We have demonstrated that a buried gettering layer can be formed with a single MeV ion implantation without damaging the top device region. The strong gettering efficiency of carbon implant and its linear dependence on dose are confirmed. A surprising feature of the carbon implanted layers is that no extended defects are formed after annealing for implant doses up to 2×1016 cm−2 at 3 MeV, compared to a layer of small precipitates and dislocations in the case of oxygen implantation. It is suggested that the carbon-related gettering centers are point defects or their clusters.

Mobile code is now a nearly inescapable component of modern computing, thanks to client-side code that runs within web browsers. The usual tension between security and functionality is particularly acute in a mobile-code setting, and current platforms disappoint on both dimensions. We introduce a new architecture for secure mobile code, with which developers can use, publish, and share mobile code securely across trust domains. This architecture enables new kinds of distributed applications, and makes it easier to reuse and evolve code from untrusted providers. The architecture gives mobile code considerable expressive power: it can securely access distributed, persistent, shared information from multiple trust domains, unlike web applications bound by the same-origin policy. The core of our approach is analyzing how flows of information within mobile code affect confidentiality and integrity. Because mobile code is untrusted, this analysis requires novel constraints on information flow and authority. We show that these constraints offer principled enforcement of strong security while avoiding the limitations of current mobile-code security mechanisms. We evaluate our approach by demonstrating a variety of mobilecode applications, showing that new functionality can be offered along with strong security.

In order to identify reliable markers of corneal epithelial stem cells, we employed an inducible transgenic "pulse-chase" murine model (K5Tta × TRE-H2BGFP) to localize, purify, and characterize slow cycling cells in the cornea. The retention of GFP labeling in slowly dividing cells allowed for localization of these cells to the corneal limbus and their subsequent purification by FACS. Transcriptome analysis from slow cycling cells identified differentially expressed genes when comparing to GFP -faster-dividing cells. RNA-Seq data from corneal epithelium were compared to epidermal hair follicle stem cell RNA-Seq to identify genes representing common putative stem cell markers or determinants, which included Sox9, Fzd7, Actn1, Anxa3 and Krt17. Overlapping retention of GFP and immunohistochemical expression of Krt15, ΔNp63, Sox9, Actn1, Fzd7 and Krt17 were observed in our transgenic model. Our analysis presents an array of novel genes as putative corneal stem cell markers.Loss of the regenerative capacity of the ocular surface through the absence of corneal epithelial stem cells is a potentially blinding condition. Lack of definitive molecular markers to reproducibility locate, purify and expand corneal epithelial stem cells has hampered the ability to understand their biology and to use these cells for therapeutic transplantation.Stem cells from the cornea reside between the corneal periphery and the conjunctiva, known as the limbus. Limbal stem cells (LSCs) are clonogenic, regenerating new tissue in vivo and in vitro 1 exhibiting slow cycling phenotypic characteristics 2 . Classically, these cells have been characterized by the ability to retain tritiated thymidine or bromodeoxyurdine (BrdU) for long periods, yet have high proliferative potential 3-7 . More recently, a transgenic system that can genetically label slow cycling cells with GFP has been used to identify label retaining cells (LRCs) in skin 8,9 , sweat glands 10 , salivary glands 11 and the cornea 12 . In this model, one parental strain harbors the H2B-GFP transgene under the control of a tetracycline (doxycycline; dox) regulatory element (TRE), creating a tet-off system. The second strain expresses a transcription factor regulated by tetracycline (tTA) under the control of a cell-type-specific Keratin 5 (K5) promoter. Thus, K5 expressing cells will have nuclear GFP labeling in the "pulse" period, which is then turned off with dox administration, beginning the "chase" period.This approach allowed for the purification of cells and their subsequent molecular characterization of LRCs using next generation sequencing (NGS), yielding genes marking (and in some cases determining) "stemness". Thus, the molecular markers are identified without a pre-conceived notion as to which genes may be related to stemness. Comparison of these data from corneal epithelium with prior similar characterization of hair follicle stem cells (HFSCs) 13 were performed to identify common stem cell markers in these developmentally related tissues.

Systemic lupus erythematosus (SLE) is a complex, multifactorial autoimmune disease characterized by the dysregulation of T and B cells that leads to hyperactivity of B cells and production of autoantibodies, and involves both environmental and genetic factors. Interleukin-10 (IL-10) is a candidate susceptibility gene in SLE. In particular, three IL-10 promoter singlenucleotide polymorphisms (SNPs; À1082A/G, À819T/C and À592A/C) are strongly associated with the pathogenesis of SLE. We found that the homozygous GCC haplotype linked to greater SLE severity confers higher IL-10 gene transcriptional activity than the ATA haplotype in macrophages that encounter apoptotic cells, because of the differential DNA binding to the À592 SNP by a nuclear protein uniquely induced by apoptotic cells. We identified this protein as poly(ADP-ribose) polymerase-1, confirmed its physiological role and characterized its molecular properties in modulating IL-10 production during phagocytosis of apoptotic cells. This study unveils a novel direct link between DNA damage repair/apoptosis pathways and IL-10-mediated immune regulation.

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