John and Tara to present at Student Seminar on Thursday (24.June) at noon in BSB

John and Tara will be presenting Student Seminar this week in BSB at noon. I have asked the speakers to provide a brief overview for their talks. Hope to see you there!

Background for John’s talk

Metwbolic syndrome is a collective term for some common, associated disorders including central obesity, dyslipidemia, insulin resistance, hypertension, and cardiovascular and renal disease connected to these conditions. It has a major impact on health care costs in the developed world. In the United States, for example, its prevalence reaches 25% of the population, and is estimated to cost approximately $30 billion annually.

By using consomic strains involving Lyon Hypertensive (LH), an established rat model for metabolic syndrome, our lab has previously identified chromosome 17 of the rat to carry significant risk factors for several metabolic syndrome traits, including obesity, dyslipidemia, left ventricular hypertrophy, and insulin resistance.

In this talk I will present my upcoming projects, both of them involving sequencing: a fine-mapping of genotypic landscape between LH and its normotensive counterpart, the Lyon Normotensive (LN) strain through SNP discovery, and a relative expression level and alternative splicing analysis through next-gen RNA-seq.

Background for Tara’s talk

Title: Contributions of genes in the complement system to the pathogenesis of atypical hemolytic uremic syndrome

Abstract: Atypical hemolytic uremic syndrome (aHUS, OMIM) is characterized by acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia. aHUS is far less common and more severe than typical HUS, which is caused by E. coli infection and manifests as diarrheal illness. Anecdotally aHUS is a rare disease with an estimate of a total of 600 cases reported in the USA. The pathogenesis of the disease is linked to dysregulation of the alternative pathway of the complement cascade. Mutations in the complement regulators factor H (CFH), membrane cofactor protein (MCP), factor B (CFB), and factor I (CFI), complement component 3 (C3), and thrombomodulin (THBD) have been implicated in aHUS. Since only 50% of aHUS patients have mutations in known disease causing genes, we hypothesize that there are other genes associated with disease. We are using several different approaches in determining which other genes are involved in the pathogenesis of aHUS.


Posted on June 22, 2010, in Student Seminar and tagged , , , , , . Bookmark the permalink. Leave a comment.

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