The design and implementation of PowerMill

In this paper we discuss the design and implemen-tation of the simulator PowerMill, a novel transistor level simulator for the simulation of current and power behavior in vlsi circuits. With a new transistor mod-eling technology and a versatile event driven simu-lation algorithm, PowerMill is capable of simulating detailed current behavior in modern deep-submicron cmos circuits, including sophisticated circuitries such as exclusive-or gates and sense-ampliers, with speed and capacity approaching conventional gate level sim-ulators. The high accuracy and speed have made it possible for designers to study and verify detailed cur-rent behavior of large functional blocks or even an en-tire chip with a reasonable amount of CPU resources, making it a de facto industry standard for power sim-ulation.

Characterizing and Modeling Control-Plane Traffic for Mobile Core Network

In this paper, we first carry out to our knowledge the first in-depth characterization of control-plane traffic, using a real-world control-plane trace for 37,325 UEs sampled at a real-world LTE Mobile Core Network (MCN). Our analysis shows that control events exhibit significant diversity in device types and time-of-day among UEs. Second, we study whether traditional probability distributions that have been widely adopted for modeling Internet traffic can model the control-plane traffic originated from individual UEs. Our analysis shows that the inter-arrival time of the control events as well as the sojourn time in the UE states of EMM and ECM for the cellular network cannot be modeled as Poisson processes or other traditional probability distributions. We further show that the reasons that these models fail to capture the control-plane traffic are due to its higher burstiness and longer tails in the cumulative distribution than the traditional models. Third, we propose a two-level hierarchical state-machine-based traffic model for UE clusters derived from our adaptive clustering scheme based on the Semi-Markov Model to capture key characteristics of mobile network control-plane traffic -- in particular, the dependence among events generated by each UE, and the diversity in device types and time-of-day among UEs. Finally, we show how our model can be easily adjusted from LTE to 5G to support modeling 5G control-plane traffic, when the sizable control-plane trace for 5G UEs becomes available to train the adjusted model. The developed control-plane traffic generator for LTE/5G networks is open-sourced to the research community to support high-performance MCN architecture design R&D

Myricetin inhibits proliferation of cisplatin-resistant cancer cells through a p53-dependent apoptotic pathway

Cisplatin is a commonly used drug for cancer treatment by crosslinking DNA, leading to apoptosis of cancer cells, resistance to cisplatin treatment often occurs, leading to relapse. Therefore, there is a need for the development of more effective treatment strategies that can overcome chemoresistance. Myricetin is a flavonoid from fruits and vegetables, showing anticancer activity in various cancer cells. In this study, we found myricetin exhibited greater cytotoxicity than cisplatin in two cisplatin-resistant ovarian cancer cell lines, OVCAR-3 and A2780/CP70, and it was less cytotoxic to the normal ovarian cell line IOSE-364. Myricetin selectively induced apoptosis in both cisplatin-resistant cancer cell lines, but did not induce apoptosis in the normal ovarian cell line. It induced both Bcl-2 family-dependent intrinsic and DR5 dependent extrinsic apoptosis in OVCAR-3 cells. P53, a multifunctional tumor suppressor, regulated apoptosis in OVCAR-3 cells through a Bcl-2 family protein-dependent pathway. Myricetin did not induce cell cycle arrest in either ovarian cancer cell line. Because of its potency and selectivity against cisplatin-resistant cancer cells, myricetin could potentially be used to overcome cancer chemoresistance against platinum-based therapy

Myricetin inhibits proliferation of cisplatin-resistant cancer cells through a p53-dependent apoptotic pathway

Cisplatin is a commonly used drug for cancer treatment by crosslinking DNA, leading to apoptosis of cancer cells, resistance to cisplatin treatment often occurs, leading to relapse. Therefore, there is a need for the development of more effective treatment strategies that can overcome chemoresistance. Myricetin is a flavonoid from fruits and vegetables, showing anticancer activity in various cancer cells. In this study, we found myricetin exhibited greater cytotoxicity than cisplatin in two cisplatin-resistant ovarian cancer cell lines, OVCAR-3 and A2780/CP70, and it was less cytotoxic to the normal ovarian cell line IOSE-364. Myricetin selectively induced apoptosis in both cisplatinresistant cancer cell lines, but did not induce apoptosis in the normal ovarian cell line. It induced both Bcl-2 familydependent intrinsic and DR5 dependent extrinsic apoptosis in OVCAR-3 cells. P53, a multifunctional tumor suppressor, regulated apoptosis in OVCAR-3 cells through a Bcl-2 family protein-dependent pathway. Myricetin did not induce cell cycle arrest in either ovarian cancer cell line. Because of its potency and selectivity against cisplatin-resistant cancer cells, myricetin could potentially be used to overcome cancer chemoresistance against platinum-based therapy

Research on energy extraction characteristics of an adaptive deformation oscillating-wing

Oscillating foil machines represent a type of flow energy harvesters which perform pitching and plunging motions simultaneously to harness the energy from incoming stream. In this paper, a new adaptive deformation oscillating wing was proposed and the theoretical performance of such a concept was studied here through unsteady two-dimensional simulations using an in-house developed computational fluid dynamics code. During operation, the proposed oscillating foil whose initial shape is symmetric can be deformed into a cambered foil, which aims to produce large lift force. Our numerical results suggest that the power efficiency of the proposed oscillating foil can be about 16.1% higher than the conventional oscillating foil without deformation. In addition, the effects of the maximum bending displacement and effective angle of attack on the efficiency of proposed oscillating foil were also discussed in this work

The flavonoid nobiletin inhibits tumor growth and angiogenesis of ovarian cancers via the Akt pathway

Despite its importance, the death rate of ovarian cancer has remained unchanged over the past five decades, demanding an improvement in prevention and treatment of this malignancy. With no known carcinogens, targeted prevention is currently unavailable, and efforts in early detection of this malignancy by screening biomarkers have failed. The inhibition of angiogenesis, also known as angioprevention, is a promising strategy to limit the growth of solid tumors, including ovarian cancers. Nobiletin, a polymethoxy flavonoid compound isolated from the tiansheng plant, has been shown to inhibit the growth of multiple types of human cancers. However, there are no reports involving the effect on nobiletin on human ovarian cancer. The present report shows that nobiletin potently decreases the viability of ovarian cancer cells in vitro. However, nobiletin does not affect the viability of normal ovarian epithelial cells at \u3c40 µM. The antitumor activity of nobiletin was also observed in athymic mouse models and in chicken chorioallantoic membrane (CAM) models. The anti-neoplastic activity of nobiletin was due to its ability to inhibit angiogenesis. We also studied the molecular mechanisms by which nobiletin suppresses angiogenesis. We observed that nobiletin inhibits secretion of the key angiogenesis mediators, Akt, HIF-1α, NF-κB and vascular epithelial growth factor (VEGF) by ovarian cancer cells. Transient transfection experiments showed that nobiletin inhibits production of HIF-1α by downregulation of Akt. Such decreased levels of HIF-1α were responsible for nobiletin-induced suppression of VEGF. Our data suggest that nobiletin may be a promising anti-angiogenic agent relevant for therapy of ovarian cancers

Sesn3 protects against diet‐induced nonalcoholic steatohepatitis in mice via suppression of the TGFβ signal transduction

Sesn3 belongs to the three‐member sestrin protein family. Sestrins have been implicated in anti‐oxidative stress, AMPK and mTOR signal transduction, and metabolic homeostasis. However, the role of Sesn3 in the development of nonalcoholic steatohepatitis (NASH) has not been previously studied. In this work, we generated Sesn3 whole‐body knockout and liver‐specific transgenic mice to investigate the hepatic function of Sesn3 in diet‐induced NASH. With only 4 weeks of dietary treatment, Sesn3 knockout mice developed severe NASH phenotype as characterized by hepatic steatosis, inflammation, and fibrosis. Strikingly, after 8‐week feeding with a NASH‐inducing diet, Sesn3 transgenic mice were largely protected against NASH development. Transcriptomic analysis revealed that multiple extracellular matrix related processes were upregulated including TGFβ signaling and collagen production. Further biochemical and cell biological analyses have illustrated a critical control of the TGFβ‐Smad pathway by Sesn3 at the TGFβ receptor and Smad3 levels. First, Sesn3 inhibits the TGFβ receptor through an interaction with Smad7; second, Sesn3 directly inhibits the Smad3 function through protein‐protein interaction and cytosolic retention