Abstract-Large-scale (or massive) multiple-input multipleoutput (MIMO) is expected to be one of the key technologies in next-generation multi-user cellular systems based on the upcoming 3GPP LTE Release 12 standard, for example. In this work, we propose-to the best of our knowledge-the first VLSI design enabling high-throughput data detection in single-carrier frequency-division multiple access (SC-FDMA)-based large-scale MIMO systems. We propose a new approximate matrix inversion algorithm relying on a Neumann series expansion, which substantially reduces the complexity of linear data detection. We analyze the associated error, and we compare its performance and complexity to those of an exact linear detector. We present corresponding VLSI architectures, which perform exact and approximate soft-output detection for large-scale MIMO systems with various antenna/user configurations. Reference implementation results for a Xilinx Virtex-7 XC7VX980T FPGA show that our designs are able to achieve more than 600 Mb/s for a 128 antenna, 8 user 3GPP LTE-based large-scale MIMO system. We finally provide a performance/complexity trade-off comparison using the presented FPGA designs, which reveals that the detector circuit of choice is determined by the ratio between BS antennas and users, as well as the desired error-rate performance.Index Terms-Approximate matrix inversion, FPGA design, large-scale (or massive) MIMO, linear soft-output detection, minimum mean square error (MMSE), Neumann series, VLSI.

The endoplasmic reticulum (ER) is the cellular organelle responsible for protein folding and assembly, lipid and sterol biosynthesis, and calcium storage. The unfolded protein response (UPR) is an adaptive intracellular stress response to accumulation of unfolded or misfolded proteins in the ER. In this study, we show that the most conserved UPR sensor inositol‐requiring enzyme 1 α (IRE1α), an ER transmembrane protein kinase/endoribonuclease, is required to maintain hepatic lipid homeostasis under ER stress conditions through repressing hepatic lipid accumulation and maintaining lipoprotein secretion. To elucidate physiological roles of IRE1α‐mediated signalling in the liver, we generated hepatocyte‐specific Ire1α‐null mice by utilizing an albumin promoter‐controlled Cre recombinase‐mediated deletion. Deletion of Ire1α caused defective induction of genes encoding functions in ER‐to‐Golgi protein transport, oxidative protein folding, and ER‐associated degradation (ERAD) of misfolded proteins, and led to selective induction of pro‐apoptotic UPR trans‐activators. We show that IRE1α is required to maintain the secretion efficiency of selective proteins. In the absence of ER stress, mice with hepatocyte‐specific Ire1α deletion displayed modest hepatosteatosis that became profound after induction of ER stress. Further investigation revealed that IRE1α represses expression of key metabolic transcriptional regulators, including CCAAT/enhancer‐binding protein (C/EBP) β, C/EBPδ, peroxisome proliferator‐activated receptor γ (PPARγ), and enzymes involved in triglyceride biosynthesis. IRE1α was also found to be required for efficient secretion of apolipoproteins upon disruption of ER homeostasis. Consistent with a role for IRE1α in preventing intracellular lipid accumulation, mice with hepatocyte‐specific deletion of Ire1α developed severe hepatic steatosis after treatment with an ER stress‐inducing anti‐cancer drug Bortezomib, upon expression of a misfolding‐prone human blood clotting factor VIII, or after partial hepatectomy. The identification of IRE1α as a key regulator to prevent hepatic steatosis provides novel insights into ER stress mechanisms in fatty liver diseases associated with toxic liver injuries.

Abstract-Cloud computing services allow users to lease computing resources from large scale data centers operated by service providers. Using cloud services, users can deploy a wide variety of applications dynamically and on-demand. Most cloud service providers use machine virtualization to provide flexible and costeffective resource sharing. However, few studies have investigated the impact of machine virtualization in the cloud on networking performance.In this paper, we present a measurement study to characterize the impact of virtualization on the networking performance of the Amazon Elastic Cloud Computing (EC2) data center. We measure the processor sharing, packet delay, TCP/UDP throughput and packet loss among Amazon EC2 virtual machines. Our results show that even though the data center network is lightly utilized, virtualization can still cause significant throughput instability and abnormal delay variations. We discuss the implications of our findings on several classes of applications.

CREBH is a liver-specific transcription factor that is localized in the endoplasmic reticulum (ER) membrane. Our previous work demonstrated that CREBH is activated by ER stress or inflammatory stimuli to induce an acute-phase hepatic inflammation. Here we demonstrate that CREBH is a key metabolic regulator of hepatic lipogenesis, fatty acid (FA) oxidation, and lipolysis under metabolic stress. Saturated FA, insulin signals, or an atherogenic high-fat diet can induce CREBH activation in the liver. Under the normal chow diet, CrebH knockout mice display a modest decrease in hepatic lipid contents but an increase in plasma triglycerides (TG). After feeding an atherogenic high-fat diet, massive accumulation of hepatic lipid metabolites and significant increase in plasma TG levels were observed in the CrebH knockout mice. Along with the hypertriglyceridemia phenotype, the CrebH null mice displayed significantly reduced body weight gain, diminished abdominal fat, and increased non-alcoholic steatohepatitis (NASH) activities under the atherogenic high-fat diet. Gene expression analysis and chromatin-immunoprecipitation (ChIP) assay indicated that CREBH is required to activate expression of the genes encoding functions involved in de novo lipogenesis, TG and cholesterol biosynthesis, FA elongation and oxidation, lipolysis, and lipid transport. Supporting the role of CREBH in lipogenesis and lipolysis, forced expression of an activated form of CREBH protein in the liver significantly increases accumulation of hepatic lipids but reduces plasma TG levels in mice. All together our study shows that CREBH plays a key role in maintaining lipid homeostasis by regulating expression of the genes involved in hepatic lipogenesis, FA oxidation, and lipolysis under metabolic stress. The identification of CREBH as a stress-inducible metabolic regulator has important implications in the understanding and treatment of metabolic disease.

Airborne particulate matter selectively activates endoplasmic reticulum stress response in the lung and liver tissues.