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| Wednesday, September 5, 2012
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6:00 PM - 7:30 PM
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Mapping the Neuronal Methylome at the Epigenetic Interface of Genes and Environment
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RSVP to lmavros@mit.edu if you would like to attend.
Speaker: Janine LaSalle, Ph.D., Professor, Medical Microbiology and Immunology, MIND Institute, Genome Center, UC Davis
MIT Building 46-3002 (Singleton Auditorium), 43 Vassar Street, Cambridge, MA 02139
Please visit our website for further details, including talk abstract.
The SCSB Autism and Developmental Disorders Colloquium Series is sponsored by the Simons Center for the Social Brain at MIT.
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Lee Mavros Rushton
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| Thursday, September 6, 2012
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Noon - 1:00 PM
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Aggressive periodontitis in children and adolescents: what have we learned so far?
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Speaker: Luciana M. Shaddox, DDS, MS, Ph.D., Associate Professor, Department of Periodontology, College of Dentistry University of Florida
Location: The Forsyth Institute, Seminar Rooms A & B, 245 First Street, 17th Floor, Cambridge
Abstract: Aggressive periodontitis (AgP) is a rare and rapidly progressing form of periodontitis which is often characterized by early age of onset and a family aggregation. Due to the severe nature of this disease, it is thought that AgP is associated with the presence of a highly virulent flora and/or a high level of subject susceptibility. The objectives of our studies are to define immunological mechanisms and bacterial profile associations with localized AgP (LAP) disease onset and response to treatment in African-American children/adolescents. Our studies so far have shown that AgP patients exhibit a hyper-inflammatory response when exposed to bacterial antigens and this response may be related to the severe tissue destruction observed in this disease. We have also observed that healthy siblings respond to LPS with a heightened inflammatory response when compared to healthy controls but to a lesser extent of that observed in their LAP siblings. Our more recent data show that this inflammatory profile seems to be slightly higher in females and in older subjects with permanent dentition affected. The microbial profile studies in this population so far indicate a strong association of LAP with Aggregatibacter actinomycetemcomitans (Aa), as well as Filifactor alocis. Our more recent data analysis have shown an association of Aa with some Streptococcus species, however, Filifactor alocis, Eubacterium nodatum, and Porphyromonas gingivalis are found in samples that do not contain any Aa. In addition, comparing Aa positive patients with Aa negative patients, we found a slightly different inflammatory profile but no significant differences in clinical parameters. Analysis of response patterns to conventional treatment is also enlightening regarding LAP in this population. Our studies are ongoing in this population and our results are providing us with important knowledge regarding LAP mechanisms and how to best prevent and treat it.
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Pam Quattrocchi
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Week of Sunday, September 2, 2012
