Development of A 16:1 serializer for data transmission at 5 Gbps

Radiation tolerant, high speed and low power serializer ASIC is critical for optical link systems in particle physics experiments. Based on a commercial 0.25 μm silicon-onsapphire CMOS technology, we design a 16:1 serializer with 5 Gbps serial data rate. This ASIC has been submitted for fabrication. The post-layout simulation indicates the deterministic jitter is 54 ps (pk-pk) and random jitter is 3 ps (rms). The power consumption of the serializer is 500 mW. The design details and post layout simulation results are presented in this paper

High-Speed Serial Optical Link Test Bench Using FPGA with Embedded Transceivers

We develop a custom Bit Error Rate test bench based on Altera’s Stratix II GX transceiver signal integrity development kit, demonstrate it on point-to-point serial optical link with data rate up to 5 Gbps, and compare it with commercial stand alone tester. The 8B/10B protocol is implemented and its effects studied. A variable optical attenuator is inserted in the fibre loop to induce transmission degradation and to measure receiver sensitivity. We report comparable receiver sensitivity results using the FPGA based tester and commercial tester. The results of the FPGA also shows that there are more one-tozero bit flips than zero-to-one bit flips at lower error rate. In 8B/10B coded transmission, there are more word errors than bit flips, and the total error rate is less than two times that of non-coded transmission. Total error rate measured complies with simulation results, according to the protocol setup

The Design of a High Speed Low Power Phase Locked Loop

The upgrade of the ATLAS Liquid Argon Calorimeter readout system calls for the development of radiation tolerant, high speed and low power serializer ASIC. We have designed a phase locked loop using a commercial 0.25-μm Silicon-on- Sapphire (SoS) CMOS technology. Post-layout simulation indicates that tuning range is 3.79 – 5.01 GHz and power consumption is 104 mW. The PLL has been submitted for fabrication. The design and simulation results are presented

Optical Data Transmission ASICs for the High-Luminosity LHC (HL-LHC) Experiments

We present the design and test results of two optical data transmission ASICs for the High-Luminosity LHC (HL-LHC) experiments. These ASICs include a two-channel serializer (LOCs2) and a single-channel Vertical Cavity Surface Emitting Laser (VCSEL) driver (LOCld1V2). Both ASICs are fabricated in a commercial 0.25-um Silicon-on-Sapphire (SoS) CMOS technology and operate at a data rate up to 8 Gbps per channel. The power consumption of LOCs2 and LOCld1V2 are 1.25 W and 0.27 W at 8-Gbps data rate, respectively. LOCld1V2 has been verified meeting the radiation-tolerance requirements for HL-LHC experiments.Comment: 9 pages, 12 figure

The 120Gbps VCSEL Array Based Optical Transmitter (ATx) Development for the High-Luminosity LHC (HL-LHC) Experiments

The integration of a Verticle Cavity Surface-Emitting Laser (VCSEL) array and a driving Application-Specific Integrated Circuit (ASIC) in a custom optical array transmitter module (ATx) for operation in the detector front-end is constructed, assembled and tested. The ATx provides 12 parallel channels with each channel operating at 10 Gbps. The optical transmitter eye diagram passes the eye mask and the bit-error rate (BER) less than 1E-12 transmission is achieved at 10 Gbps/ch. The overall insertion loss including the radiation induced attenuation is sufficiently low to meet the proposed link budget requirement.Comment: 10 pages, 9 figure

Preparation and characterization of carbon nanofluid by a plasma arc nanoparticles synthesis system

Heat dissipation from electrical appliances is a significant issue with contemporary electrical devices. One factor in the improvement of heat dissipation is the heat transfer performance of the working fluid. In this study, we used plasma arc technology to produce a nanofluid of carbon nanoparticles dispersed in distilled water. In a one-step synthesis, carbon was simultaneously heated and vaporized in the chamber, the carbon vapor and particles were then carried to a collector, where cooling furnished the desired carbon/water nanofluid. The particle size and shape were determined using the light-scattering size analyzer, SEM, and TEM. Crystal morphology was examined by XRD. Finally, the characterization include thermal conductivity, viscosity, density and electric conductivity were evaluated by suitable instruments under different temperatures. The thermal conductivity of carbon/water nanofluid increased by about 25% at 50°C compared to distilled water. The experimental results demonstrated excellent thermal conductivity and feasibility for manufacturing of carbon/water nanofluids

Anti-Arthritic Effects of Magnolol in Human Interleukin 1β-Stimulated Fibroblast-Like Synoviocytes and in a Rat Arthritis Model

Fibroblast-like synoviocytes (FLS) play an important role in the pathologic processes of destructive arthritis by producing a number of catabolic cytokines and metalloproteinases (MMPs). The expression of these mediators is controlled at the transcriptional level. The purposes of this study were to evaluate the anti-arthritic effects of magnolol (5,5′-Diallyl-biphenyl-2,2′-diol), the major bioactive component of the bark of Magnolia officinalis, by examining its inhibitory effects on inflammatory mediator secretion and the NF-κB and AP-1 activation pathways and to investigate its therapeutic effects on the development of arthritis in a rat model. The in vitro anti-arthritic activity of magnolol was tested on interleukin (IL)-1β-stimulated FLS by measuring levels of IL-6, cyclooxygenase-2, prostaglandin E2, and matrix metalloproteinases (MMPs) by ELISA and RT-PCR. Further studies on how magnolol inhibits IL-1β-stimulated cytokine expression were performed using Western blots, reporter gene assay, electrophoretic mobility shift assay, and confocal microscope analysis. The in vivo anti-arthritic effects of magnolol were evaluated in a Mycobacterium butyricum-induced arthritis model in rats. Magnolol markedly inhibited IL-1β (10 ng/mL)-induced cytokine expression in a concentration-dependent manner (2.5–25 µg/mL). In clarifying the mechanisms involved, magnolol was found to inhibit the IL-1β-induced activation of the IKK/IκB/NF-κB and MAPKs pathways by suppressing the nuclear translocation and DNA binding activity of both transcription factors. In the animal model, magnolol (100 mg/kg) significantly inhibited paw swelling and reduced serum cytokine levels. Our results demonstrate that magnolol inhibits the development of arthritis, suggesting that it might provide a new therapeutic approach to inflammatory arthritis diseases

Microtubular Stability Affects pVHL-Mediated Regulation of HIF-1alpha via the p38/MAPK Pathway in Hypoxic Cardiomyocytes

BACKGROUND: Our previous research found that structural changes of the microtubule network influence glycolysis in cardiomyocytes by regulating the hypoxia-inducible factor (HIF)-1α during the early stages of hypoxia. However, little is known about the underlying regulatory mechanism of the changes of HIF-1α caused by microtubule network alternation. The von Hippel-Lindau tumor suppressor protein (pVHL), as a ubiquitin ligase, is best understood as a negative regulator of HIF-1α. METHODOLOGY/PRINCIPAL FINDINGS: In primary rat cardiomyocytes and H9c2 cardiac cells, microtubule-stabilization was achieved by pretreating with paclitaxel or transfection of microtubule-associated protein 4 (MAP4) overexpression plasmids and microtubule-depolymerization was achieved by pretreating with colchicine or transfection of MAP4 siRNA before hypoxia treatment. Recombinant adenovirus vectors for overexpressing pVHL or silencing of pVHL expression were constructed and transfected in primary rat cardiomyocytes and H9c2 cells. With different microtubule-stabilizing and -depolymerizing treaments, we demonstrated that the protein levels of HIF-1α were down-regulated through overexpression of pVHL and were up-regulated through knockdown of pVHL in hypoxic cardiomyocytes. Importantly, microtubular structure breakdown activated p38/MAPK pathway, accompanied with the upregulation of pVHL. In coincidence, we found that SB203580, a p38/MAPK inhibitor decreased pVHL while MKK6 (Glu) overexpression increased pVHL in the microtubule network altered-hypoxic cardiomyocytes and H9c2 cells. CONCLUSIONS/SIGNIFICANCE: This study suggests that pVHL plays an important role in the regulation of HIF-1α caused by the changes of microtubular structure and the p38/MAPK pathway participates in the process of pVHL change following microtubule network alteration in hypoxic cardiomyocytes