Comparative Study of PID Based VMC and Fuzzy Logic Controllers for Flyback Converter

In this paper performance of flyback converter by using PID controller and Fuzzy controller are studied, compared and analyzed. The above study is done for 200W, 230V A.C input 48V DC output. Design of fuzzy controller is based on the heuristic knowledge of converter behaviour, and tuning of fuzzy inference requires some expertise to minimize unproductive trial and error. The design of PID control is based on the frequency response of the converter. For the DC-DC converters, the performance of the fuzzy controller was superior in some respects to that of the PID controller. The fuzzy controller is easily to develop, they cover a wide range of operating conditions, and they are more readily customizable in natural language terms. Simulation is done in Matlab environment to show the performance variations of above mentioned converters using both Fuzzy & PID controllers

Quasi Switched Capacitor based integrated Boost Series Parallel Fly-back Converter for energy Storage Applications

711-715A quasi-Switched Capacitor technique (QSC) is used to control the switch in Interconnected Boost Series Parallel Fly-Back Converter (IBSPFC). The QSC based IBSPFC does not require any snubber circuits for all the MOSFET switches presented at primary and secondary side and power can also be transferred even if one the winding gets damage. The primary side winding of the fly-back transformer is coupled in series across with bulk capacitor to minimize switch voltage stress and the secondary winding of the 1:1 fly-back transformer is coupled with dc voltage source, three switches and capacitor which forms a Quasi switched capacitor technique. Working techniques of quasi-switched capacitor with IBSPFC have been introduced. A 75v input, 100v output and DC-DC isolated Converter switching at frequency of 100 kHz is modeled using FPGA SPARTAN6LX9 and experimental results have been presented

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes