje cell firing rate and elevated downstream Akt signaling. Prolonged 7,8-DHF administration persistently improved ataxia when treatment commenced near disease onset but was ineffective when treatment was started late. These data suggest that 7,8-DHF, which is orally bioavailable and crosses the blood-brain barrier, is a promising therapeutic for SCA6 and argue for the importance of early intervention for SCA6.

Loss of Flocculus Purkinje Cell Firing Precision Leads to Impaired Gaze Stabilization in a Mouse Model of Spinocerebellar Ataxia Type 6 (SCA6).

Spinocerebellar Ataxia Type 6 (SCA6) is a mid-life onset neurodegenerative disease characterized by progressive ataxia, dysarthria, and eye movement impairment. This autosomal dominant disease is caused by the expansion of a CAG repeat tract in the CACNA1A gene that encodes the α1A subunit of the P/Q type voltage-gated Ca2+ channel. Mouse models of SCA6 demonstrate impaired locomotive function and reduced firing precision of cerebellar Purkinje in the anterior vermis. Here, to further assess deficits in other cerebellar-dependent behaviors, we characterized the oculomotor phenotype of a knock-in mouse model with hyper-expanded polyQ repeats (SCA684Q). We found a reduction in the efficacy of the vestibulo-ocular reflex (VOR) and optokinetic reflex (OKR) in SCA6 mutant mice, without a change in phase, compared to their litter-matched controls. Additionally, VOR motor learning was significantly impaired in SCA684Q mice. Given that the floccular lobe of the cerebellum plays a vital role in the generation of OKR and VOR calibration and motor learning, we investigated the firing behavior and morphology of floccular cerebellar Purkinje cells. Overall, we found a reduction in the firing precision of floccular lobe Purkinje cells but no morphological difference between SCA684Q and wild-type mice. Taken together, our findings establish that gaze stabilization and motor learning are impaired in SCA684Q mice and suggest that altered cerebellar output contributes to these deficits.

"I Spent Most of Freshers in my Room"-A Qualitative Study of the Social Experiences of University Students on the Autistic Spectrum.

Autistic university students face extra challenges in both their academic and social life. Barriers to socialising appear to be less well understood and supported by universities than academic requirements. Semi-structured interviews were conducted with ten autistic university students to explore their social experiences. Questions explored their social experiences, satisfaction with social life, disclosure of ASD to others, and the impact of mental wellbeing on university life. Thematic analysis indicated most participants were unsatisfied with their social lives and experienced mental health issues. Factors exacerbating social isolation included lack of suitable social events, lack of social support and feeling unable to disclose to peers. Factors which reduced social isolation included joining an autism or special interest society and receiving social mentoring.

Molecular Identity and Location Influence Purkinje Cell Vulnerability in Autosomal-Recessive Spastic Ataxia of Charlevoix-Saguenay Mice.

Patterned cell death is a common feature of many neurodegenerative diseases. In patients with autosomal-recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) and mouse models of ARSACS, it has been observed that Purkinje cells in anterior cerebellar vermis are vulnerable to degeneration while those in posterior vermis are resilient. Purkinje cells are known to express certain molecules in a highly stereotyped, patterned manner across the cerebellum. One patterned molecule is zebrin, which is expressed in distinctive stripes across the cerebellar cortex. The different zones delineated by the expression pattern of zebrin and other patterned molecules have been implicated in the patterning of Purkinje cell death, raising the question of whether they contribute to cell death in ARSACS. We found that zebrin patterning appears normal prior to disease onset in Sacs-/- mice, suggesting that zebrin-positive and -negative Purkinje cell zones develop normally. We next observed that zebrin-negative Purkinje cells in anterior lobule III were preferentially susceptible to cell death, while anterior zebrin-positive cells and posterior zebrin-negative and -positive cells remained resilient even at late disease stages. The patterning of Purkinje cell innervation to the target neurons in the cerebellar nuclei (CN) showed a similar pattern of loss: neurons in the anterior CN, where inputs are predominantly zebrin-negative, displayed a loss of Purkinje cell innervation. In contrast, neurons in the posterior CN, which is innervated by both zebrin-negative and -positive puncta, had normal innervation. These results suggest that the location and the molecular identity of Purkinje cells determine their susceptibility to cell death in ARSACS.

Field-Portable Microplastic Sensing in Aqueous Environments: A Perspective on Emerging Techniques.

Microplastics (MPs) have been found in aqueous environments ranging from rural ponds and lakes to the deep ocean. Despite the ubiquity of MPs, our ability to characterize MPs in the environment is limited by the lack of technologies for rapidly and accurately identifying and quantifying MPs. Although standards exist for MP sample collection and preparation, methods of MP analysis vary considerably and produce data with a broad range of data content and quality. The need for extensive analysis-specific sample preparation in current technology approaches has hindered the emergence of a single technique which can operate on aqueous samples in the field, rather than on dried laboratory preparations. In this perspective, we consider MP measurement technologies with a focus on both their eventual field-deployability and their respective data products (e.g., MP particle count, size, and/or polymer type). We present preliminary demonstrations of several prospective MP measurement techniques, with an eye towards developing a solution or solutions that can transition from the laboratory to the field. Specifically, experimental results are presented from multiple prototype systems that measure various physical properties of MPs: pyrolysis-differential mobility spectroscopy, short-wave infrared imaging, aqueous Nile Red labeling and counting, acoustophoresis, ultrasound, impedance spectroscopy, and dielectrophoresis.

Templated α-Synuclein Inclusion Formation Is Independent of Endogenous Tau.

Synucleinopathies including Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are characterized by neuronal intracellular inclusions of α-synuclein. PD dementia (PDD) and DLB are collectively the second most common cause of neurodegenerative dementia. In addition to associated inclusions, Lewy body diseases (LBDs) have dopaminergic neurodegeneration, motor defects and cognitive changes. The microtubule-associated protein tau has been implicated in LBDs, but the exact role of the protein and how it influences formation of α-synuclein inclusions is unknown. Reducing endogenous tau levels is protective in multiple models of Alzheimer's disease (AD), tauopathies, and in some transgenic synucleinopathy mouse models. Recombinant α-synuclein and tau proteins interact in vitro Here, we show tau and α-synuclein colocalize at excitatory presynaptic terminals. However, tau heterozygous and tau knock-out mice do not show a reduction in fibril-induced α-synuclein inclusions formation in primary cortical neurons, or after intrastriatal injections of fibrils at 1.5 month or six months later. At six months following intrastriatal injections, wild-type, tau heterozygous and tau knock-out mice showed a 50% reduction in dopamine neurons in the substantia nigra pars compacta (SNc) compared with mice injected with α-synuclein monomer, but there were no statistically significant differences across genotypes. These data suggest the role of tau in the pathogenesis of LBDs is distinct from AD, and Lewy pathology formation may be independent of endogenous tau.

The diagnosis of respiratory disease in children using a phone-based cough and symptom analysis algorithm: The smartphone recordings of cough sounds 2 (SMARTCOUGH-C 2) trial design.

The diagnosis of acute respiratory diseases in children can be challenging, and no single objective diagnostic test exists for common pediatric respiratory diseases. Previous research has demonstrated that ResAppDx, a cough sound and symptom-based analysis algorithm, can identify common respiratory diseases at the point of care. We present the study protocol for SMARTCOUGH-C 2, a prospective diagnostic accuracy trial of a cough and symptom-based algorithm in a cohort of children presenting with acute respiratory diseases. The objective of the study is to assess the performance characteristics of the ResAppDx algorithm in the diagnosis of common pediatric acute respiratory diseases.

Losing the Beat: Contribution of Purkinje Cell Firing Dysfunction to Disease, and Its Reversal.

The cerebellum is a brain structure that is highly interconnected with other brain regions. There are many contributing factors to cerebellar-related brain disease, such as altered afferent input, local connectivity, and/or cerebellar output. Purkinje cells (PC) are the principle cells of the cerebellar cortex, and fire intrinsically; that is, they fire spontaneous action potentials at high frequencies. This review paper focuses on PC intrinsic firing activity, which is altered in multiple neurological diseases, including ataxia, Huntington Disease (HD) and autism spectrum disorder (ASD). Notably, there are several cases where interventions that restore or rescue PC intrinsic activity also improve impaired behavior in these mouse models of disease. These findings suggest that rescuing PC firing deficits themselves may be sufficient to improve impairment in cerebellar-related behavior in disease. We propose that restoring PC intrinsic firing represents a good target for drug development that might be of therapeutic use for several disorders.

S-EQUOL: a neuroprotective therapeutic for chronic neurocognitive impairments in pediatric HIV.

Chronic neurocognitive impairments, commonly associated with pediatric human immunodeficiency virus type 1 (PHIV), are a detrimental consequence of early exposure to HIV-1 viral proteins. Strong evidence supports S-Equol (SE) as an efficacious adjunctive neuroprotective and/or neurorestorative therapeutic for neurocognitive impairments in adult ovariectomized female HIV-1 transgenic (Tg) rats. There remains, however, a critical need to assess the therapeutic efficacy of SE when treatment occurs at an earlier age (i.e., resembling a therapeutic for children with PHIV) and across the factor of biological sex. Utilization of a series of signal detection operant tasks revealed prominent, sex-dependent neurocognitive deficits in the HIV-1 Tg rat, characterized by alterations in stimulus-reinforcement learning, the response profile, and temporal processing. Early (i.e., postnatal day 28) initiation of SE treatment precluded the development of chronic neurocognitive impairments in all (i.e., 100%) HIV-1 Tg animals, albeit not for all neurocognitive domains. Most notably, the therapeutic effects of SE are generalized across the factor of biological sex, despite the presence of endogenous hormones. Results support, therefore, the efficacy of SE as a neuroprotective therapeutic for chronic neurocognitive impairments in the post-cART era; an adjunctive therapeutic that demonstrates high efficacy in both males and females. Optimizing treatment conditions by evaluating multiple factors (i.e., age, neurocognitive domains, and biological sex) associated with PHIV and HIV-1 associated neurocognitive disorders (HAND) affords a key opportunity to improve the therapeutic efficacy of SE.

The effect of school exposure and personal contact on attitudes towards bullying and autism in schools: A cohort study with a control group.

LAY ABSTRACT: Autistic children are more likely than non-autistic children to be bullied at school. This study therefore explored whether the kind of school setting and the level of personal contact with autistic people can affect children's attitudes towards bullying and autism. Surveys were completed at the beginning and end of the school year by 775 children aged 11-12 years, from six schools: three with specialist centres for autistic children and three without. Participants read stories describing bullying situations, then provided their views in relation to the story and in relation to autism. Children in schools with centres increased their feelings of anger, pity, sadness and shame in response to the bullying situations. In contrast, children in schools with no centre showed less sociable responses to bullying, except in response to a story describing an autistic child, being excluded by classmates. Furthermore, children who increased the time they spent with autistic individuals over the course of the year showed a greater rise in positive attitudes towards autistic people. This highlights the need for both personal contact and an inclusive school environment, to improve attitudes towards autism and reduce tolerance for bullying.

Dose-dependent effects of alcohol injections on omission-contingency learning have an inverted-U pattern.

Previous examinations of the long-term effects of alcohol exposure on omission-contingency learning have produced mixed results across different age or sex groups, with evidence for faster learning or no effect. However, none of these experiments made comparisons using the same exposure-dose across the age/sex groups. Here, we exposed rats to 6 weeks of alcohol injections (3 days/week, 1.75 or 3.5 g/kg/24-h, i.p. broken up into 2 injections/day) in adolescent/early adult males or females (PND27-66) or adult males (PND62-101). We then tested the rats in autoshaping and omission-contingency tasks. In contrast to our hypotheses, the low 1.75-g/kg/24-h dose led to slower omission learning and the higher 3.5-g/kg/24-h dose had no effect. There were no age- or sex-differences in omission learning. Additionally, during autoshaping training, rats exposed in adolescence/early adulthood had a faster shift to sign-tracking in their sign-tracking/goal-tracking ratios than rats exposed in adulthood, with no consistent effect of alcohol exposure or sex-differences. Our results suggest complex effects of alcohol on the neural substrates of omission-contingency learning at different doses, which will require future investigation.

Phytoremediation of slightly brackish, polycyclic aromatic hydrocarbon-contaminated groundwater from 250 ft below land surface: A pilot-scale study using salt-tolerant, endophyte-enhanced hybrid poplar trees at a Superfund site in the Central Valley of California, April-November 2019.

Slightly brackish groundwater contaminated by polycyclic aromatic hydrocarbons (PAHs) at a Superfund site in the Central Valley of California was pumped from 250 feet below land surface to a water storage tank using solar power and then gravity-fed into 18, 330-gallon intermediate bulk containers (totes) as follows: (1) Five totes contained planting medium with three salt-tolerant hybrid poplar trees per tote (n = 15); (2) Seven totes contained planting medium with three salt-tolerant hybrid poplar trees per tote and inoculated with the naturally occurring, PAH-degrading endophyte Pseudomonas putida PD1 (n = 21); (3) Three totes contained planting medium only (n = 0); (4) One tote contained groundwater with three PD1-inoculated trees (n = 3) and one tote contained groundwater with three regular trees (n = 3); and (5) One tote contained groundwater only (n = 0). All trees grew well during the 7-month growing season in spite of the area's hot, dry air temperature, little precipitation, tote-influent chloride concentrations of 290 mg/L, and tote-influent naphthalene concentrations that ranged from 650 to 5,100 mg/L. PD1-inoculated trees initially had 56% larger tree area (tree height × tree width) than regular trees and up to 69% larger tree area by the end of the growing season, indicating some conferred phytoprotection to the PAH contamination. All trees had similar trunk caliper (diameter) and leaf chlorophyll content by the end of the growing season. Total naphthalene removal ranged from 88% to 100% across all totes. The lowest naphthalene removal of 88% was observed in a tote that contained only planting medium and indicates substantial adsorption of naphthalene onto the high organic content of the planting medium. Contaminant removal due to uptake by the hybrid poplar trees was confirmed by the detection of naphthalene in in vivo passive samplers placed in tree trunks. Benzene, toluene, ethylbenzene, total xylenes, 2-methylnaphthalene, 1,2,4-trimethylbenzene, and isopropylbenzene were also detected. These results from the pilot-scale study indicate that a full-scale application of using salt-tolerant hybrid poplar trees at this site could effectively decrease naphthalene concentrations in groundwater pumped from the deep aquifer. These initial results provide hope for similar application at other contaminated sites characterized by groundwater at considerable depths, especially at Superfund sites where costly pump-and-treat systems have been used long-term to treat low levels of groundwater contamination.

Nondestructive Extraction and Identification of Microplastics from Freshwater Sport Fish Stomachs.

Microplastics were extracted from freshwater sport fish stomachs containing substantial biomass and identified using optical microscopy, scanning electron microscopy plus energy-dispersive X-ray spectroscopy (SEM/EDS), and Fourier transform infrared (FTIR) micro-spectroscopy with automated spectral mapping. An extraction method is presented that uses a negatively pressurized sieve stack and purified water to preserve plastic surface characteristics and any adsorbed persistent organic pollutants (POPs). This nondestructive extraction method for large predators' stomachs enables multiple trophic-level studies from one fish sampling event and provides other dietary and behavioral data. FTIR-identified microplastics 50-1500 µm, including polyethylene (two with plastic additive POPs), styrene acrylonitrile, polystyrene, and nylon and polyethylene terephthalate fibers 10-50 µm wide. SEM/EDS revealed characteristic surface weathering on the plastic surfaces. The nylon fibers appear to be from human fishing activities, suggesting options for management. Some particles visually identified as potential plastics were revealed by micro-spectroscopy to be mineralized, natural polyamide proteins, or nonplastic shell pieces. A low-cost, reflective sample preparation method with stable particle mounting was developed to enable automated mapping, improved FTIR throughput, and lower detection size limit. This study yielded 37 intact prey items set aside for future analyses.

The impact of a school-based musical contact intervention on prosocial attitudes, emotions and behaviours: A pilot trial with autistic and neurotypical children.

Children with autism are more likely to be socially excluded than their neurotypical peers. Since the majority of children with autism attend mainstream schools, interventions are needed to improve the attitudes and behaviours of their peers. Many studies highlight the influence of contact on positive attitudes and reduced discrimination. Group music-making provides an ideal opportunity for positive contact to occur in the classroom. This study evaluated the impact of music-based contact with autistic peers on the attitudes, emotions and behaviours of neurotypical children. Changes in those with autism were also assessed. Neurotypical participants ( n = 55) aged 10-11 years took part in an 11-week music programme designed to increase social interaction, which either did or did not include contact with autistic children ( n = 10). Measures of attitudes, emotions and behaviours were assessed at baseline and follow-up. In response to a hypothetical scenario depicting social exclusion of a child with autism, neurotypical participants in the contact group showed a greater increase in prosocial emotions and a greater decrease in tendency to be a victim than those in the no-contact group. Participants with autism also showed a 19.7% decrease in victimisation. Implications of group music-making for tackling social exclusion of children with autism are discussed.