An Effective Fairness Scheme for Named Data Networking

Named data networking (NDN) is a revolutionary approach to cater for modern and future Internet usage trends. The advancements in web services, social networks and cloud computing have shifted Internet utilization towards information delivery. Information-centric networking (ICN) enables content-awareness in the network layer and adopts name-based routing through the NDN architecture. Data delivery in NDN is receiver-driven pull-based and governed by requests (interests) sent out by the receiver. The ever-increasing share of high-volume media streams traversing the Internet due to the popularity and availability of video-streaming services can put a strain on network resources and lead to congestion. Since most congestion control techniques proposed for NDN are receiver-based and rely on the users to adjust their interest rates, a fairness scheme needs to be implemented at the intermediate network nodes to ensure that “rogue” users do not monopolize the available network resources. This paper proposes a fairness-based active queue management at network routers which performs per-flow interest rate shaping in order to ensure fair allocation of resources. Different congestion scenarios for both single path and multipath network topologies have been simulated to test the effectiveness of the proposed fairness scheme. Performance of the scheme is evaluated using Jain’s fairness index as a fairness metric.

Biological sex and age shape melanoma tumour evolution

Many cancer types display sex and age disparity in incidence and outcome. Here, we establish a mathematical approach using cancer mutational data to analyze how sex and age shape the tumour genome. We model how age-related (clock-like) somatic mutations that arise during cell division, and extrinsic (environmental) mutations accumulate in cancer genomes. As a proof-of-concept, we apply our approach to melanoma, a cancer driven by cell-intrinsic age-related mutations and extrinsic ultraviolet light-induced mutations, and show these mutation types differ in magnitude, chronology and by sex in the distinct molecular melanoma subtypes.Our model confirms age and sex are determinants of cellular mutation rate, shaping the final mutation composition. We show mathematically for the first time how, similar to non-cancer tissues, melanoma genomes reflect a decline in cell division during ageing. We find clock-like mutations strongly correlate with the acquisition of ultraviolet light-induced mutations, but critically, males present a higher number and rate of cell division-linked mutations. These data indicate the contribution of environmental damage to melanoma likely extends beyond genetic damage to affect cell division.