Autism spectrum disorder (ASD) is a family of neurodevelopmental disorders characterized by restrictive interests, repetitive behaviors, deficits in social understanding and interactions, impairments in language development and communications skills. Associated symptoms also include self-injurious behavior, aggression and epilepsy (Amminger et al. 2007). During the last decade, ASD cases in North America indicate a dramatic increase with a prevalence of Received October 21, 2009; revised manuscript received January 18, 2010; Accepted January 19, 2010. Address correspondence and reprint requests to Dr Derrick MacFabe, Kilee Patchell-Evans Autism Research Group, The University of Western Ontario, London, Ontario, Canada N6A 5C2. E-mail: dmacfabe@uwo.caAbbreviations used: ASD, autism spectrum disorder; BUT, butyric acid; CL, cardiolipin; DMA, dimethyl acetal; ESI-MS, electrospray ionization mass spectrometry; FAME, fatty acid methyl ester; FID, flame ionization detection; GC/MS, gas chromatography/mass spectrometry; ICV, intracerebroventricular; PBS, phosphate-buffered saline; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PPA, propionic acid; PS, phosphatidylserine; PUFA, polyunsaturated fatty acids; SM, sphingomyelin. AbstractRecent studies have demonstrated intraventricular infusions of propionic acid (PPA) a dietary and enteric short-chain fatty acid can produce brain and behavioral changes similar to those observed in autism spectrum disorder (ASD). The effects of PPA were further evaluated to determine if there are any alterations in brain lipids associated with the ASD-like behavioral changes observed following intermittent intraventricular infusions of PPA, the related enteric metabolite butyric acid (BUT) or phosphate-buffered saline vehicle. Both PPA and BUT produced significant increases (p < 0.001) in locomotor activity (total distance travelled and stereotypy). PPA and to a lesser extent BUT infusions decreased the levels of total monounsaturates, total x6 fatty acids, total phosphatidylethanolamine plasmalogens, the ratio of x6 : x3 and elevated the levels of total saturates in separated phospholipid species. In addition, total acylcarnitines, total longchain (C12-C24) acylcarnitines, total short-chain (C2 to C9) acylcarnitines, and the ratio of bound to free carnitine were increased following infusions with PPA and BUT. These results provide evidence of a relationship between changes in brain lipid profiles and the occurrence of ASD-like behaviors using the autism rodent model. We propose that altered brain fatty acid metabolism may contribute to ASD. Keywords: carnitine, clostridia, gap junctions, lipids, mitochondria, movement disorder, short-chain fatty acids. one in every 150 children under the age of 5 years (Bertrand et al. 2001;Herbert et al. 2006). Evidence exists for a strong genetic contribution to ASD. However, the lack of complete concordance as well as variances in the severity of autism in monozygotic twins (Hu et al. 2006) indicate that the recent ...

9 Barley and yeast β-glucans were selected, together with lecithin, to encapsulate resveratrol by 10 emulsification-evaporation method to develop new and safer antifungal formulations. Different 11 emulsification techniques were used: high-shear, high pressure and high pressure and 12 temperature emulsification. Morphology, crystallinity, encapsulation efficiency and in vitro 13 antifungal activity against Botrytis cinerea of the different formulations were evaluated. No 14 significant differences between each emulsification procedure in particle size (below 90 nm) and 15 in encapsulation efficiency (70-100%) were observed; only barley β-glucan emulsions showed 16 lower efficiency due to the formation of a gel that retained most of the active compound. A 17 great influence of the emulsification method and the encapsulating material on the crystallinity 18 of the particles was observed. The highest antifungal activity (up to 53% growth inhibition) was 19 obtained by the formulations with yeast β-glucans, indicating an enhanced absorption of 20 encapsulated resveratrol through the cell wall of the fungus at the presence of (1-3, 1-6)-β-21 glucans. 22

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The present data highlights that onychomycosis may be a growing medical concern among ageing patients.

Alterations in the composition of the gut microbiome and/or immune system function may have a role in the development of autism spectrum disorders (ASD). The current study examined the effects of prenatal and early life administration of lipopolysaccharide (LPS), a bacterial mimetic, and the short chain fatty acid, propionic acid (PPA), a metabolic fermentation product of enteric bacteria, on developmental milestones, locomotor activity, and anxiety-like behavior in adolescent male and female offspring. Pregnant Long-Evans rats were subcutaneously injected once a day with PPA (500 mg/kg) on gestation days G12–16, LPS (50 µg/kg) on G15–16, or vehicle control on G12–16 or G15–16. Male and female offspring were injected with PPA (500 mg/kg) or vehicle twice a day, every second day from postnatal days (P) 10–18. Physical milestones and reflexes were monitored in early life with prenatal PPA and LPS inducing delays in eye opening. Locomotor activity and anxiety were assessed in adolescence (P40–42) in the elevated plus maze (EPM) and open-field. Prenatal and postnatal treatments altered behavior in a sex-specific manner. Prenatal PPA decreased time spent in the centre of the open-field in males and females while prenatal and postnatal PPA increased anxiety behavior on the EPM in female rats. Prenatal LPS did not significantly influence those behaviors. Evidence for the double hit hypothesis was seen as females receiving a double hit of PPA (prenatal and postnatal) displayed increased repetitive behavior in the open-field. These results provide evidence for the hypothesis that by-products of enteric bacteria metabolism such as PPA may contribute to ASD, altering development and behavior in adolescent rats similar to that observed in ASD and other neurodevelopmental disorders.

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Individual vulnerability factors influencing the function of the hypothalamic-pituitary-adrenal (HPA) axis may contribute to the risk of the development of persistent musculoskeletal pain after traumatic stress exposure. The objective of the study was to evaluate the association between polymorphisms in the gene encoding FK506 binding protein 51, FKBP5, a glucocorticoid receptor co-chaperone, and musculoskeletal pain severity six weeks after two common trauma exposures. The study included data from two prospective emergency department-based cohorts: a discovery cohort (n=949) of European Americans experiencing motor vehicle collision and a replication cohort of adult European American women experiencing sexual assault (n=53). DNA was collected from trauma survivors at the time of initial assessment. Overall pain and neck pain six weeks after trauma exposure were assessed using a 0–10 numeric rating scale. After adjustment for multiple comparisons, six FKBP5 polymorphisms showed significant association (minimum p <0.0001) with both overall and neck pain in the discovery cohort. The association of rs3800373, rs9380526, rs9394314, rs2817032, and rs2817040 with neck pain and/or overall pain six weeks after trauma was replicated in the sexual assault cohort, showing the same direction of the effect in each case. The results of this study indicate that genetic variants in FKBP5 influence the severity of musculoskeletal pain symptoms experienced during the weeks after motor vehicle collision and sexual assault. These results suggest that glucocorticoid pathways influence the development of persistent post-traumatic pain, and that such pathways may be a target of pharmacologic interventions aimed at improving recovery after trauma.