The E3 architecture: enabling future cellular networks with cognitive and self‐x capabilities

Future mobile networks are expected to be complex heterogeneous systems. On the one hand this will enable users to take advantage of a number of different access technologies. On the other hand it will seriously affect network management procedures since more extensive operations and decisions will have to be dealt with. To tackle these challenges a number of new dynamic mechanisms need to be designed. It is imperative that certain network management tasks have to be performed without human intervention to reduce the OPEX costs and achieve faster responses in different events. To achieve this goal, the introduction of self‐x functionalities, combined with cognitive mechanisms and the ability to reconfigure network entities and terminals, is required. Moreover, the introduction of a new pilot channel needs to be considered to assist the terminals in selecting the most suitable radio access technology according to their requirements. We present the functional architecture of an evolved network that was designed in the context of the EU‐funded IP project ‘E³: End‐to‐End Efficiency’. This architecture aims to enhance existing procedures usually performed in traditional operation and maintenance systems (e.g. spectrum management, network planning, configuration actions). We explain the rationale of our design and provide specific examples to illustrate the role of the different functional entities and their interfaces. A considerable part of this architecture has recently been approved as a feasibility study by the ETSI Committee Reconfigurable Radio System. Copyright © 2010 John Wiley & Sons, Ltd.     

BET Inhibition Upregulates SIRT1 and Alleviates Inflammatory Responses

Control of histone acetylation is a part of the epigenetic mechanism that regulates gene expression and chromatin architecture. The members of the bromodomain and extra terminal domain (BET) protein family are a group of epigenetic readers that recognize histone acetylation, whereas histone deacetyl‐ ases such as sirtuin 1 (SIRT1) function as epigenetic erasers. We observed that BET inhibition by the specific inhibitor JQ1 upregulated SIRT1 expression and activated SIRT1. Moreover, we observed that BET inhibition functionally reversed the pro‐inflammatory effect of SIRT1 inhibition in a cellular lung disease model. SIRT1 activation is desirable in many age‐related, metabolic and inflammatory diseases; our results suggest that BET protein inhibition would be beneficial in treatment of those conditions. Most importantly, our findings demonstrate a novel mechanism of SIRT1 activation by inhibition of the BET proteins.     

Cement-based additive manufacturing: experimental investigation of process quality

The International Journal of Advanced Manufacturing Technology - The interest in additive manufacturing (AM) of cement-based materials is steadily increasing. Moreover, there is a growing need for...     

A simple algorithm for the nonlinear dynamic analysis of networks

A simple and economical algorithm is presented for the nonlinear dynamic analysis of networks, with lumped masses on the nodes, bars obeying uniaxial stress-strain laws and no damping. The step-by-step algorithm of the trapezoidal rule is used, combined with the predictor-corrector technique, with only two corrections per step. The prediction of an upper-bound for the eigenfrequencies permits the use of a constant steplength throughout the whole algorithm. An example problem and an error analysis of the algorithm are presented.