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| Tuesday, November 15, 2011
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12:30 PM - 1:30 PM
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4:00 PM - 5:00 PM
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All-natural solutions to heart regeneration by zebrafish
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| Description: |
Cardiovascular Seminar Series
Kenneth D. Poss, Associate Professor, Cell Biology, Duke University Medical Center
Folkman (Enders) Auditorium, John F. Enders Research Bldg., Children's Hospital
Host: Department of Cardiology | Children’s Hospital Boston
This conference is supported by the Faye and Karen Sinclair Research Fund for Congenital Heart Disease
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Michelle Merry
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4:00 PM - 5:00 PM
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| Thursday, November 17, 2011
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Noon - 1:00 PM
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Sex Steriods and the Skeleton
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Speaker: Sundeep Khosla, MD, Mayo Clinic
Location: The Forsyth Institute, Seminar Room A, 245 First St., Cambridge
Summary: Estrogen deficiency is the major cause of early postmenopausal bone loss in women and also contributes to the late phase of bone loss in aging women. Considerable work over the past decade has shown, however, that estrogen is also the dominant regulator of bone metabolism in men. These studies, in turn, have provided important information regarding the dose-relationships between estrogen levels and bone turnover/bone loss that are also relevant to women. Initial studies in a male with homozygous deletions in estrogen receptor (ER)á and in additional men deficient in the enzyme responsible for the final step in estrogen synthesis, aromatase, demonstrated that even in men, estrogen was required for epiphyseal closure and the acquisition of bone mass during growth. Using a direct interventional design, we subsequently showed that estrogen was the major sex steroid regulating bone resorption in men, with both estrogen and testosterone contributing to the maintenance of bone formation. Studies using raloxifene in men found that only men with low endogenous estradiol levels had a beneficial skeletal response to a selective estrogen receptor modulator (SERM); these findings are entirely consistent with data in women showing that raloxifene has beneficial skeletal effects in estrogen-deficient, postmenopausal women, but causes bone loss in estrogen-sufficient, premenopausal women.
While women develop relatively rapid and severe estrogen deficiency following the menopause, men have a more gradual onset of sex steroid deficiency with aging. Although total estradiol or testosterone levels decrease modestly over life in men, aging men have much more dramatic decreases in non-SHBG-bound (“bioavailable”) estrogen and testosterone levels. These declining estrogen levels, in particular, have been shown to correlate with rates of bone loss and fracture risk in men. More recent studies using central and peripheral quantitative computed tomography, which can separately assess age-related changes in trabecular versus cortical bone, have demonstrated that while decreases in cortical bone (at the radius, tibia, and femur) begin with the onset of sex steroid deficiency in women and men, trabecular bone loss (at the spine, femur, and radius/tibia) begins in young adult life in both sexes, with an acceleration of bone loss around the menopausal transition in women. These data, which are consistent with recent mouse studies, indicate that while cortical bone loss seems to be largely dependent on changes in estrogen levels, a substantial proportion of trabecular bone loss in independent of changes estrogen (or testosterone) levels. In summary, estrogen has emerged as the dominant regulator of bone metabolism in women and in men, although there clearly are estrogen-independent mechanisms leading to bone loss over life in both sexes, particularly in trabecular bone.
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Pam Quattrocchi
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7:00 PM - 9:00 PM
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Genome Engineering and the Construction of New Genetic Codes
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| Description: |
IEEE Computer and Engineering in Medicine and Biology Societies, MIT biological engineering and biomedical engineering student group (BE-BMES), and GBC/ACM
Speaker: Peter Carr, MIT Lincoln Laboratory
Location: Broad Institute Auditorium (MIT building NE-30)
Our capacity to engineer genetic material is moving beyond the level of single genes to the scale of genomes. Still, our ability to paint effectively on a canvas as large as a genome is minute, dwarfed by our growing ability to synthesize DNA, which is in turn dwarfed by our ability to sequence. Current attempts to engineer at this scale are first and foremost an exploration of to what extent living systems can be re-designed and modified.
The rE. coli project is a collaborative effort to re-engineer the genetic code of E. coli strain MG1655. We are nearing completion of the first organism engineered throughout its genome to remove every instance of one of its 64 codons. The result will be a hole in the genetic code, a plug-and-play opportunity for programming in new chemical functions not seen in nature. It will also be the first step towards generating organisms with an orthogonal genetic code, unable to correctly translate genomes from outside their own genome. This feature is predicted to block the ability of viruses/bacteriophage to infect. In a more distant envisioning, crops with such a feature would be unable to cross with wild strains. Such engineered organisms will in a sense be protected behind a genetic firewall.
Peter Andrew Carr leads the research program in synthetic biology at MIT Lincoln Laboratory. A central goal of his work is to expand the scope of what can be achieved by genetic engineering, from single genes to the engineering of complete genomes. Topics of focus include: 1) the rE. coli project, which aims to rewrite the genetic code by genome-scale reformatting of the E. coli chromosome. 2) microfluidic gene and protein synthesis for high throughput production (and prototyping) of genetic systems; and 3) programming genomes for improved control and biosafety.
Dr. Carr holds a Bachelors degree in Biochemistry from Harvard College and a Ph.D. in Biochemistry and Molecular Biophysics from Columbia University. Following his post-doctoral research in the lab of Peter S. Kim (Whitehead Institute for Biomedical Research), he started and led the GeneFab research team under Prof. Joe Jacobson at the MIT Media Lab and the Center for Bits and Atoms.
This joint meeting of the Boston Chapters of the IEEE Computer and Engineering in Medicine and Biology Societies, the MIT biological engineering and biomedical engineering student group (BE-BMES) and GBC/ACM will be held in the Broad Institute Auditorium (MIT building NE-30). The Broad Institute is on Main St between Vassar and Ames streets. You can see it on a map at this location. The auditorium is on the ground floor near the entrance.
Up-to-date information about this and other talks is available online at http://ewh.ieee.org/r1/boston/computer/. You can sign up to receive updated status information about this talk and informational emails about future talks at http://mailman.mit.edu/mailman/listinfo/ieee-cs, our self-administered mailing list.
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| Contact: |
Peter Mager
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| Friday, November 18, 2011
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8:30 AM - 9:30 AM
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Week of Sunday, November 13, 2011
