Waste Reduction at the University of Richmond: Recommendations for a Greener, Cleaner Campus

Connecting with the University of Richmond goals of stewardship and academic achievement both in and outside the classroom, we have constructed a plan for making the University campus more sustainable. By applying knowledge acquired throughout our Environmental Studies education, and understanding its connection to global issues, we hope to make a positive, lasting impact on our campus community. In the 2017 Strategic Plan, the University describes a vision of modelling the way that colleges and universities can effectively meet the challenges of our time (UR Strategic Plan, 2017). Although there is a broad range of environmental issues that can be addressed by universities, we focus on a solution to address food waste on the University of Richmond campus. Paper prepared for the Environmental Studies Senior Seminar/Geography Capstone. Faculty Advisor: Dr. David Salisbur

The Ursinus Weekly, March 12, 1962

Nobel Prize-winner here tonight: Dr. Linus Pauling to address special forum on Science and international relations • Book No more war! Dr. Pauling\u27s credo • Local high school pupils invited to PSEA panel • UC students attend I.C.G. convention • Student-faculty talent show to finish Campus Chest charity drive Friday • College\u27s concert band to perform next Thursday • Lauderdale braces for Spring influx • Civil liberty\u27s Cox visits U.C. campus • Campus Chest activities continue this week • Ursinus invites public to use College Library • St. Pat\u27s twist theme of frosh dance Saturday • Pre-med club to see films depicting Caesarian birth • Editorial: Just this once • Penna. folk festival planned for Harrisburg • Ursinus in the past • Curtain Club offers two plays; One-act shows given last Thursday • Women\u27s hairbreadth victories mark basketball play; Sansenbach stars • High scoring continues; Intramural finish nears • Mermaids win two in week\u27s action • Sports publicist evaluates season • Intramural corner • Cindermen seem strong as five lettermen return • Chief McClure hustles vagrant to county jail • Collegeville tops Phoenix YMCA basketball league • Collegeville firemen take part in Phila. exhibit • Faculty hoopsters triumph in benefit against girls • Graduate grantshttps://digitalcommons.ursinus.edu/weekly/1314/thumbnail.jp

31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016) : part two

Background The immunological escape of tumors represents one of the main ob- stacles to the treatment of malignancies. The blockade of PD-1 or CTLA-4 receptors represented a milestone in the history of immunotherapy. However, immune checkpoint inhibitors seem to be effective in specific cohorts of patients. It has been proposed that their efficacy relies on the presence of an immunological response. Thus, we hypothesized that disruption of the PD-L1/PD-1 axis would synergize with our oncolytic vaccine platform PeptiCRAd. Methods We used murine B16OVA in vivo tumor models and flow cytometry analysis to investigate the immunological background. Results First, we found that high-burden B16OVA tumors were refractory to combination immunotherapy. However, with a more aggressive schedule, tumors with a lower burden were more susceptible to the combination of PeptiCRAd and PD-L1 blockade. The therapy signifi- cantly increased the median survival of mice (Fig. 7). Interestingly, the reduced growth of contralaterally injected B16F10 cells sug- gested the presence of a long lasting immunological memory also against non-targeted antigens. Concerning the functional state of tumor infiltrating lymphocytes (TILs), we found that all the immune therapies would enhance the percentage of activated (PD-1pos TIM- 3neg) T lymphocytes and reduce the amount of exhausted (PD-1pos TIM-3pos) cells compared to placebo. As expected, we found that PeptiCRAd monotherapy could increase the number of antigen spe- cific CD8+ T cells compared to other treatments. However, only the combination with PD-L1 blockade could significantly increase the ra- tio between activated and exhausted pentamer positive cells (p= 0.0058), suggesting that by disrupting the PD-1/PD-L1 axis we could decrease the amount of dysfunctional antigen specific T cells. We ob- served that the anatomical location deeply influenced the state of CD4+ and CD8+ T lymphocytes. In fact, TIM-3 expression was in- creased by 2 fold on TILs compared to splenic and lymphoid T cells. In the CD8+ compartment, the expression of PD-1 on the surface seemed to be restricted to the tumor micro-environment, while CD4 + T cells had a high expression of PD-1 also in lymphoid organs. Interestingly, we found that the levels of PD-1 were significantly higher on CD8+ T cells than on CD4+ T cells into the tumor micro- environment (p < 0.0001). Conclusions In conclusion, we demonstrated that the efficacy of immune check- point inhibitors might be strongly enhanced by their combination with cancer vaccines. PeptiCRAd was able to increase the number of antigen-specific T cells and PD-L1 blockade prevented their exhaus- tion, resulting in long-lasting immunological memory and increased median survival

A Kinetic-Based Model of Radiation-Induced Intercellular Signalling

It is now widely accepted that intercellular communication can cause significant variations in cellular responses to genotoxic stress. The radiation-induced bystander effect is a prime example of this effect, where cells shielded from radiation exposure see a significant reduction in survival when cultured with irradiated cells. However, there is a lack of robust, quantitative models of this effect which are widely applicable. In this work, we present a novel mathematical model of radiation-induced intercellular signalling which incorporates signal production and response kinetics together with the effects of direct irradiation, and test it against published data sets, including modulated field exposures. This model suggests that these so-called "bystander" effects play a significant role in determining cellular survival, even in directly irradiated populations, meaning that the inclusion of intercellular communication may be essential to produce robust models of radio-biological outcomes in clinically relevant in vivo situations