Hybrid Message Passing Algorithm for Downlink FDD Massive MIMO-OFDM Channel Estimation

The design of message passing algorithms on factor graphs has been proven to be an effective manner to implement channel estimation in wireless communication systems. In Bayesian approaches, a prior probability model that accurately matches the channel characteristics can effectively improve estimation performance. In this work, we study the channel estimation problem in a frequency division duplexing (FDD) downlink massive multiple-input multiple-output (MIMO) orthogonal frequency division multiplexing (OFDM) system. As the prior probability, we propose the Markov chain two-state Gaussian mixture with large variance difference (TSGM-LVD) model to exploit the structured sparsity in the angle-frequency domain of the massive MIMO-OFDM channel. In addition, we present a new method to derive the hybrid message passing (HMP) rule, which can calculate the message with mixed linear and non-linear model. To the best of the authors' knowledge, we are the first to apply the HMP rule to practical communication systems, designing the HMP-TSGM-LVD algorithm under the structured turbo-compressed sensing (STCS) framework. Simulation results demonstrate that the proposed HMP-TSGM-LVD algorithm converges faster and outperforms its counterparts under a wide range of simulation settings

Tailoring density estimation via reproducing kernel moment matching

Moment matching is a popular means of parametric density estimation. We extend this technique to nonparametric estimation of mixture models. Our approach works by embedding distributions into a reproducing kernel Hilbert space, and performing moment matching in that space. This allows us to tailor density estimators to a function class of interest (i.e., for which we would like to compute expectations). We show our density estimation approach is useful in applications such as message compression in graphical models, and image classification and retrieval

A novel fouling control strategy for forward osmosis membrane during sludge thickening via self-forming protective layer

Severe membrane fouling significantly limited forward osmosis (FO) process for sludge thickening (FST). Here, a novel antifouling strategy by loading a self-forming protective layer on FO membrane surface was proposed in this study. The protective layer was coated on FO membrane surface via a short-term FO process using activated sludge as the feed solution. Results indicated that the self-forming protective layer made FO membrane surface more negatively charged and more hydrophilic. As for the control FO (C-FO) membrane, the water flux decreased approximately 66% of the initial flux in Cycle 2 of FST process and thus resulting in the sludge concentration only increased to 40 g/L. In contrast, the flux decline rate of modified FO (M−FO) membrane was about 22%, and the corresponding sludge concentration still rose to 50 g/L. It suggested that the M−FO membrane with a protective layer had a better sludge thickening efficiency and a lower flux decline during sludge thickening compared to the C-FO membrane. Furthermore, less deposited foulants and better fouling reversibility were observed for M−FO membrane after two cycles of sludge thickening, implying that the protective layer effectively mitigated FO membrane fouling during sludge thickening. This phenomenon could be attributed to the excellent barrier effect of the protective layer and the enhanced surface hydrophilicity and negative charge, which improved the antifouling performance of the FO membrane. The findings of this study were conducive to better understanding of FO membrane fouling mechanisms and further development of fouling mitigation strategy via a protective layer.</p

A novel fouling control strategy for forward osmosis membrane during sludge thickening via self-forming protective layer

Severe membrane fouling significantly limited forward osmosis (FO) process for sludge thickening (FST). Here, a novel antifouling strategy by loading a self-forming protective layer on FO membrane surface was proposed in this study. The protective layer was coated on FO membrane surface via a short-term FO process using activated sludge as the feed solution. Results indicated that the self-forming protective layer made FO membrane surface more negatively charged and more hydrophilic. As for the control FO (C-FO) membrane, the water flux decreased approximately 66% of the initial flux in Cycle 2 of FST process and thus resulting in the sludge concentration only increased to 40 g/L. In contrast, the flux decline rate of modified FO (M−FO) membrane was about 22%, and the corresponding sludge concentration still rose to 50 g/L. It suggested that the M−FO membrane with a protective layer had a better sludge thickening efficiency and a lower flux decline during sludge thickening compared to the C-FO membrane. Furthermore, less deposited foulants and better fouling reversibility were observed for M−FO membrane after two cycles of sludge thickening, implying that the protective layer effectively mitigated FO membrane fouling during sludge thickening. This phenomenon could be attributed to the excellent barrier effect of the protective layer and the enhanced surface hydrophilicity and negative charge, which improved the antifouling performance of the FO membrane. The findings of this study were conducive to better understanding of FO membrane fouling mechanisms and further development of fouling mitigation strategy via a protective layer.</p

Notch2 controls hepatocyte-derived cholangiocarcinoma formation in mice.

Liver cancer comprises a group of malignant tumors, among which hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) are the most common. ICC is especially pernicious and associated with poor clinical outcome. Studies have shown that a subset of human ICCs may originate from mature hepatocytes. However, the mechanisms driving the trans-differentiation of hepatocytes into malignant cholangiocytes remain poorly defined. We adopted lineage tracing techniques and an established murine hepatocyte-derived ICC model by hydrodynamic injection of activated forms of AKT (myr-AKT) and Yap (YapS127A) proto-oncogenes. Wild-type, Notch1 flox/flox , and Notch2 flox/flox mice were used to investigate the role of canonical Notch signaling and Notch receptors in AKT/Yap-driven ICC formation. Human ICC and HCC cell lines were transfected with siRNA against Notch2 to determine whether Notch2 regulates biliary marker expression in liver tumor cells. We found that AKT/Yap-induced ICC formation is hepatocyte derived and this process is strictly dependent on the canonical Notch signaling pathway in vivo. Deletion of Notch2 in AKT/Yap-induced tumors switched the phenotype from ICC to hepatocellular adenoma-like lesions, while inactivation of Notch1 in hepatocytes did not result in significant histomorphological changes. Finally, in vitro studies revealed that Notch2 silencing in ICC and HCC cell lines down-regulates the expression of Sox9 and EpCAM biliary markers. Notch2 is the major determinant of hepatocyte-derived ICC formation in mice

Combined treatment with MEK and mTOR inhibitors is effective in vitro and in vivo models of hepatocellular carcinoma

Background: Hepatocellular carcinoma (HCC) is the most common primary liver cancer histotype, characterized by high biological aggressiveness and scarce treatment options. Recently, we have established a clinically relevant murine HCC model by co-expressing activated forms of v-akt murine thymoma viral oncogene homolog (AKT) and oncogene c-mesenchymal-epithelial transition (c-Met) proto-oncogenes in the mouse liver via hydrodynamic tail vein injection (AKT/c-MET mice). Tumor cells from these mice demonstrated high activity of the AKT/mammalian target of rapamycin (mTOR) and Ras/Mitogen-activated protein kinase (MAPK) signaling cascades, two pathways frequently co-induced in human HCC. Methods: Here, we investigated the therapeutic efficacy of sorafenib, regorafenib, the MEK inhibitor PD901 as well as the pan-mTOR inhibitor MLN0128 in the AKT/c-Met preclinical HCC model. Results: In these mice, neither sorafenib nor regorafenib demonstrated any efficacy. In contrast, administration of PD901 inhibited cell cycle progression of HCC cells in vitro. Combined PD901 and MLN0128 administration resulted in a pronounced growth constraint of HCC cell lines. In vivo, treatment with PD901 or MLN0128 alone moderately slowed HCC growth in AKT/c-MET mice. Importantly, the simultaneous administration of the two drugs led to a stable disease with limited tumor progression in mice. Mechanistically, combined mitogen-activated extracellular signal-regulated kinase (MEK) and mTOR inhibition resulted in a stronger cell cycle inhibition and growth arrest both in vitro and in vivo. Conclusions: Our study indicates that combination of MEK and mTOR inhibitors might represent an effective therapeutic approach against human HCC