GPUHElib and DistributedHElib: Distributed Computing Variants of HElib, a Homomorphic Encryption Library

Homomorphic Encryption, an encryption scheme only developed in the last five years, allows for arbitrary operations to be performed on encrypted data. Using this scheme, a user can encrypt data, and send it to an online service. The online service can then perform an operation on the data and generate an encrypted result. This encrypted result is then sent back to the user, who decrypts it. This decryption produces the same data as if the operation performed by the online service had been performed on the unencrypted data. This is revolutionary because it allows for users to rely on online services, even untrusted online services, to perform operations on their data, without the online service gaining any knowledge from their data. A prominent implementation of homomorphic encryption is HElib. While one is able to perform homomorphic encryption with this library, there are problems with it. It, like all other homomorphic encryption libraries, is slow relative to other encryption systems. Thus there is a need to speed it up. Because homomorphic encryption will be deployed on online services, many of them distributed systems, it is natural to modify HElib to utilize some of the tools that are available on them in an attempt to speed up run times. Thus two modified libraries were designed: GPUHElib, which utilizes a GPU, and DistributedHElib, which utilizes a distributed computing design. These designs were then tested against the original library to see if they provided any speed up

Research Data Services in Academic Libraries: Data Intensive Roles for the Future?

Objectives: The primary objectives of this study are to gauge the various levels of Research Data Service academic libraries provide based on demographic factors, gauging RDS growth since 2011, and what obstacles may prevent expansion or growth of services. Methods: Survey of academic institutions through stratified random sample of ACRL library directors across the U.S. and Canada. Frequencies and chi-square analysis were applied, with some responses grouped into broader categories for analysis. Results: Minimal to no change for what services were offered between survey years, and interviews with library directors were conducted to help explain this lack of change. Conclusion: Further analysis is forthcoming for a librarians study to help explain possible discrepancies in organizational objectives and librarian sentiments of RDS

FAK regulates IL-33 expression by controlling chromatin accessibility at c-Jun motifs

Focal adhesion kinase (FAK) localizes to focal adhesions and is overexpressed in many cancers. FAK can also translocate to the nucleus, where it binds to, and regulates, several transcription factors, including MBD2, p53 and IL-33, to control gene expression by unknown mechanisms. We have used ATAC-seq to reveal that FAK controls chromatin accessibility at a subset of regulated genes. Integration of ATAC-seq and RNA-seq data showed that FAK-dependent chromatin accessibility is linked to differential gene expression, including of the FAK-regulated cytokine and transcriptional regulator interleukin-33 (Il33), which controls anti-tumor immunity. Analysis of the accessibility peaks on the Il33 gene promoter/enhancer regions revealed sequences for several transcription factors, including ETS and AP-1 motifs, and we show that c-Jun, a component of AP-1, regulates Il33 gene expression by binding to its enhancer in a FAK kinase-dependent manner. This work provides the first demonstration that FAK controls transcription via chromatin accessibility, identifying a novel mechanism by which nuclear FAK regulates biologically important gene expression

Nuclear FAK and Runx1 cooperate to regulate IGFBP3, cell cycle progression and tumor growth

Abstract Nuclear focal adhesion kinase (FAK) is a potentially important regulator of gene expression in cancer, impacting both cellular function and the composition of the surrounding tumor microenvironment. Here, we report in a murine model of skin squamous cell carcinoma (SCC) that nuclear FAK regulates Runx1-dependent transcription of insulin-like growth factor binding protein 3 (IGFBP3), and that this regulates SCC cell-cycle progression and tumor growth in vivo. Furthermore, we identified a novel molecular complex between FAK and Runx1 in the nucleus of SCC cells and showed that FAK interacted with a number of Runx1-regulatory proteins, including Sin3a and other epigenetic modifiers known to alter Runx1 transcriptional function through posttranslational modification. These findings provide important new insights into the role of FAK as a scaffolding protein in molecular complexes that regulate gene transcription. Cancer Res; 77(19); 5301–12. ©2017 AACR.</jats:p

Modeling the Compton Camera Response for Extended Voxel Sources

The analysis and interpretation of coincidence events in a Compton camera requires the comparison of the expected rates of observed events from sources with various emission rates, energy spectra and spatial distributions. Radioactive source distributions are often represented by the activity distributed among numerous voxels; each voxel having uniform internal activity and spectra within a cube. In this paper a mathematical model is constructed that predicts the expected rate of coincident Compton events from the rate of emissions from a single voxel source. This detailed model incorporates (1) the finite voxel size, (2) the blurring of the “Compton cone” by the limitations of energy resolution in the detectors and (3) the uncertainty in the Compton cone-axis due to the limited spatial resolution and ‘lever-arm’ separation between the coincident interactions. The resultant rates can be used to generate the system response matrix for source reconstruction and, therefore, are directly applicable in list-mode MLEM source reconstruction algorithms

The Lantern Vol. 67, No. 2, Spring 2000

• Dearest Yarn-Spinner • My Poem, This Tongue In Your Eye • 15th & Rodman • Vision • Linguistics • Casting Cartesian Shadows • On the Defensive • Sea Sick but Still Docked • Urban Dreams • Wolf of the Steppes • Josephine • Happy Birthday to Me • I Have Never Been to Africa • Pa-pou • Onion[s] • Intimacy • Three Trick Pony • Blazer • In My Tea • Emmaless • Dreamcatcher • Repetition • With the Turn of the Reel • Fault Lines • The Shrink Is In • The dancE • Exam • Another Post-Apocalyptic Christmas • The Circumstances of My Prolonged Depressionhttps://digitalcommons.ursinus.edu/lantern/1156/thumbnail.jp

Toll-like receptor orchestrates a tumor suppressor response in non-small cell lung cancer

Targeting early-stage lung cancer is vital to improve survival. However, the mechanisms and components of the early tumor suppressor response in lung cancer are not well understood. In this report, we study the role of Toll-like receptor 2 (TLR2), a regulator of oncogene-induced senescence, which is a key tumor suppressor response in premalignancy. Using human lung cancer samples and genetically engineered mouse models, we show that TLR2 is active early in lung tumorigenesis, where it correlates with improved survival and clinical regression. Mechanistically, TLR2 impairs early lung cancer progression via activation of cell intrinsic cell cycle arrest pathways and the proinflammatory senescence-associated secretory phenotype (SASP). The SASP regulates non-cell autonomous anti-tumor responses, such as immune surveillance of premalignant cells, and we observe impaired myeloid cell recruitment to lung tumors after Tlr2 loss. Last, we show that administration of a TLR2 agonist reduces lung tumor growth, highlighting TLR2 as a possible therapeutic target.F.R.M. is funded by a Wellcome Trust clinical research fellowship through the Edinburgh Clinical Academic Track (ECAT) program (203913/Z/16/Z), a Wellcome Trust-ISSF3 award (IS3-R1.07 20/21), and a Wellcome Trust iTPA award (209710/Z/17/Z). J.C.A. core lab funding was received from Cancer Research UK (C47559/A16243, Training and Career Development Board – Career Development Fellowship), the University of Edinburgh (Chancellor’s Fellowship), and the Ministry of Science and Innovation of the Government of Spain (Proyecto PID2020-117860GB-100 financiado por MCIN/AEI/10.13039/501100011033). S.W. is supported by a Cancer Research UK senior fellowship (A29576). J.C. is supported by a Wellcome Trust clinical lectureship through the ECAT program (203913/Z/16/Z). M.M. is supported by a CRUK Edinburgh Centre Award (C157/A25140). S.V. and J.F.P. are funded by National Institute on Aging (NIA) grants (R01AG 68048-1 and UG3CA 268103-1)