Developing standard pedestrian-equivalent factors: passenger car–equivalent approach for dealing with pedestrian diversity

Similar to vehicular traffic, pedestrians, despite having diverse capabilities and body sizes, can be classified as heterogeneous. The use of vehicular traffic resolves the diversity issue with a conversion of heterogeneous vehicle flow into an equivalent flow with the use of passenger car–equivalent (PCE) factors. Analysis of pedestrian flow has yet to incorporate pedestrian diversity analysis implicitly into the design of pedestrian facilities, although some form of adjustment has been suggested. This paper introduces the concept of PCE-type factors for mixed pedestrian traffic called standard pedestrian-equivalent (SPE) factors. Estimates of SPE factors are made relative to the average commuter. The equivalent total travel time approach for PCE estimation was adapted to consider the effects of the differences in physical and operational characteristics of pedestrians, particularly walking speed and body size. Microsimulation of pedestrians was employed to evaluate hypothetical pedestrian proportions so as to generate corresponding flow relationships. Walking speeds and body sizes were varied across different flow conditions, walkway widths, and proportions of other pedestrian types. The first part of this paper explores how the two pedestrian characteristics (walking speed and body size) influence estimated SPE factors. The second part is a case study in which field-collected data illustrate SPE factors calculated for older adults, obese pedestrians, and their combination. An application of SPE factors demonstrates the robustness of the methodology in bridging the gap between pedestrian compositions and planning practice

A fast and accurate energy source emulator for wireless sensor networks

The capability to either minimize energy consumption in battery-operated devices, or to adequately exploit energy harvesting from various ambient sources, is central to the development and engineering of energy-neutral wireless sensor networks. However, the design of effective networked embedded systems targeting unlimited lifetime poses several challenges at different architectural levels. In particular, the heterogeneity, the variability, and the unpredictability of many energy sources, combined to changes in energy required by powered devices, make it difficult to obtain reproducible testing conditions, thus prompting the need of novel solutions addressing these issues. This paper introduces a novel embedded hardware-software solution aimed at emulating a wide spectrum of energy sources usually exploited to power sensor networks motes. The proposed system consists of a modular architecture featuring small factor form, low power requirements, and limited cost. An extensive experimental characterization confirms the validity of the embedded emulator in terms of flexibility, accuracy, and latency while a case study about the emulation of a lithium battery shows that the hardware-software platform does not introduce any measurable reduction of the accuracy of the model. The presented solution represents therefore a convenient solution for testing large-scale testbeds under realistic energy supply scenarios for wireless sensor networks

Mutational mechanisms shaping the coding and noncoding genome of germinal center derived B-cell lymphomas

B cells have the unique property to somatically alter their immunoglobulin (IG) genes by V(D)J recombination, somatic hypermutation (SHM) and class-switch recombination (CSR). Aberrant targeting of these mechanisms is implicated in lymphomagenesis, but the mutational processes are poorly understood. By performing whole genome and transcriptome sequencing of 181 germinal center derived B-cell lymphomas (gcBCL) we identified distinct mutational signatures linked to SHM and CSR. We show that not only SHM, but presumably also CSR causes off-target mutations in non-IG genes. Kataegis clusters with high mutational density mainly affected early replicating regions and were enriched for SHM- and CSR-mediated off-target mutations. Moreover, they often co-occurred in loci physically interacting in the nucleus, suggesting that mutation hotspots promote increased mutation targeting of spatially co-localized loci (termed hypermutation by proxy). Only around 1% of somatic small variants were in protein coding sequences, but in about half of the driver genes, a contribution of B-cell specific mutational processes to their mutations was found. The B-cell-specific mutational processes contribute to both lymphoma initiation and intratumoral heterogeneity. Overall, we demonstrate that mutational processes involved in the development of gcBCL are more complex than previously appreciated, and that B cell-specific mutational processes contribute via diverse mechanisms to lymphomagenesis

Expression profiling during arabidopsis/downy mildew interaction reveals a highly-expressed effector that attenuates responses to salicylic acid

Plants have evolved strong innate immunity mechanisms, but successful pathogens evade or suppress plant immunity via effectors delivered into the plant cell. Hyaloperonospora arabidopsidis (Hpa) causes downy mildew on Arabidopsis thaliana, and a genome sequence is available for isolate Emoy2. Here, we exploit the availability of genome sequences for Hpa and Arabidopsis to measure gene-expression changes in both Hpa and Arabidopsis simultaneously during infection. Using a high-throughput cDNA tag sequencing method, we reveal expression patterns of Hpa predicted effectors and Arabidopsis genes in compatible and incompatible interactions, and promoter elements associated with Hpa genes expressed during infection. By resequencing Hpa isolate Waco9, we found it evades Arabidopsis resistance gene RPP1 through deletion of the cognate recognized effector ATR1. Arabidopsis salicylic acid (SA)-responsive genes including PR1 were activated not only at early time points in the incompatible interaction but also at late time points in the compatible interaction. By histochemical analysis, we found that Hpa suppresses SA-inducible PR1 expression, specifically in the haustoriated cells into which host-translocated effectors are delivered, but not in non-haustoriated adjacent cells. Finally, we found a highly-expressed Hpa effector candidate that suppresses responsiveness to SA. As this approach can be easily applied to host-pathogen interactions for which both host and pathogen genome sequences are available, this work opens the door towards transcriptome studies in infection biology that should help unravel pathogen infection strategies and the mechanisms by which host defense responses are overcome