An Extended Virtual Aperture Imaging Model for Through-the-wall Sensing and Its Environmental Parameters Estimation

Through-the-wall imaging (TWI) radar has been given increasing attention in recent years. However, prior knowledge about environmental parameters, such as wall thickness and dielectric constant, and the standoff distance between an array and a wall, is generally unavailable in real applications. Thus, targets behind the wall suffer from defocusing and displacement under the conventional imag¬ing operations. To solve this problem, in this paper, we first set up an extended imaging model of a virtual aperture obtained by a multiple-input-multiple-output array, which considers the array position to the wall and thus is more applicable for real situations. Then, we present a method to estimate the environmental parameters to calibrate the TWI, without multiple measurements or dominant scatter¬ers behind-the-wall to assist. Simulation and field experi¬ments were performed to illustrate the validity of the pro¬posed imaging model and the environmental parameters estimation method

East-West Partnerships for Poverty Reduction: Experience Review and Institutional Innovation

As a general rule, companies have focused most of their improvement initiatives in manufacturing and operations, leaving their internal service processes behind. This study presents a FRACAS process which is underperforming in terms of lead time. The process is studied in detail and the people who work with it were interviewed to find out how they think the process inhibits their work. The contribution this study makes is that it provides an example of what lean FRACAS could mean. The studied process presents itself as non-compliant with what the employees wish from such a process. This in turn causes these employees to underperform since they think that the process does not seem to provide value to neither themselves nor the customers

Ultrafast Relaxation Dynamics of Photoexcited Dirac Fermion in The Three Dimensional Dirac Semimetal Cadmium Arsenide

Three dimensional (3D) Dirac semimetals which can be seen as 3D analogues of graphene have attracted enormous interests in research recently. In order to apply these ultrahigh-mobility materials in future electronic/optoelectronic devices, it is crucial to understand the relaxation dynamics of photoexcited carriers and their coupling with lattice. In this work, we report ultrafast transient reflection measurements of the photoexcited carrier dynamics in cadmium arsenide (Cd3As2), which is one of the most stable Dirac semimetals that have been confirmed experimentally. By using low energy probe photon of 0.3 eV, we probed the dynamics of the photoexcited carriers that are Dirac-Fermi-like approaching the Dirac point. We systematically studied the transient reflection on bulk and nanoplate samples that have different doping intensities by tuning the probe wavelength, pump power and lattice temperature, and find that the dynamical evolution of carrier distributions can be retrieved qualitatively by using a two-temperature model. This result is very similar to that of graphene, but the carrier cooling through the optical phonon couplings is slower and lasts over larger electron temperature range because the optical phonon energies in Cd3As2 are much lower than those in graphene

Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of β-catenin, and enhanced tumor cell invasion

AbstractEGF receptor (EGFR) overexpression correlates with metastasis in a variety of carcinomas, but the underlying mechanisms are poorly understood. We demonstrated that EGF disrupted cell-cell adhesion and caused epithelial-to-mesenchymal transition (EMT) in human tumor cells overexpressing EGFR, and also induced caveolin-dependent endocytosis of E-cadherin, a cell-cell adhesion protein. Chronic EGF treatment resulted in transcriptional downregulation of caveolin-1 and induction of the transcriptional repressor Snail, correlating with downregulation of E-cadherin expression. Caveolin-1 downregulation enhanced β-catenin-TCF/LEF-1 transcriptional activity in a GSK-3β-independent manner. Antisense RNA-mediated reduction of caveolin-1 expression in EGFR-overexpressing tumor cells recapitulated these EGF-induced effects and enhanced invasion into collagen gels. We propose that EGF-induced negative regulation of caveolin-1 plays a central role in the complex cellular changes leading to metastasis

Site-specific relapse pattern of the triple negative tumors in Chinese breast cancer patients

BACKGROUND: It has been reported that triple negative phenotype is characterized by aggressive clinical history in Western breast cancer patients, however its pattern of metastatic spread had never been reported in the Chinese population. Considering racial disparities, we sought to analyze the spread pattern for different sites of first recurrence in Chinese triple negative breast cancers. METHODS: A retrospective study of 1662 patients was carried out from a large database of breast cancer patients undergoing surgery between January 1, 2000 and March 31, 2004 at the Cancer Hospital, Fudan University, Shanghai, China. Survival curves were generated using the Kaplan-Meier method and annual relapse hazards were estimated by the hazard function. RESULTS: We found a statistically significant difference in relapse-free survival (RFS) for locoregional and visceral recurrence (P = 0.007 and P = 0.025, respectively) among the triple negative, ERBB2+ and HR+/ERBB2- subgroups in univariate analysis. In the multivariate Cox proportional hazards regression analysis, RFS for either locoregional or visceral relapse in the triple negative category was inferior to that in HR+/ERBB2- patients (P = 0.027 and P = 0.005, respectively), but comparable to that in ERBB2+ women (both P >0.05). Furthermore, the early relapse peak appeared later in the triple negative group than that in the ERBB2+ counterpart for both locoregional and visceral relapse. On the other hand, when compared with triple negative breast cancers, a significantly lower risk of developing bone relapse was discerned for ERBB2+ women (P = 0.048; HR = 0.384, 95% CI 0.148-0.991), with the borderline significance for HR+/ERBB2- breast cancers (P = 0.058; HR = 0.479, 95% CI 0.224-1.025). In terms of bone metastasis, the hazard rate remained higher for the triple negative category than that for the ERBB2+ subtype. CONCLUSION: Based on the site-specific spread pattern in different subgroups, the triple negative category of breast cancers in the Chinese population exhibits a different pattern of relapse, which indicates that different organotropism may be due to the different intrinsic subtypes. A better knowledge of the triple negative category is warranted for efficacious systemic regimens to decrease and/or delay the relapse hazard

Blocking interaction between SHP2 and PD‐1 denotes a novel opportunity for developing PD‐1 inhibitors

Small molecular PD‐1 inhibitors are lacking in current immuno‐oncology clinic. PD‐1/PD‐L1 antibody inhibitors currently approved for clinical usage block interaction between PD‐L1 and PD‐1 to enhance cytotoxicity of CD8+ cytotoxic T lymphocyte (CTL). Whether other steps along the PD‐1 signaling pathway can be targeted remains to be determined. Here, we report that methylene blue (MB), an FDA‐approved chemical for treating methemoglobinemia, potently inhibits PD‐1 signaling. MB enhances the cytotoxicity, activation, cell proliferation, and cytokine‐secreting activity of CTL inhibited by PD‐1. Mechanistically, MB blocks interaction between Y248‐phosphorylated immunoreceptor tyrosine‐based switch motif (ITSM) of human PD‐1 and SHP2. MB enables activated CTL to shrink PD‐L1 expressing tumor allografts and autochthonous lung cancers in a transgenic mouse model. MB also effectively counteracts the PD‐1 signaling on human T cells isolated from peripheral blood of healthy donors. Thus, we identify an FDA‐approved chemical capable of potently inhibiting the function of PD‐1. Equally important, our work sheds light on a novel strategy to develop inhibitors targeting PD‐1 signaling axis