University of Bielsko-Biała

About: University of Bielsko-Biała is a education organization based out in Bielsko-Biala, Poland. It is known for research contribution in the topics: Finite element method & Activated sludge. The organization has 905 authors who have published 2013 publications receiving 11675 citations. The organization is also known as: Academy of Technology and Humanities in Bielsko-Biała.

An overview of energy efficiency techniques in cluster computing systems

Abstract: Two major constraints demand more consideration for energy efficiency in cluster computing: (a) operational costs, and (b) system reliability. Increasing energy efficiency in cluster systems will reduce energy consumption, excess heat, lower operational costs, and improve system reliability. Based on the energy-power relationship, and the fact that energy consumption can be reduced with strategic power management, we focus in this survey on the characteristic of two main power management technologies: (a) static power management (SPM) systems that utilize low-power components to save the energy, and (b) dynamic power management (DPM) systems that utilize software and power-scalable components to optimize the energy consumption. We present the current state of the art in both of the SPM and DPM techniques, citing representative examples. The survey is concluded with a brief discussion and some assumptions about the possible future directions that could be explored to improve the energy efficiency in cluster computing.

Self-regulation of the inflammatory response by peroxisome proliferator-activated receptors

Abstract: The peroxisome proliferator-activated receptor (PPAR) family includes three transcription factors: PPARα, PPARβ/δ, and PPARγ. PPAR are nuclear receptors activated by oxidised and nitrated fatty acid derivatives as well as by cyclopentenone prostaglandins (PGA2 and 15d-PGJ2) during the inflammatory response. This results in the modulation of the pro-inflammatory response, preventing it from being excessively activated. Other activators of these receptors are nonsteroidal anti-inflammatory drug (NSAID) and fatty acids, especially polyunsaturated fatty acid (PUFA) (arachidonic acid, ALA, EPA, and DHA). The main function of PPAR during the inflammatory reaction is to promote the inactivation of NF-κB. Possible mechanisms of inactivation include direct binding and thus inactivation of p65 NF-κB or ubiquitination leading to proteolytic degradation of p65 NF-κB. PPAR also exert indirect effects on NF-κB. They promote the expression of antioxidant enzymes, such as catalase, superoxide dismutase, or heme oxygenase-1, resulting in a reduction in the concentration of reactive oxygen species (ROS), i.e., secondary transmitters in inflammatory reactions. PPAR also cause an increase in the expression of IκBα, SIRT1, and PTEN, which interferes with the activation and function of NF-κB in inflammatory reactions.