A Framework for Qualitative Communications Using Big Packet Protocol

In the current Internet architecture, a packet is a minimal or fundamental unit upon which different actions such as classification,forwarding, or discarding are performed by the network nodes.When faced with constrained or poor network conditions, a packet is subjected to undesirable drops and re-transmissions, resulting in unpredictable delays and subsequent traffic overheads in the network. Alternately, we introduce qualitative communication services which allow partial, yet timely, delivery of a packet instead of dropping it entirely. These services allow breaking down packet payloads into smaller units (called chunks), enabling much finer granularity of bandwidth utilization. We propose Packet Wash as a new operation in forwarding nodes to support qualitative services. Upon packet error or network congestion, the forwarding node selectively removes some chunk(s)from the payload based on the relationship among the chunks or the individual significance level of each chunk. We also present a qualitative communication framework as well as a Packet Wash directive implemented in a newly evolved data plane technology,called Big Packet Protocol (BPP)Comment: Accepted in NEAT workshop, ACM SIGCOMM, August 2019, Beijing, Chin

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

White paper on 6G networking

This white paper is one of the twelve new themed 6G White Papers led by the 6G Flagship program. It involved the participation of more than 50 experts and enthusiasts of future 6G technologies. In this white paper, we intend to shed light on advanced features relevant to networking that would shape the evolution beyond 5G, ultimately leading to the 6G mobile system