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We report extensive new measurements of the longitudinal relaxation time T 1 of 1 2 9 Xe nuclear spins in solid xenon. For temperatures T 0.05 T, we found T 1 on the order of hours, in goodagreement with previous measurements and with the predicted phonon-scattering limit for the spin-rotation interaction. For T > 120 K, our new data show that T 1 can be much shorter than the phonon scattering limit. For B = 0.06 T, a field often used to accumulate hyperpolarized xenon, T 1 is ∼6 s near the Xe melting point T m = 161.4 K. From T = 50 K to T m , the new data are in excellent agreement with the theoretical prediction that the relaxation is due to (i) modulation of the spin-rotation interaction by phonons, and (ii) modulation of the dipole-dipole interaction by vacancy diffusion.

We demonstrate an all-optical 133Cs scalar magnetometer, operating in nonzero magnetic field, in which the magnetic resonance is driven by an effective oscillating magnetic field provided by the AC Stark shift of an intensity-modulated laser beam. We achieve a projected shot-noise-limited sensitivity of 1.7fT/Hz and measure a technical noise floor of 40fT/Hz. These results are essentially identical to a coil-driven scalar magnetometer using the same setup. This all-optical scheme offers advantages over traditional coil-driven magnetometers for use in arrays and in magnetically sensitive fundamental physics experiments, e.g., searches for a permanent electric dipole moment of the neutron.

Targeted expression of the SV40 large T-antigen oncoprotein (T-Ag) induces cardiomyocyte proliferation in the atria and ventricles of transgenic mice. Previous studies have identified the p53 tumor suppressor, p107 (a homologue of the retinoblastoma tumor suppressor), and p193 (a novel BH3 only proapoptosis protein) as prominent TAg binding proteins in cardiomyocyte cell lines derived from these transgenic mice. To further explore the significance of these protein-protein interactions in the regulation of cardiomyocyte proliferation, a transgene comprising the human atrial natriuretic factor (ANF) promoter and sequences encoding a mutant T-Ag lacking the p53 binding domain was generated. Repeated micro-injection of this DNA gave rise to genetically mosaic animals with minimal transgene content, suggesting that widespread cardiac expression of mutant T-Ag was deleterious. This notion was supported by the observation that the transgene was selectively lost from the cardiac myocytes (but not the cardiac fibroblasts) in the mosaic animals. Crosses between the mosaic mice and animals expressing a cardiac restricted dominant negative p53 resulted in transgene transmission with ensuing overt cardiac tumorigenesis. Transfection of the mutant T-Ag in embryonic stem (ES) cell-derived cardiomyocytes resulted in wide-spread cell death with characteristics typical of apoptosis. Co-transfection with a dominant negative p53 transgene rescued mutant TAg-induced cell death in the ES-derived cardiomyocyte cultures, resulting in a marked proliferative response similar to that seen in vivo with the rescued transgenic mouse study. These results indicate that T-Ag expression in the absence of p53 functional abrogation results in cardiomyocyte death.

A 193-kDa SV40 large T antigen (T-Ag)-binding protein, designated p193, was identified and cloned. Inspection of the deduced amino acid sequence revealed the presence of a short motif similar to the Bcl-2 homology (BH) domain 3, suggesting that p193 may be a member of a family of apoptosis promoting proteins containing only BH3 motifs. In support of this, p193 expression promoted apoptosis in NIH-3T3 cells. Deletion of the BH3 motif abolished p193 apoptosis activity. p193-induced apoptosis was antagonized by co-expression of Bcl-X(L). Immune cytologic analysis indicated that p193 is localized to the cytoplasm of transfected cells. p193-induced apoptosis was also antagonized by co-expression of T-Ag, which resulted in the cytoplasmic localization of both proteins. The p193 binding site was mapped to an N-terminal region of T-Ag previously implicated in transforming activity. These results suggest that T-Ag possesses an antiapoptosis activity, independent of p53 sequestration, which is actuated by T-Ag/p193 binding in the cytoplasm.

Between 1500 and 1700, London grew from a minor national capital to the largest city in Europe. The defining period of growth was the period from 1550 to 1650, the midpoint of which coincided with the end of Elizabeth I's reign and the height of Shakespeare's theatrical career. In Material London ca. 1600, Lena Cowen Orlin and a distinguished group of social, intellectual, urban, architectural, and agrarian historians, archaeologists, cultural anthropologists, and literary critics explore the ideas, structures, and practices that distinguished London before the Great Fire, basing their investigations on the material traces in artifacts, playtexts, documents, graphic arts, and archaeological remains.In order to evoke "material London, ca. 1600", each scholar examines a different aspect of one of the great world cities at a critical moment in Western history. Several chapters give broad panoramic and authoritative views: what architectural forms charaterized the built city around 1600; how London's citizens incorporated the new commercialism of their culture into their moral views. Other essays offer sharply focused studies: how Irish mantles were adopted as elite fashions in the hybrid culture of the court; how the city authorities clashed with the church hierarchy over the building of a small bookshop; how London figured in Ben Jonson's exploration of the role of the poet. Although all the authors situate the material world of early modern London -- its objects, products, literatures, built environment, and economics practices -- in its broader political and cultural contexts, provocative debates and exchanges remain both within and between the essays as to what constitutes "materialLondon, ca. 1600".