State-Compute Replication: Parallelizing High-Speed Stateful Packet Processing

With the slowdown of Moore's law, CPU-oriented packet processing in software will be significantly outpaced by emerging line speeds of network interface cards (NICs). Single-core packet-processing throughput has saturated. We consider the problem of high-speed packet processing with multiple CPU cores. The key challenge is state--memory that multiple packets must read and update. The prevailing method to scale throughput with multiple cores involves state sharding, processing all packets that update the same state, i.e., flow, at the same core. However, given the heavy-tailed nature of realistic flow size distributions, this method will be untenable in the near future, since total throughput is severely limited by single core performance. This paper introduces state-compute replication, a principle to scale the throughput of a single stateful flow across multiple cores using replication. Our design leverages a packet history sequencer running on a NIC or top-of-the-rack switch to enable multiple cores to update state without explicit synchronization. Our experiments with realistic data center and wide-area Internet traces shows that state-compute replication can scale total packet-processing throughput linearly with cores, deterministically and independent of flow size distributions, across a range of realistic packet-processing programs

BMP-6 promotes E-cadherin expression through repressing δEF1 in breast cancer cells

<p>Abstract</p> <p>Background</p> <p>Bone morphogenetic protein-6 (BMP-6) is critically involved in many developmental processes. Recent studies indicate that BMP-6 is closely related to tumor differentiation and metastasis.</p> <p>Methods</p> <p>Quantitative RT-PCR was used to determine the expression of BMP-6, E-cadherin, and δEF1 at the mRNA level in MCF-7 and MDA-MB-231 breast cancer cells, as well as in 16 breast cancer specimens. Immunoblot analysis was used to measure the expression of δEF1 at the protein level in δEF1-overexpressing and δEF1-interfered MDA-MB-231 cells. Luciferase assay was used to determine the rhBMP-6 or δEF1 driven transcriptional activity of the E-cadherin promoter in MDA-MB-231 cells. Quantitative CHIP assay was used to detect the direct association of δEF1 with the E-cadherin proximal promoter in MDA-MB-231 cells.</p> <p>Results</p> <p>MCF-7 breast cancer cells, an ER⁺cell line that expressed high levels of BMP-6 and E-cadherin exhibited very low levels of δEF1 transcript. In contrast, MDA-MB-231 cells, an ER^-cell line had significantly reduced BMP-6 and E-cadherin mRNA levels, suggesting an inverse correlation between BMP-6/E-cadherin and δEF1. To determine if the same relationship exists in human tumors, we examined tissue samples of breast cancer from human subjects. In 16 breast cancer specimens, the inverse correlation between BMP-6/E-cadherin and δEF1 was observed in both ER⁺cases (4 of 8 cases) and ER^-cases (7 of 8 cases). Further, we found that BMP-6 inhibited δEF1 transcription, resulting in an up-regulation of E-cadherin mRNA expression. This is consistent with our analysis of the E-cadherin promoter demonstrating that BMP-6 was a potent transcriptional activator. Interestingly, ectopic expression of δEF1 was able to block BMP-6-induced transactivation of E-cadherin, whereas RNA interference-mediated down-regulation of endogenous δEF1 in breast cancer cells abolished E-cadherin transactivation by BMP-6. In addition to down-regulating the expression of δEF1, BMP-6 also physically dislodged δEF1 from E-cadherin promoter to allow the activation of E-cadherin transcription.</p> <p>Conclusion</p> <p>We conclude that repression of δEF1 plays a key role in mediating BMP-6-induced transcriptional activation of E-cadherin in breast cancer cells. Consistent with the fact that higher level of δEF1 expression is associated with more invasive phenotype of breast cancer cells, our collective data suggests that δEF1 is likely the switch through which BMP-6 restores E-cadherin-mediated cell-to-cell adhesion and prevents breast cancer metastasis.</p

Photo-response of Two-Dimensional Ruddlesden-Popper Perovskite Films for Photovoltaics

Two-dimensional (2D) Ruddlesden-Popper (RP) perovskites have emerged as a prospective candidate to address the instability issues of traditional perovskite solar cells. However, the mechanisms of charge carrier transport of 2D perovskite films obtained by the solution process still remain elusive. In this work, we proposed a novel characterization technique based on the Kelvin probe force microscopy (KPFM) to investigate the micro-scale morphology and surface potential (SP) of the BA2MA3Pb4I13 films. In additionally, a Xenon laser source was adopted to realize the in-situ scanning of the light response of the perovskite film. The obvious increase in surface potential values in the same scanning area before and after white light illumination indicated the emergence of photo-generated charge carriers. Based on the unique photophysical properties and form formation features of the hot-cast BA2MA3Pb4I13 films, we fabricated the 2D perovskite solar cells (PSCs) with an efficiency of 10.95%. As a result, the in-situ KPFM is capable to serve as an effective approach to investigating the charge carrier behaviors in the 2D perovskites for photovoltaic applications

Design of a Novel Telerehabilitation System with a Force-Sensing Mechanism

Many stroke patients are expected to rehabilitate at home, which limits their access to proper rehabilitation equipment, treatment, or assessment by therapists. We have developed a novel telerehabilitation system that incorporates a human-upper-limb-like device and an exoskeleton device. The system is designed to provide the feeling of real therapist–patient contact via telerehabilitation. We applied the principle of a series elastic actuator to both the master and slave devices. On the master side, the therapist can operate the device in a rehabilitation center. When performing passive training, the master device can detect the therapist’s motion while controlling the deflection of elastic elements to near-zero, and the patient can receive the motion via the exoskeleton device. When performing active training, the design of the force-sensing mechanism in the master device can detect the assisting force added by the therapist. The force-sensing mechanism also allows force detection with an angle sensor. Patients’ safety is guaranteed by monitoring the motor’s current from the exoskeleton device. To compensate for any possible time delay or data loss, a torque-limiter mechanism was also designed in the exoskeleton device for patients’ safety. Finally, we successfully performed a system performance test for passive training with transmission control protocol/internet protocol communication

Real-Time Evaluation of the Signal Processing of sEMG Used in Limb Exoskeleton Rehabilitation System

As an important branch of medical robotics, a rehabilitation training robot for the hemiplegic upper limbs is a research hotspot of rehabilitation training. Based on the motion relearning program, rehabilitation technology, human anatomy, mechanics, computer science, robotics, and other fields of technology are covered. Based on an sEMG real-time training system for rehabilitation, the exoskeleton robot still has some problems that need to be solved in this field. Most of the existing rehabilitation exoskeleton robotic systems are heavy, and it is difficult to ensure the accuracy and real-time performance of sEMG signals. In this paper, we design a real-time training system for the upper limb exoskeleton robot based on the EMG signal. It has four main characteristics: light weight, portability, high precision, and low delay. This work includes the structure of the rehabilitation robotic system and the method of signal processing of the sEMG. An experiment on the accuracy and time delay of the sEMG signal processing has been done. In the experimental results, the recognition accuracy of the sEMG is 94%, and the average delay time is 300 ms, which meets the accuracy and real-time requirements

Evolution of Microstructures and Mechanical Properties of Nb-V Alloyed Ultra-High Strength Hot Stamping Steel in Austenitizing Process

Clarifying the influence of Nb and V microalloying on the ultra-high strength hot stamping steel (UHSHSS) and exploring appropriate process parameters are the basis for effectively regulating properties of the final product. In this study, the effects of different austenitizing temperatures and holding times on the phase transitions, grain sizes and mechanical properties of 22MnB5NbV with Nb and V alloyed are studied by using JMatPro thermodynamic calculations and experiments. By comparing with 22MnB5 without Nb and V alloyed, the effects of Nb and V elements on quenching microstructures, grain sizes and mechanical properties of UHSHSS are analyzed. The suitable austenitizing process parameters of 22MnB5NbV have been obtained. The results show that the grain size of Nb-V-alloyed UHSHSS grows with the increase in the austenitizing temperature and holding time. The 22MnB5NbV steel can be completely austenitized while the austenitizing temperatures ≥870 °C and holding time ≥3 min. Combined with the actual production process, the best austenitizing temperature and holding time are 930 °C and 3 min. Under these conditions, the average grain size is 7.7 μm, the tensile strength, elongation and strength-ductility product are 1570.8 MPa, 6.6% and 10.4 GPa·%, respectively. With the addition of Nb and V elements, the nanoscale precipitates lead to the refinement of the quenched structure and grain size, and the comprehensive properties of UHSHSS have been effectively promoted, in which the elongation and strong-plastic products are increased by ~0.6% and ~1.2 GPa·%, respectively

BMP-6 promotes E-cadherin expression through repressing δEF1 in breast cancer cells-5

<p><b>Copyright information:</b></p><p>Taken from "BMP-6 promotes E-cadherin expression through repressing δEF1 in breast cancer cells"</p><p>http://www.biomedcentral.com/1471-2407/7/211</p><p>BMC Cancer 2007;7():211-211.</p><p>Published online 13 Nov 2007</p><p>PMCID:PMC2217560.</p><p></p>o generate δEF1-interfered stable transfectants. Control cells were treated with a scrambled siRNA. The efficiency of δEF1 protein knockdown was examined by western blot, using an anti-ZEB antibody. Actin was used as a loading control. (b) δEF1-interfered MDA-MB-231 cell were transiently transfected with luciferase E-caherin promoter constructs. After transfection for 24 h, cells were treated with 200 ng/ml rhBMP-6. The luciferase activity of the extracts was determined 24 h after BMP-6 treatment using a Betascope analyzer. Luciferase values are normalized with Renilla activities. * indicates p < 0.05 in unpaired student t test when compared with vector alone

BMP-6 promotes E-cadherin expression through repressing δEF1 in breast cancer cells-7

<p><b>Copyright information:</b></p><p>Taken from "BMP-6 promotes E-cadherin expression through repressing δEF1 in breast cancer cells"</p><p>http://www.biomedcentral.com/1471-2407/7/211</p><p>BMC Cancer 2007;7():211-211.</p><p>Published online 13 Nov 2007</p><p>PMCID:PMC2217560.</p><p></p>lysis in MDA-MB-231 cells, using an unrelated anti-FLAG antibody or an anti-ZEB antibody directed against the N-terminal epitopes of δEF1. The amplified human E-cadherin promoter fragment is shown (-175/+21). (b) For quantitative CHIP assay, MDA-MB-231 cells were treated with or without 200 ng/ml rhBMP-6. Cell lysates were collected after 72 h. The IP was performed using anti-ZEB antibody (10 μg) with anti-FLAG antibody (10 μg) as a negative control. DNA fragments containing the E-cadherin promoter region (-175/+21) were amplified by quantitative PCR from anti-ZEB and anti-FLAG immunoprecipitated samples. Data represent three independent experiments. * indicates p < 0.05 in unpaired t-test when compared with un-treated group

BMP-6 promotes E-cadherin expression through repressing δEF1 in breast cancer cells-4

<p><b>Copyright information:</b></p><p>Taken from "BMP-6 promotes E-cadherin expression through repressing δEF1 in breast cancer cells"</p><p>http://www.biomedcentral.com/1471-2407/7/211</p><p>BMC Cancer 2007;7():211-211.</p><p>Published online 13 Nov 2007</p><p>PMCID:PMC2217560.</p><p></p> δEF1-binding sites are indicated