Large-scale unit commitment under uncertainty: an updated literature survey

The Unit Commitment problem in energy management aims at finding the optimal production schedule of a set of generation units, while meeting various system-wide constraints. It has always been a large-scale, non-convex, difficult problem, especially in view of the fact that, due to operational requirements, it has to be solved in an unreasonably small time for its size. Recently, growing renewable energy shares have strongly increased the level of uncertainty in the system, making the (ideal) Unit Commitment model a large-scale, non-convex and uncertain (stochastic, robust, chance-constrained) program. We provide a survey of the literature on methods for the Uncertain Unit Commitment problem, in all its variants. We start with a review of the main contributions on solution methods for the deterministic versions of the problem, focussing on those based on mathematical programming techniques that are more relevant for the uncertain versions of the problem. We then present and categorize the approaches to the latter, while providing entry points to the relevant literature on optimization under uncertainty. This is an updated version of the paper "Large-scale Unit Commitment under uncertainty: a literature survey" that appeared in 4OR 13(2), 115--171 (2015); this version has over 170 more citations, most of which appeared in the last three years, proving how fast the literature on uncertain Unit Commitment evolves, and therefore the interest in this subject

Loss of amphiregulin reduces myoepithelial cell coverage of mammary ducts and alters breast tumor growth

Abstract Background Amphiregulin (AREG), a ligand of the epidermal growth factor receptor, is not only essential for proper mammary ductal development, but also associated with breast cancer proliferation and growth. In the absence of AREG, mammary ductal growth is stunted and fails to expand. Furthermore, suppression of AREG expression in estrogen receptor-positive breast tumor cells inhibits in-vitro and in-vivo growth. Methods We crossed AREG-null (AREG−/−) mice with the murine luminal B breast cancer model, MMTV-PyMT (PyMT), to generate spontaneous breast tumors that lack AREG (AREG−/− PyMT). We evaluated tumor growth, cytokeratin-8 (K8)-positive luminal cells, cytokeratin-14 (K14)-positive myoepithelial cells, and expression of AREG, Ki67, and PyMT. Primary myoepithelial cells from nontumor-bearing AREG+/+ mice underwent fluorescence-activated cell sorting and were adapted to culture for in-vitro coculture studies with AT-3 cells, a cell line derived from C57Bl/6 PyMT mammary tumors. Results Intriguingly, PyMT-induced lesions progress more rapidly in AREG−/− mice than in AREG+/+ mice. Quantification of K8+ luminal and K14+ myoepithelial cells in non-PyMT AREG−/− mammary glands showed fewer K14+ cells and a thinner myoepithelial layer. Study of AT-3 cells indicated that coculture with myoepithelial cells or exposure to AREG, epidermal growth factor, or basic fibroblast growth factor can suppress PyMT expression. Late-stage AREG−/− PyMT tumors are significantly less solid in structure, with more areas of papillary and cystic growth. Papillary areas appear to be both less proliferative and less necrotic. In The Cancer Genome Atlas database, luminal-B invasive papillary carcinomas have lower AREG expression than luminal B invasive ductal carcinomas. Conclusions Our study has revealed a previously unknown role of AREG in myoepithelial cell development and PyMT expression. AREG expression is essential for proper myoepithelial coverage of mammary ducts. Both AREG and myoepithelial cells can suppress PyMT expression. We find that lower AREG expression is associated with invasive papillary breast cancer in both the MMTV-PyMT model and human breast cancer

Bioprotective Lactic Acid Bacteria and Lactic Acid as a Sustainable Strategy to Combat <i>Escherichia coli</i> O157:H7 in Meat

Human infection by Enterohemorrhagic Escherichia coli (EHEC) constitutes a serious threat to public health and a major concern for the meat industry. Presently, consumers require safer/healthier foods with minimal chemical additives, highlighting the need for sustainable solutions to limit and prevent risks. This work evaluated the ability of two antagonistic lactic acid bacteria (LAB) strains, Lactiplantibacillus plantarum CRL681 and Enterococcus mundtii CRL35, and their combination in order to inhibit EHEC in beef (ground and vacuum sealed meat discs) at 8 °C during 72 h. The effect of lower lactic acid (LA) concentrations was evaluated. Meat color was studied along with how LAB strains interfere with the adhesion of Escherichia coli to meat. The results indicated a bacteriostatic effect on EHEC cells when mixed LAB strains were inoculated. However, a bactericidal action due to a synergism between 0.6% LA and LAB occurred, producing undetectable pathogenic cells at 72 h. Color parameters (a*, b* and L*) did not vary in bioprotected meat discs, but they were significantly modified in ground meat after 24 h. In addition, LAB strains hindered EHEC adhesion to meat. The use of both LAB strains plus 0.6% LA, represents a novel, effective and ecofriendly strategy to inactivate EHEC in meat

Revista española de pedagogía

Resumen basado en el de la publicaciónSe quiere comprobar si se confirman los mismos resultados que los obtenidos en otros estudios sobre la inteligencia con adultos y en qué grado o, sí por el contrario, son diferentes a ellos. Los participantes han sido 191 estudiantes de educación secundaria. De ellos, 86 eran mujeres y, 105 hombres. Su nivel socioeconómico era de clase media. Se les pidió que hicieran estimaciones de su propia inteligencia y de la de su familia. Los resultados confirmaron que los hombres hacían estimaciones más altas que las mujeres especialmente en la inteligencia matemática y espacial. Los resultados están de acuerdo con el conjunto de investigaciones y se han interpretado en términos de influencias sociales y familiares.MadridBiblioteca de Educación del Ministerio de Educación, Cultura y Deporte; Calle San Agustín, 5 - 3 planta; 28014 Madrid; Tel. +34917748000; [email protected]