The Gut Microbiome’s Influence on Autism Spectrum Disorder

In recent years, research on the gut microbiome has revealed that microbiota in the gut have profound effects on physical health, mental health, and even neurological disorders like Autism Spectrum Disorder (ASD). The colonization of an infant's microbiome begins in the womb through the placenta and amniotic fluid and continues with the consumption of breast milk. Studies have found that this period is critical for neurodevelopment, and factors such as diet, infection, and stress can lead to irregular neurological development. For patients with ASD, regulation of the gut microbiome has also been found to have great importance for reducing neuropsychiatric symptoms. With greater links being found between children with ASD and lowered gastrointestinal function, the gut microbiome may be crucial to improving the landscape of ASD diagnosis and developing an FDA-approved treatment that is designed to specifically target autism symptoms. This thesis aims to identify the viability of using cytokine levels as a new way to aid in the diagnosis of ASD in addition to analyzing how microbiota therapy treatment effectiveness is impacted by antibiotic use in early life. Through exploratory secondary analysis, this work shows that thought-provoking trends exist for certain cytokine levels among individuals with ASD. Additionally, the ability of microbiota transfer therapy to reduce ASD symptoms was not affected by the amount of antibiotics used in the first 48 months of life.Plan II Honors Progra

Secrets of Success: Identifying Success Factors in Institutional Repositories

4th International Conference on Open RepositoriesThis presentation was part of the session : Conference PresentationsDate: 2009-05-19 08:30 AM – 09:30 AMThere is little agreement on which factors lead to successful institutional repositories. Researchers primarily cite content recruitment and services as key factors; however, there has also been discussion of measuring IR success in terms of how well the IR furthers the overall goals of the library. This paper examines the topic of IRs and success. Our findings are based on a comparative case study of five IRs in colleges and universities. We argue that success should be measured by both internal (e.g., content or services) as well as external factors - how well the IR fulfills or brings the library closer to achieving its long-term goals in terms of service to the academic community.Institute of Museum and Library Service

Noggin depletion in adipocytes promotes obesity in mice.

ObjectiveObesity has increased to pandemic levels and enhanced understanding of adipose regulation is required for new treatment strategies. Although bone morphogenetic proteins (BMPs) influence adipogenesis, the effect of BMP antagonists such as Noggin is largely unknown. The aim of the study was to define the role of Noggin, an extracellular BMP inhibitor, in adipogenesis.MethodsWe generated adipose-derived progenitor cells and a mouse model with adipocyte-specific Noggin deletion using the AdiponectinCre transgenic mouse, and determined the adipose phenotype of Noggin-deficiency.ResultsOur studies showed that Noggin is expressed in progenitor cells but declines in adipocytes, possibly allowing for lipid accumulation. Correspondingly, adipocyte-specific Noggin deletion in vivo promoted age-related obesity in both genders with no change in food intake. Although the loss of Noggin caused white adipose tissue hypertrophy, and whitening and impaired function in brown adipose tissue in both genders, there were clear gender differences with the females being most affected. The females had suppressed expression of brown adipose markers and thermogenic genes including peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1alpha) and uncoupling protein 1 (UCP1) as well as genes associated with adipogenesis and lipid metabolism. The males, on the other hand, had early changes in a few BAT markers and thermogenic genes, but the main changes were in the genes associated with adipogenesis and lipid metabolism. Further characterization revealed that both genders had reductions in VO2, VCO2, and RER, whereas females also had reduced heat production. Noggin was also reduced in diet-induced obesity in inbred mice consistent with the obesity phenotype of the Noggin-deficient mice.ConclusionsBMP signaling regulates female and male adipogenesis through different metabolic pathways. Modulation of adipose tissue metabolism by select BMP antagonists may be a strategy for long-term regulation of age-related weight gain and obesity

Interdépendance du potentiel d'exploitation et la structure d'habitat dans la région de l'Atakora

Le département de l’Atakora est une région très contrastée et jusqu’à présent très peu explorée. Son élément le plus saillant est la Chaîne de l’Atakora, une des rares élévations montagneuses de cette partie de l’Afrique occidentale. Le haut-plateau de l’Atakora est caractérisé par une densité de la population relativement basse, comparée au reste de la région, et une végétation variée, qui est jusqu’à présent extrêmement mal connu. Il contraste fortement avec son piémont à l’ouest de la chaîne qui est très densément peuplé et exploité de manière intensive. Notre recherche a été consacrée à la question de savoir si ce sont des facteurs dépendant du géopotentiel ou plutôt des données socio-économiques qui sont responsables pour la disparité actuelle de ce paysage. Partant de l’hypothèse que non seulement les conditions socio-économiques mais aussi les conditions naturelles sont beaucoup plus favorables dans le piémont que sur le plateau, nous avons - par une approche interdisciplinaire - effectué une analyse et une évaluation de ces facteurs. Des méthodes de la télédétection, de la pédologie, de la botanique et de la géographie agraire ont été employées

NASAs Land, Atmosphere near Real-Time Capability for EOS (LANCE): Delivering Data and Imagery to Meet the Needs of near Real-Time Applications

No abstract availabl

Altered brain energetics induces mitochondrial fission arrest in Alzheimer's Disease.

Altered brain metabolism is associated with progression of Alzheimer's Disease (AD). Mitochondria respond to bioenergetic changes by continuous fission and fusion. To account for three dimensional architecture of the brain tissue and organelles, we applied 3-dimensional electron microscopy (3D EM) reconstruction to visualize mitochondrial structure in the brain tissue from patients and mouse models of AD. We identified a previously unknown mitochondrial fission arrest phenotype that results in elongated interconnected organelles, "mitochondria-on-a-string" (MOAS). Our data suggest that MOAS formation may occur at the final stages of fission process and was not associated with altered translocation of activated dynamin related protein 1 (Drp1) to mitochondria but with reduced GTPase activity. Since MOAS formation was also observed in the brain tissue of wild-type mice in response to hypoxia or during chronological aging, fission arrest may represent fundamental compensatory adaptation to bioenergetic stress providing protection against mitophagy that may preserve residual mitochondrial function. The discovery of novel mitochondrial phenotype that occurs in the brain tissue in response to energetic stress accurately detected only using 3D EM reconstruction argues for a major role of mitochondrial dynamics in regulating neuronal survival

The Proteasome Activators Blm10/PA200 Enhance the Proteasomal Degradation of N-Terminal Huntingtin.

The Blm10/PA200 family of proteasome activators modulates the peptidase activity of the core particle (20S CP). They participate in opening the 20S CP gate, thus facilitating the degradation of unstructured proteins such as tau and Dnm1 in a ubiquitin- and ATP-independent manner. Furthermore, PA200 also participates in the degradation of acetylated histones. In our study, we use a combination of yeast and human cell systems to investigate the role of Blm10/PA200 in the degradation of N-terminal Huntingtin fragments (N-Htt). We demonstrate that the human PA200 binds to N-Htt. The loss of Blm10 in yeast or PA200 in human cells results in increased mutant N-Htt aggregate formation and elevated cellular toxicity. Furthermore, Blm10 in vitro accelerates the proteasomal degradation of soluble N-Htt. Collectively, our data suggest N-Htt as a new substrate for Blm10/PA200-proteasomes and point to new approaches in Huntington\u27s disease (HD) research

Use of a multi-virus array for the study of human viral and retroviral pathogens: gene expression studies and ChIP-chip analysis

BACKGROUND: Since the discovery of human immunodeficiency virus (HIV-1) twenty years ago, AIDS has become one of the most studied diseases. A number of viruses have subsequently been identified to contribute to the pathogenesis of HIV and its opportunistic infections and cancers. Therefore, a multi-virus array containing eight human viruses implicated in AIDS pathogenesis was developed and its efficacy in various applications was characterized. RESULTS: The amplified open reading frames (ORFs) of human immunodeficiency virus type 1, human T cell leukemia virus types 1 and 2, hepatitis C virus, Epstein-Barr virus, human herpesvirus 6A and 6B, and Kaposi's sarcoma-associated herpesvirus were spotted on glass slides and hybridized to DNA and RNA samples. Using a random priming method for labeling genomic DNA or cDNA probes, we show specific detection of genomic viral DNA from cells infected with the human herpesviruses, and effectively demonstrate the inhibitory effects of a cellular cyclin dependent kinase inhibitor on viral gene expression in HIV-1 and KSHV latently infected cells. In addition, we coupled chromatin immunoprecipitation with the virus chip (ChIP-chip) to study cellular protein and DNA binding. CONCLUSIONS: An amplicon based virus chip representing eight human viruses was successfully used to identify each virus with little cross hybridization. Furthermore, the identity of both viruses was correctly determined in co-infected cells. The utility of the virus chip was demonstrated by a variety of expression studies. Additionally, this is the first demonstrated use of ChIP-chip analysis to show specific binding of proteins to viral DNA, which, importantly, did not require further amplification for detection