Economic optimization for configuration and sizing of micro integrated energy systems

Abstract Based on analysis of construction and operation of micro integrated energy systems (MIES), this paper presents economic optimization for their configuration and sizing. After presenting typical models for MIES, a residential community MIES is developed by analyzing residential direct energy consumption within a general design procedure. Integrating with available current technologies and local resources, the systematic design considers a prime mover, fed by natural gas, with wind power, photovoltaic generation, and two storage devices serving thermal energy and power to satisfy cooling, heating and electricity demands. Control strategies for MIES also are presented in this study. Multi-objective formulas are obtained by analyzing annual cost and dumped renewable energy to achieve optimal coordination of energy supply and demand. According to historical load data and the probability distribution of distributed generation output, clustering methods based on K-means and discretization methods are employed to obtain typical scenarios representative of uncertainties. The modified non-dominated sorting genetic algorithm is applied to find the Pareto frontier of the constructed multi-objective formulas. In addition, aiming to explore the Pareto frontier, the dumped energy cost ratio is defined to check the energy balance in different MIES designs and provide decision support for the investors. Finally, simulations and comparision show the appropriateness of the developed model and the applicability of the adopted optimization algorithm

Adeno-Associated Virus-Mediated RNAi against Mutant Alleles Attenuates Abnormal Calvarial Phenotypes in an Apert Syndrome Mouse Model

Apert syndrome (AS), the most severe form of craniosynostosis, is caused by missense mutations including Pro253Arg(P253R) of fibroblast growth factor receptor 2 (FGFR2), which leads to enhanced FGF/FGFR2-signaling activity. Surgical correction of the deformed skull is the typical treatment for AS. Because of constant maldevelopment of sutures, the corrective surgery is often executed several times, resulting in increased patient challenge and complications. Biological therapies targeting the signaling of mutant FGFR2 allele, in combination with surgery, may bring better outcome. Here we screened and found a small interfering RNA (siRNA) specifically targeting the Fgfr2-P253R allele, and we revealed that it inhibited osteoblastic differentiation and matrix mineralization by reducing the signaling of ERK1/2 and P38 in cultured primary calvarial cells and calvarial explants from Apert mice (Fgfr2+/P253R). Furthermore, AAV9 carrying short hairpin RNA (shRNA) (AAV9-Fgfr2-shRNA) against mutant Fgfr2 was delivered to the skulls of AS mice. Results demonstrate that AAV9-Fgfr2-shRNA attenuated the premature closure of coronal suture and the decreased calvarial bone volume of AS mice. Our study provides a novel practical biological approach, which will, in combination with other therapies, including surgeries, help treat patients with AS while providing experimental clues for the biological therapies of other genetic skeletal diseases. Keywords: craniosynostosis, Apert syndrome, Fgfr2, adeno-associated virus, RNAi, molecular therap