Recent studies suggest a role for the microbiota in autism spectrum disorders (ASD), potentially arising from their role in modulating the immune system and gastrointestinal (GI) function or from gut–brain interactions dependent or independent from the immune system. GI problems such as chronic constipation and/or diarrhea are common in children with ASD, and significantly worsen their behavior and their quality of life. Here we first summarize previously published data supporting that GI dysfunction is common in individuals with ASD and the role of the microbiota in ASD. Second, by comparing with other publically available microbiome datasets, we provide some evidence that the shifted microbiota can be a result of westernization and that this shift could also be framing an altered immune system. Third, we explore the possibility that gut–brain interactions could also be a direct result of microbially produced metabolites.

Background: Autism spectrum disorders (ASD) are complex neurobiological disorders that impair social interactions and communication and lead to restricted, repetitive, and stereotyped patterns of behavior, interests, and activities. The causes of these disorders remain poorly understood, but gut microbiota, the 1013 bacteria in the human intestines, have been implicated because children with ASD often suffer gastrointestinal (GI) problems that correlate with ASD severity. Several previous studies have reported abnormal gut bacteria in children with ASD. The gut microbiome-ASD connection has been tested in a mouse model of ASD, where the microbiome was mechanistically linked to abnormal metabolites and behavior. Similarly, a study of children with ASD found that oral non-absorbable antibiotic treatment improved GI and ASD symptoms, albeit temporarily. Here, a small open-label clinical trial evaluated the impact of Microbiota Transfer Therapy (MTT) on gut microbiota composition and GI and ASD symptoms of 18 ASD-diagnosed children.

Results: MTT involved a 2-week antibiotic treatment, a bowel cleanse, and then an extended fecal microbiota transplant (FMT) using a high initial dose followed by daily and lower maintenance doses for 7–8 weeks. The Gastrointestinal Symptom Rating Scale revealed an approximately 80% reduction of GI symptoms at the end of treatment, including significant improvements in symptoms of constipation, diarrhea, indigestion, and abdominal pain. Improvements persisted 8 weeks after treatment. Similarly, clinical assessments showed that behavioral ASD symptoms improved significantly and remained improved 8 weeks after treatment ended. Bacterial and phage deep sequencing analyses revealed successful partial engraftment of donor microbiota and beneficial changes in the gut environment. Specifically, overall bacterial diversity and the abundance of Bifidobacterium, Prevotella, and Desulfovibrio among other taxa increased following MTT, and these changes persisted after treatment stopped (followed for 8 weeks).

Conclusions: This exploratory, extended-duration treatment protocol thus appears to be a promising approach to alter the gut microbiome and virome and improve GI and behavioral symptoms of ASD. Improvements in GI symptoms, ASD symptoms, and the microbiome all persisted for at least 8 weeks after treatment ended, suggesting a long-term impact.

High proportions of autistic children suffer from gastrointestinal (GI) disorders, implying a link between autism and abnormalities in gut microbial functions. Increasing evidence from recent high-throughput sequencing analyses indicates that disturbances in composition and diversity of gut microbiome are associated with various disease conditions. However, microbiome-level studies on autism are limited and mostly focused on pathogenic bacteria. Therefore, here we aimed to define systemic changes in gut microbiome associated with autism and autism-related GI problems. We recruited 20 neurotypical and 20 autistic children accompanied by a survey of both autistic severity and GI symptoms. By pyrosequencing the V2/V3 regions in bacterial 16S rDNA from fecal DNA samples, we compared gut microbiomes of GI symptom-free neurotypical children with those of autistic children mostly presenting GI symptoms. Unexpectedly, the presence of autistic symptoms, rather than the severity of GI symptoms, was associated with less diverse gut microbiomes. Further, rigorous statistical tests with multiple testing corrections showed significantly lower abundances of the genera Prevotella, Coprococcus, and unclassified Veillonellaceae in autistic samples. These are intriguingly versatile carbohydrate-degrading and/or fermenting bacteria, suggesting a potential influence of unusual diet patterns observed in autistic children. However, multivariate analyses showed that autism-related changes in both overall diversity and individual genus abundances were correlated with the presence of autistic symptoms but not with their diet patterns. Taken together, autism and accompanying GI symptoms were characterized by distinct and less diverse gut microbial compositions with lower levels of Prevotella, Coprococcus, and unclassified Veillonellaceae.

Materials produced for the workshop hosted by the Humane Cities Initiative, Institute for Humanities Research, Arizona State University. Participants were sent this package of archival materials and links to brief online sources for advance readings. Also enclosed are PDF renderings of introductory powerpoint files by Spindler and Pagan, and an audio recording of the discussion joined in progress.

Presentation slides regarding the history of Victory Village, the trailer park built in 1945-46 to provide housing for WWII Veterans and their families at Arizona State University's Tempe campus. A presentation of research from University Archives records conducted in the summer of 2018. The presentation was videotaped as a lecture for Professor Volker Benkert's online World War II history class.

A two-part presentation from the ASU Library and Knowledge Enterprise Research Data Management Office. Presented at the 2023 Rocky Mountain Advanced Computing Consortium (RMACC).

Session 1: Data management planning is an integral step in the research data life cycle. Large amounts of data and lengthy code accompanying supercomputing runs are no exception. Planning before analysis will benefit research and the researcher by providing a clear strategy for collecting, storing, analyzing, and sharing the data at the end of the research cycle. Supercomputing can require significant storage beyond scratch space, but researchers typically need to be informed of what tools are appropriate and available. Framed within the planning phase of the life cycle, this presentation presents ASU’s Storage Selector as a quick and easy tool to find the most appropriate storage resources provided by the university to help researchers choose a proper storage and management solution for their research data at the right time in their project. We will also explore the DMP Tool, developed by the California Digital Library, which provides a resource-rich platform for writing data management plans, including institutional-specific guidance, feedback request, and public plans that can be used as guides.

Session 2: This presentation overviews the ongoing working relationship between the ASU Library Open Science and Scholarly Communication division, Research Data Management Office, and Research Computing. We will explore these teams’ interdisciplinary relationships and interdependence as the institution increasingly supports open science practices and initiatives. We will include case studies regarding the decision-making process, data-sharing decisions, and opportunities and challenges when transferring research data from a high-performance computing environment to the ASU Research Data Repository. Finally, we will share lessons learned as we intentionally shepherd research data from active project management and storage to final publication and preservation.