Integrating Data Science Ethics into an Undergraduate Major

We present a programmatic approach to incorporating ethics into an undergraduate major in statistical and data sciences. We discuss departmental-level initiatives designed to meet the National Academy of Sciences recommendation for weaving ethics into the curriculum from top-to-bottom as our majors progress from our introductory courses to our senior capstone course, as well as from side-to-side through co-curricular programming. We also provide six examples of data science ethics modules used in five different courses at our liberal arts college, each focusing on a different ethical consideration. The modules are designed to be portable such that they can be flexibly incorporated into existing courses at different levels of instruction with minimal disruption to syllabi. We conclude with next steps and preliminary assessments

Macrophage-specific expression of IL-37 in hyperlipidemic mice attenuates atherosclerosis

Copyright © 2017 by The American Association of Immunologists, Inc. inflammation, as well as the formation of lipid-laden macrophage foam cells within the vessel wall. IL-37 is recognized as an important anti-inflammatory cytokine expressed especially by immune cells. This study was undertaken to elucidate the role of macrophage-expressed IL-37 in reducing the production and effects of proinflammatory cytokines, preventing foam cell formation, and reducing the development of atherosclerosis. Expression of human IL-37 was achieved with a macrophage-specific overexpression system, using the CD68 promoter in mouse primary bone marrow-derived macrophages via retroviral transduction. Macrophage IL-37 expression in vitro resulted in decreased mRNA (e.g., IL-1B, IL-6, and IL-12) and secreted protein production (e.g., IL-6, M-CSF, and ICAM-1) of key inflammatory mediators. IL-37 expression also inhibited macrophage proliferation, apoptosis, and transmigration, as well as reduced lipid uptake, compared with controls in vitro. The in vivo effects of macrophage-expressed IL-37 were investigated through bone marrow transplantation of transduced hematopoietic stem cells into irradiated atherosclerosis-prone Ldlr2/2 mice. After 10 wk on a high-fat/high-cholesterol diet, mice with IL-37-expressing macrophages showed reduced disease pathogenesis, which was demonstrated by significantly less arterial plaque development and systemic inflammation compared with control mice. The athero-protective effect of macrophage-expressed IL-37 has implications for development of future therapies to treat atherosclerosis, as well as other chronic inflammatory diseases

MicroRNA 302a is a novel modulator of cholesterol homeostasis and atherosclerosis

© 2014 American Heart Association, Inc. OBJECTIVE - : Macrophage foam cell formation is a key feature of atherosclerosis. Recent studies have shown that specific microRNAs (miRs) are regulated in modified low-density lipoprotein-treated macrophages, which can affect the cellular cholesterol homeostasis. Undertaking a genome-wide screen of miRs regulated in primary macrophages by modified low-density lipoprotein, miR-302a emerged as a potential candidate that may play a key role in macrophage cholesterol homeostasis. APPROACH AND RESULTS - : The objective of this study was to assess the involvement of miR-302a in macrophage lipid homeostasis and if it can influence circulating lipid levels and atherosclerotic development when it is inhibited in a murine atherosclerosis model. We found that transfection of primary macrophages with either miR-302a or anti-miR-302a regulated the expression of ATP-binding cassette (ABC) transporter ABCA1 mRNA and protein. Luciferase reporter assays showed that miR-302a repressed the 3′ untranslated regions (UTR) activity of mouse Abca1 by 48% and human ABCA1 by 45%. In addition, transfection of murine macrophages with miR-302a attenuated cholesterol efflux to apolipoprotein A-1 (apoA-1) by 38%. Long-term in vivo administration of anti-miR-302a to mice with low-density lipoprotein receptor deficiency (Ldlr) fed an atherogenic diet led to an increase in ABCA1 in the liver and aorta as well as an increase in circulating plasma high-density lipoprotein levels by 35% compared with that of control mice. The anti-miR-302a-treated mice also displayed reduced atherosclerotic plaque size by ≈25% and a more stable plaque morphology with reduced signs of inflammation. CONCLUSIONS - : These studies identify miR-302a as a novel modulator of cholesterol efflux and a potential therapeutic target for suppressing atherosclerosis

Sphingosine 1-phosphate modulates antigen capture by murine langerhans cells via the S1P2 receptor subtype

Dendritic cells (DCs) play a pivotal role in the development of cutaneous contact hypersensitivity (CHS) and atopic dermatitis as they capture and process antigen and present it to T lymphocytes in the lymphoid organs. Recently, it has been indicated that a topical application of the sphingolipid sphingosine 1-phosphate (S1P) prevents the inflammatory response in CHS, but the molecular mechanism is not fully elucidated. Here we indicate that treatment of mice with S1P is connected with an impaired antigen uptake by Langerhans cells (LCs), the initial step of CHS. Most of the known actions of S1P are mediated by a family of five specific G protein-coupled receptors. Our results indicate that S1P inhibits macropinocytosis of the murine LC line XS52 via S1P2 receptor stimulation followed by a reduced phosphatidylinositol 3-kinase (PI3K) activity. As down-regulation of S1P2 not only diminished S1P-mediated action but also enhanced the basal activity of LCs on antigen capture, an autocrine action of S1P has been assumed. Actually, S1P is continuously produced by LCs and secreted via the ATP binding cassette transporter ABCC1 to the extracellular environment. Consequently, inhibition of ABCC1, which decreased extracellular S1P levels, markedly increased the antigen uptake by LCs. Moreover, stimulation of sphingosine kinase activity, the crucial enzyme for S1P formation, is connected not only with enhanced S1P levels but also with diminished antigen capture. These results indicate that S1P is essential in LC homeostasis and influences skin immunity. This is of importance as previous reports suggested an alteration of S1P levels in atopic skin lesions

Cluster of differentiation 43 deficiency in leukocytes leads to reduced atherosclerosis - Brief report

© 2014 American Heart Association, Inc.OBJECTIVE - : The aim of this study was to investigate the role of cluster of differentiation 43 (CD43), an integral membrane glycoprotein with both proadhesive and antiadhesive activities, in atherosclerosis. APPROACH AND RESULTS - : Low-density lipoprotein receptor-deficient mice were lethally irradiated and reconstituted with either bone marrow from CD43 mice or from wild-type controls. We found that mice lacking the CD43 on their leukocytes had significantly less severe atherosclerosis and that, contrary to our expectation, macrophage infiltration into the vessel wall was not affected by the lack of CD43 in the leukocytes. However, we found that CD43 mediates cholesterol homeostasis in macrophages by facilitating cholesterol efflux. This resulted in a significant reduction in storage of cholesterol in the aorta of mice lacking CD43 in the leukocytes. CONCLUSIONS - : CD43 may be an important mediator of macrophage lipid homeostasis, thereby affecting macrophage foam cell formation and ultimately atherosclerotic plaque development

Curriculum Guidelines for Undergraduate Programs in Data Science

The Park City Math Institute (PCMI) 2016 Summer Undergraduate Faculty Program met for the purpose of composing guidelines for undergraduate programs in Data Science. The group consisted of 25 undergraduate faculty from a variety of institutions in the U.S., primarily from the disciplines of mathematics, statistics and computer science. These guidelines are meant to provide some structure for institutions planning for or revising a major in Data Science

Weldability of Duplex Stainless Steels - Thermal Cycle and Nitrogen Effects : Duplex stainless steel weld microstructures were investigated as a function of weld thermal cycles and shielding gas nitrogen content

Much development work has been performed worldwide on the welding of duplex stainless steels (DSSs), where losses in base metal nitrogen during welding have been compensated by filler metal and nitrogen additions to the shielding gas. However, some heat-affected zone (HAZ) microstructural changes have not always responded consistently to nitrogen mixtures added to the shielding gas. In this work, DSS weld microstructures were investigated as a function of weld thermal cycles and shielding gas nitrogen content. Physical simulations, actual gas tungsten arc welding (GTAW) in controlled atmospheres, and entrapped nitrogen measurements were used to relate to the weld austenite-to-ferrite (A/F) phase ratios. Results showed the thermal cycles had a stronger effect on the weld A/F ratio than shielding gas nitrogen content. Physical simulations and actual GTAW trials also showed the A/F ratio changes in the opposite way in the fusion zone than in the HAZ. Reheating was also found to have an important effect on the microstructure. The above findings should allow fabricators to better design the welding process with DSS. Better control of nitrogen-containing shielding gas mixtures, along with heat input limitations, should result in more consistent weld properties and wider use of DSS by industry

Cluster of differentiation 43 deficiency in leukocytes leads to reduced atherosclerosis - Brief report

© 2014 American Heart Association, Inc. OBJECTIVE - : The aim of this study was to investigate the role of cluster of differentiation 43 (CD43), an integral membrane glycoprotein with both proadhesive and antiadhesive activities, in atherosclerosis. APPROACH AND RESULTS - : Low-density lipoprotein receptor-deficient mice were lethally irradiated and reconstituted with either bone marrow from CD43 mice or from wild-type controls. We found that mice lacking the CD43 on their leukocytes had significantly less severe atherosclerosis and that, contrary to our expectation, macrophage infiltration into the vessel wall was not affected by the lack of CD43 in the leukocytes. However, we found that CD43 mediates cholesterol homeostasis in macrophages by facilitating cholesterol efflux. This resulted in a significant reduction in storage of cholesterol in the aorta of mice lacking CD43 in the leukocytes. CONCLUSIONS - : CD43 may be an important mediator of macrophage lipid homeostasis, thereby affecting macrophage foam cell formation and ultimately atherosclerotic plaque development

Enterprise 2.0: Research challenges and opportunities

© Springer International Publishing Switzerland 2015. Blending Web 2.0 technologies with enterprise information systems is setting up the stage for a new generation of information systems that will help enterprises open up new communication channels with their stakeholders. Contrary to traditional enterprises with top-down command flow and bottom-up feedback flow, the same flows in Enterprise 2.0 cross all levels and in all directions bringing people together in the development of creative and innovative ideas. The power of Web 2.0 technologies stems from their ability to capture real-world phenomena such as collaboration, competition, and partnership that can be converted into useful and structured information sources from which enterprises can draw information about markets’ trends, consumers’ habits, suppliers’ strategies, etc. This paper discusses the research efforts that our international research group has put into the topic of Enterprise 2.0 (aka Social Enterprise). In particular, our research group advocates that existing practices for managing enterprise information systems need to be re-visited in a way that permits to capture social relations that arise inside and outside the enterprise, to establish guidelines and techniques to assist IT practitioners integrate social relations into their design, development, and maintenance efforts of these information systems, and last but not least to identify and tackle challenges that prevent capturing social relations