Scaling of Island Growth in Pb Overlayers on Cu(001)

The growth and ordering of a Pb layer deposited on Cu(001) at 150 K has been studied using atom beam scattering. At low coverage, ordered Pb islands with a large square unit cell and nearly hexagonal internal structure are formed. This is a high order commensurate phase with 30 atoms in the unit cell. From the measurement of the island diffraction peak profiles we find a power law for the mean island - size versus coverage with an exponent $n=0.54 \pm 0.03$. A scaling behavior of growth is confirmed and a simple model describing island growth is presented. Due to the high degeneracy of the monolayer phase, different islands do not diffract coherently. Therefore, when islands merge they still diffract as separate islands and coalescence effects are thus negligible. From the result for $n$ we conclude that the island density is approximately a constant in the coverage range $0.1 < \Theta < 0.5$ where the ordered islands are observed. We thus conclude that most islands nucleate at $\Theta < 0.1$ and then grow in an approximately self similar fashion as $\Theta$ increases.Comment: 23 pages, 10 Figures (available upon request). SU-PHYS-93-443-375

Determination of step--edge barriers to interlayer transport from surface morphology during the initial stages of homoepitaxial growth

We use analytic formulae obtained from a simple model of crystal growth by molecular--beam epitaxy to determine step--edge barriers to interlayer transport. The method is based on information about the surface morphology at the onset of nucleation on top of first--layer islands in the submonolayer coverage regime of homoepitaxial growth. The formulae are tested using kinetic Monte Carlo simulations of a solid--on--solid model and applied to estimate step--edge barriers from scanning--tunneling microscopy data on initial stages of Fe(001), Pt(111), and Ag(111) homoepitaxy.Comment: 4 pages, a Postscript file, uuencoded and compressed. Physical Review B, Rapid Communications, in press

First measurement of Xi(-) polarization in photoproduction

Despite decades of studies of the photoproduction of hyperons, both their production mechanisms and their spectra of excited states are still largely unknown. While the parity-violating weak decay of hyperons offers a means of measuring their polarization, which could help discern their production mechanisms and identify their excitation spectra, no such study has been possible for doubly strange baryons in photoproduction, due to low production cross sections. However, by making use of the reaction γp→K+K+Ξ−, we have measured, for the first time, the induced polarization, P, and the transferred polarization from circularly polarized real photons, characterized by Cx and Cz, to recoiling Ξ−s. The data were obtained using the CEBAF Large Acceptance Spectrometer (CLAS) at Jefferson Lab for photon energies from just over threshold (2.4 GeV) to 5.45 GeV. These first-time measurements are compared, and are shown to broadly agree, with model predictions in which cascade photoproduction proceeds through the decay of intermediate hyperon resonances that are produced via relativistic meson exchange, offering a new step forward in the understanding of the production and polarization of doubly-strange baryons

First measurement of the helicity asymmetry E in eta photoproduction on the proton

Results are presented for the first measurement of the double-polarization helicity asymmetry E for the $\eta$ photoproduction reaction $\gamma p \rightarrow \eta p$. Data were obtained using the FROzen Spin Target (FROST) with the CLAS spectrometer in Hall B at Jefferson Lab, covering a range of center-of-mass energy W from threshold to 2.15 GeV and a large range in center-of-mass polar angle. As an initial application of these data, the results have been incorporated into the J\"ulich model to examine the case for the existence of a narrow $N^*$ resonance between 1.66 and 1.70 GeV. The addition of these data to the world database results in marked changes in the predictions for the E observable using that model. Further comparison with several theoretical approaches indicates these data will significantly enhance our understanding of nucleon resonances

Assignment of a gene (NEMI) for autosomal dominant nemaline myopathy to chromosome I

Nemaline myopathy (NEM) is a neuromuscular disorder characterized by the presence, in skeletal muscle, of nemaline rods composed at least in part of α-actinin. A candidate gene and linkage approach was used to localize the gene (NEM1) for an autosomal dominant form (MIM 161800) in one large kindred with 10 living affected family members. Markers on chromosome 19 that were linked to the central core disease gene, a marker at the complement 3 locus, and a marker on chromosome 1 at the α-actinin locus exclude these three candidate genes. The family was fully informative for APOA2, which is localized to 1q21-q23. NEM1 was assigned to chromosome 1 by close linkage for APOA2, which is localized to 1q21-q23. NEM1 was assigned to chromosome 1 by close linkage to APOA2, with a lod score of 3.8 at a recombination fraction of 0. Recombinants with NGFB (1p13) and AT3 (1q23-25.1) indicate that NEM1 lies between 1p13 and 1q25.1. In total, 47 loci were investigated on chromosomes 1, 2, 4, 5, 7–11, 14, 16, 17, and 19, with no indications of significant linkage other than to markers on chromosome 1

Treatment with anti-CD137 mAbs causes intense accumulations of liver T cells without selective antitumor immunotherapeutic effects in this organ

BACKGROUND/AIMS: Cancer therapy with agonist anti-CD137 mAbs has been shown to induce immune-mediated tumor rejections in mice, and equivalent agents of this kind are currently being tested in cancer patients. Previous reports indicated that CD137 stimulation induced polyclonal infiltrates of T lymphocytes in the liver. This study characterizes the liver infiltrates and the target dependency of the phenomena and addresses the question of whether tumors nested in the liver are a more favorable target for CD137-based immunotherapy. METHODS: Liver infiltrates were studied with conventional histology and multiple color flow cytometry of total liver leukocytes. CD137(-/-) mice, mice with a single rearrangement of the TCR (OT-1 mice) and Rag(-/-) mice were used to clarify molecular requirements. Mice implanted with MC38 colon carcinomas either subcutaneously or inside the liver were used for comparative studies under treatment with agonist anti-CD137 mAbs. RESULTS: CD137 treatment caused mononuclear inflammation in the portal spaces of the liver, which gave rise to moderate increases in transaminases without signs of cholestasis. Marked increases in the numbers of CD8+ T cells were observed, including CD8+ T lymphocytes co-expressing CD11c. Infiltrates were absent in CD137(-/-) mice and mitigated in mice harboring a single transgenic TCR on their CD8 T cells. Despite the tumor-independent accumulation of T cells in the liver, immunotherapeutic effects were not more prominent against tumors located in this organ. CONCLUSIONS: Target-dependent effects of CD137 stimulation lead to liver infiltration with T cells, but lymphocyte enrichment in this organ does not privilege this site for immunotherapeutic effects against transplanted tumors