Spatial Wireless Channel Prediction under Location Uncertainty

Spatial wireless channel prediction is important for future wireless networks, and in particular for proactive resource allocation at different layers of the protocol stack. Various sources of uncertainty must be accounted for during modeling and to provide robust predictions. We investigate two channel prediction frameworks, classical Gaussian processes (cGP) and uncertain Gaussian processes (uGP), and analyze the impact of location uncertainty during learning/training and prediction/testing, for scenarios where measurements uncertainty are dominated by large-scale fading. We observe that cGP generally fails both in terms of learning the channel parameters and in predicting the channel in the presence of location uncertainties.\textcolor{blue}{{} }In contrast, uGP explicitly considers the location uncertainty. Using simulated data, we show that uGP is able to learn and predict the wireless channel

FuSSI-Net: Fusion of Spatio-temporal Skeletons for Intention Prediction Network

Pedestrian intention recognition is very important to develop robust and safe autonomous driving (AD) and advanced driver assistance systems (ADAS) functionalities for urban driving. In this work, we develop an end-to-end pedestrian intention framework that performs well on day- and night- time scenarios. Our framework relies on objection detection bounding boxes combined with skeletal features of human pose. We study early, late, and combined (early and late) fusion mechanisms to exploit the skeletal features and reduce false positives as well to improve the intention prediction performance. The early fusion mechanism results in AP of 0.89 and precision/recall of 0.79/0.89 for pedestrian intention classification. Furthermore, we propose three new metrics to properly evaluate the pedestrian intention systems. Under these new evaluation metrics for the intention prediction, the proposed end-to-end network offers accurate pedestrian intention up to half a second ahead of the actual risky maneuver.Comment: 5 pages, 6 figures, 5 tables, IEEE Asilomar SS

The mammalian LINC complex regulates genome transcriptional responses to substrate rigidity

Mechanical integration of the nucleus with the extracellular matrix (ECM) is established by linkage between the cytoskeleton and the nucleus. This integration is hypothesized to mediate sensing of ECM rigidity, but parsing the function of nucleus-cytoskeleton linkage from other mechanisms has remained a central challenge. Here we took advantage of the fact that the LINC (linker of nucleoskeleton and cytoskeleton) complex is a known molecular linker of the nucleus to the cytoskeleton, and asked how it regulates the sensitivity of genome-wide transcription to substratum rigidity. We show that gene mechanosensitivity is preserved after LINC disruption, but reversed in direction. Combined with myosin inhibition studies, we identify genes that depend on nuclear tension for their regulation. We also show that LINC disruption does not attenuate nuclear shape sensitivity to substrate rigidity. Our results show for the first time that the LINC complex facilitates mechano-regulation of expression across the genome

Early human B cell response to Ebola virus in four U.S. survivors of infection

The human B cell response to natural filovirus infections early after recovery is poorly understood. Previous serologic studies suggest that some Ebola virus survivors exhibit delayed antibody responses with low magnitude and quality. Here, we sought to study the population of individual memory B cells induced early in convalescence. We isolated monoclonal antibodies (MAbs) from memory B cells from four survivors treated for Ebola virus disease (EVD) 1 or 3 months after discharge from the hospital. At the early time points postrecovery, the frequency of Ebola-specific B cells was low and dominated by clones that were cross-reactive with both Ebola glycoprotein (GP) and with the secreted GP (sGP) form. Of 25 MAbs isolated from four donors, only one exhibited neutralization activity. This neutralizing MAb, designated MAb EBOV237, recognizes an epitope in the glycan cap of the surface glycoprotein. In vivo murine lethal challenge studies showed that EBOV237 conferred protection when given prophylactically at a level similar to that of the ZMapp component MAb 13C6. The results suggest that the human B cell response to EVD 1 to 3 months postdischarge is characterized by a paucity of broad or potent neutralizing clones. However, the neutralizing epitope in the glycan cap recognized by EBOV237 may play a role in the early human antibody response to EVD and should be considered in rational design strategies for new Ebola virus vaccine candidates

CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis

Basal-like breast cancers (BLBC) are characterized by defects in homologous recombination (HR), deficient mitotic checkpoint, and high-proliferation activity. Here, we discover CIP2A as a candidate driver of BLBC. CIP2A was essential for DNA damage-induced initiation of mouse BLBC-like mammary tumors and for survival of HR-defective BLBC cells. CIP2A was dispensable for normal mammary gland development and for unperturbed mitosis, but selectively essential for mitotic progression of DNA damaged cells. A direct interaction between CIP2A and a DNA repair scaffold protein TopBP1 was identified, and CIP2A inhibition resulted in enhanced DNA damage-induced TopBP1 and RAD51 recruitment to chromatin in mammary epithelial cells. In addition to its role in tumor initiation, and survival of BRCA-deficient cells, CIP2A also drove proliferative MYC and E2F1 signaling in basal-like triple-negative breast cancer (BL-TNBC) cells. Clinically, high CIP2A expression was associated with poor patient prognosis in BL-TNBCs but not in other breast cancer subtypes. Small-molecule reactivators of PP2A (SMAP) inhibited CIP2A transcription, phenocopied the CIP2A-deficient DNA damage response (DDR), and inhibited growth of patient-derived BLBC xenograft. In summary, these results demonstrate that CIP2A directly interacts with TopBP1 and coordinates DNAdamage-induced mitotic checkpoint and proliferation, thereby driving BLBC initiation and progression. SMAPs could serve as a surrogate therapeutic strategy to inhibit the oncogenic activity of CIP2A in BLBCs. Significance: These results identify CIP2A as a nongenetic driver and therapeutic target in basal-like breast cancer that regulates DNA damage-induced G2-M checkpoint and proliferative signaling.Peer reviewe

Early human B cell response to Ebola virus in four U.S. survivors of infection

The human B cell response to natural filovirus infections early after recovery is poorly understood. Previous serologic studies suggest that some Ebola virus survivors exhibit delayed antibody responses with low magnitude and quality. Here, we sought to study the population of individual memory B cells induced early in convalescence. We isolated monoclonal antibodies (MAbs) from memory B cells from four survivors treated for Ebola virus disease (EVD) 1 or 3 months after discharge from the hospital. At the early time points postrecovery, the frequency of Ebola-specific B cells was low and dominated by clones that were cross-reactive with both Ebola glycoprotein (GP) and with the secreted GP (sGP) form. Of 25 MAbs isolated from four donors, only one exhibited neutralization activity. This neutralizing MAb, designated MAb EBOV237, recognizes an epitope in the glycan cap of the surface glycoprotein. In vivo murine lethal challenge studies showed that EBOV237 conferred protection when given prophylactically at a level similar to that of the ZMapp component MAb 13C6. The results suggest that the human B cell response to EVD 1 to 3 months postdischarge is characterized by a paucity of broad or potent neutralizing clones. However, the neutralizing epitope in the glycan cap recognized by EBOV237 may play a role in the early human antibody response to EVD and should be considered in rational design strategies for new Ebola virus vaccine candidates

CIP2A interacts with TopBP1 and drives basal-like breast cancer tumorigenesis

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Pull-out Behaviour of Hooked End Steel Fibres Embedded in Ultra-high Performance Mortar with Various W/B Ratios

This paper presents the fibre-matrix interfacial properties of hooked end steel fibres embedded in ultra-high performance mortars with various water/binder (W/B) ratios. The principle objective was to improve bond behaviour in terms of bond strength by reducing the (W/B) ratio to a minimum. Results show that a decrease in W/B ratio has a significant effect on the bondslip behaviour of both types of 3D fibres, especially when the W/B ratio was reduced from 0.25 to 0.15. Furthermore, the optimization in maximizing pullout load and total pullout work is found to be more prominent for the 3D fibres with a larger diameter than for fibres with a smaller diameter. On the contrary, increasing the embedded length of the 3D fibres did not result in an improvement on the maximum pullout load, but increase in the total pullout work