Background Autism, a childhood behavioral disorder, belongs to a large suite of diseases, collectively referred to as autism spectrum disorders (ASD). Though multifactorial in etiology, approximately 10% of ASD are associated with atopic dermatitis (AD). Moreover, ASD prevalence increases further as AD severity worsens, though these disorders share no common causative mutations. We assessed here the link between these two disorders in the standard, valproic acid mouse model of ASD. In prior studies, there was no evidence of skin involvement, but we hypothesized that cutaneous involvement could be detected in experiments conducted in BALB/c mice. BALB/c is an albino, laboratory-bred strain of the house mouse and is among the most widely used inbred strains used in animal experimentation. Methods We performed our studies in valproic acid (VPA)-treated BALB/c hairless mice, a standard mouse model of ASD. Mid-trimester pregnant mice received a single intraperitoneal injection of either valproic acid sodium salt dissolved in saline or saline alone on embryonic day 12.5 and were housed individually until postnatal day 21. Only the brain and epidermis appeared to be affected, while other tissues remain unchanged. At various postnatal time points, brain, skin and blood samples were obtained for histology and for quantitation of tissue sphingolipid content and cytokine levels. Results AD-like changes in ceramide content occurred by day one postpartum in both VPA-treated mouse skin and brain. The temporal co-emergence of AD and ASD, and the AD phenotype-dependent increase in ASD prevalence correlated with early appearance of cytokine markers (i.e., interleukin [IL]-4, 5, and 13), as well as mast cells in skin and brain. The high levels of interferon (IFN)γ not only in skin, but also in brain likely account for a significant decline in esterified very-long-chain N-acyl fatty acids in brain ceramides, again mimicking known IFNγ-induced changes in AD. Conclusion Baseline involvement of both AD and ASD could reflect concurrent neuro- and epidermal toxicity, possibly because both epidermis and neural tissues originate from the embryonic neuroectoderm. These studies illuminate the shared susceptibility of the brain and epidermis to a known neurotoxin, suggesting that the atopic diathesis could be extended to include ASD.

To reduce fine particulate matter (PM2.5) level, the sources of PM2.5 in terms of the composition thereof needs to be identified. In this study, the experimental burning of ten types of biomass that are typically used in Republic of Korea, collected at the regional area were to investigate the indicated organic speciation and the results obtained therefrom were applied to the chemical mass balance (CMB) model for the study area. As a result, the organic molecular markers for the biomass burning were identified as they were varying according to chemical speciation of woods and herbaceous plants and depending upon the hard- and soft characteristics of specimens. Based on the source profile from biomass burning, major sources of PM2.5 in the study area of the present study appeared as sources of biomass burning, the secondary ions, secondary particulate matters, which is including long-distance transport, wherein the three sources occupied most over 84% of entire PM2.5. In regard to the subject area distinguished into residential area and on roads, the portion of the biomass burning appeared higher in residential area than on roads, whereas the generation from vehicles of gasoline engine and burning of meats in restaurants, etc. appeared higher on roads comparing to the residential area.

Given the associated health risks, various kinds of methods have been developed to appraise the oxidative potential of particulate matter. However, a standardized experimental approach to assessing the oxidative potential has not yet been established. Researchers need to apply reasonable approaches pertinent to the characteristics of the samples and the purposes of the respective studies and to understand the limitations of each approach. In the present study, the dithiothreitol-based analytical methods of measuring the oxidative potential of particulate matter were appraised for factors that affect the experimental results, such as the sampling substrate, extraction solution, and dithiothreitol reaction. This study reveals the limitations of each experimental approach, which stem from hydrophilic and hydrophobic characteristics, according to simulated lung fluid reactions. Analyses of a Teflon filter and simulated lung fluid were suggested as the most useful procedures based on the results of prior studies.

Background: Autism, a childhood behavioral disorder, belongs to a large suite of diseases, collectively referred to as Autism Spectrum Disorders (ASD). Though multifactorial in etiology, approximately 10% of ASD are associated with atopic dermatitis (AD). Moreover, ASD prevalence increases further as AD severity worsens, though these disorders share no common causative mutations. We assessed here the link between these two disorders in the standard, valproic acid mouse model of ASD. In prior studies, there was no evidence of skin involvement, but we hypothesized that cutaneous involvement could be detected in experiments conducted in BALB/c mice. BALB/c is an albino, laboratory-bred strain of the house mouse and is among the most widely used inbred strains used in animal experimentation.Methods: We performed our studies in valproic acid (VPA)-treated BALB/c hairless mice. Mid-trimester pregnant mice received a single intraperitoneal injection of either valproic acid sodium salt dissolved in saline or saline alone on embryonic day 12.5 and were housed individually until postnatal day 21. Only the brain and epidermis appeared to be affected, while other tissues remain unchanged. At various post-natal time points, brain, skin and blood samples were obtained for histology and for quantitation of tissue sphingolipid content and cytokine levels.Results: AD-like changes in ceramide content occurred by day one post-partum in both VPA-treated mouse skin and brain. The temporal co-emergence of AD and ASD, and the AD phenotype-dependent increase in ASD prevalence correlated with the early appearance of Th2 markers (i.e., interleukin [IL]-4, 5, & 13, mast cells) in the skin and brain. The high levels of interferon (IFN)g not only in skin, but also in brain likely account for a significant decrease in very-long-chain N-acyl fatty acids in brain ceramides that again mimicked known IFNg-induced changes in AD. Conclusion: The baseline involvement of both AD and ASD could reflect concurrent neuro- and epidermal toxicity, possibly because both the epidermis and neural tissues originate from the embryonic neuroectoderm These studies illuminate the shared susceptibility of the brain and epidermis to a known neurotoxin, suggesting that ASD could be included within the atopic diathesis.