Integrated Calendar

Cryptosystems were traditionally broken by using mathematical techniques
(statistical, algebraic, combinatorial, etc). However, modern
cryptosystems are increasingly resistant to such attacks, and thus the
focus had shifted to physical attacks which try to exploit various types
of side channel information which leaks during the encryption process. In
this talk I will survey some of the recent developments in this area, and
show how to use physical attacks to break strong mathematical
cryptosystems within seconds. The presentation will be self contained,
requiring no prior knowledge in cryptography.

The $10 million Archon X PRIZE for Genomics was launched at the U.S. National Academy of Sciences in 2006 to motivate development of technologies that would provide faster, cheaper and more complete whole human diploid genome sequences. Furthermore the X PRIZE Foundation recognized that the incentive prize format was an ideal method to raise pubic awareness and provide educational opportunities about genomics as well help speed the way toward a future that encompasses personalized genomic medicine. At the time of the launch, production of a single
haploid sequence took 6 months or more, cost well upwards of $100,000 and was far from either complete or accurate. Furthermore, Sanger sequencing techniques were almost exclusively prevalent and "Next-Gen" methods were just emerging or were still deep in development. Today's sequencing technology landscape is much improved. While market forces have provided much of the incentive needed to pursue the "faster, cheaper, better" goals, the requirements of the X PRIZE contest still lie beyond current achievements- although the gap is narrowing. What are these goals and why do they remain so important?

Larry Kedes is the Scientific Director of the Archon X PRIZE

We measure apparent velocities (v_app) of the Halpha and Hbeta Balmer line cores for 449 non-binary thin disk normal DA white dwarfs (WDs) using optical spectra taken for the ESO SN Ia Progenitor surveY (SPY; Napiwotzki et al. 2001). Assuming these WDs are nearby and co-moving, we correct our velocities to the Local Standard of Rest so that the remaining stellar motions are random. By averaging over the sample, we are left with the mean gravitational redshift, : we find = = 32.57 +/- 1.17 km/s. Using the mass-radius relation from evolutionary models, this translates to a mean mass of 0.647 +0.013 -0.014 Msun. We interpret this as the mean mass for all DAs. Our results are in agreement with previous gravitational redshift studies but are significantly higher than all previous spectroscopic determinations except the recent findings of Tremblay & Bergeron (2009). Since the gravitational redshift method is independent of surface gravity from atmosphere models, we investigate the mean mass of DAs with spectroscopic Teff both above and below 12000 K; fits to line profiles give a rapid increase in the mean mass with decreasing Teff. Our results are consistent with no significant change in mean mass: ^hot = 0.640 +/- 0.014 Msun and ^cool = 0.686 +0.035 -0.039 Msun.

The neural crest is a transient embryonic structure of the vertebrate giving rise to many derivatives including craniofacial structures, most of the peripheral nervous system and melanocytes. In 1879, Marshall coined the term neural crest for an embryonic territory localized in the neural fold. This domain comprises non neural and neural ectoderm. However, it was subsequently assumed that crest cells originated exclusively from the dorsal border of the neural epithelium. We have recently found that a large number of cranial crest cells may originate from the non neural epithelium portion of the neural fold. Our very recent findings raise the intriguing possibility that the ectomesenchyme forming craniofacial structures in the vertebrate may come from a distinct domain than the bona fide neural crest cells at the origin of all other neural crest derivatives. This domain was designated metablast by James Weston in 2003. These findings also argue against a fundamental role for the appearance of neural crest cells as the most important event during evolution for the emergence of vertebrates.
I will then discuss other studies addressing mechanisms of integrin-mediated adhesion during neural crest cell migration. Using selective ablation of the β1 integrin subunit in the neural crest at the onset of migration, we found that newborn mice exhibit aberrant neuromuscular junctions leading to paralysis, and a Hirschsprung syndrome phenotype. The latter is observed as a result of incomplete colonization of the colon wall by enteric neural crest cells. The mechanism responsible for the arrest of enteric crest cells at the level of the caecum is in part mediated by a high concentration of tenascin C which in absence of β1integrin provokes premature aggregation of enteric crest cells. Clearly other adhesion systems may play a critical role in the control of earlier stages of migration of cells from the neural crest and metablast.
Monday, May 10, 2010 at 10:00 am – Belfer Building,
Botnar