A similarity-based cooperative co-evolutionary algorithm for dynamic interval multi-objective optimization problems

The file attached to this record is the author's final peer reviewed version. The Publisher's final version can be found by following the DOI link.Dynamic interval multi-objective optimization problems (DI-MOPs) are very common in real-world applications. However, there are few evolutionary algorithms that are suitable for tackling DI-MOPs up to date. A framework of dynamic interval multi-objective cooperative co-evolutionary optimization based on the interval similarity is presented in this paper to handle DI-MOPs. In the framework, a strategy for decomposing decision variables is first proposed, through which all the decision variables are divided into two groups according to the interval similarity between each decision variable and interval parameters. Following that, two sub-populations are utilized to cooperatively optimize decision variables in the two groups. Furthermore, two response strategies, rgb0.00,0.00,0.00i.e., a strategy based on the change intensity and a random mutation strategy, are employed to rapidly track the changing Pareto front of the optimization problem. The proposed algorithm is applied to eight benchmark optimization instances rgb0.00,0.00,0.00as well as a multi-period portfolio selection problem and compared with five state-of-the-art evolutionary algorithms. The experimental results reveal that the proposed algorithm is very competitive on most optimization instances

Effect of ulinastatin on growth inhibition, apoptosis of breast carcinoma cells is related to a decrease in signal conduction of JNk-2 and NF-κB

<p>Abstract</p> <p>Objective</p> <p>This study aims to investigate the <it>in vitro </it>effects of Ulinastatin (UTI) and Taxotere (TXT) on cell proliferation; cell apoptosis; xenografted tumor growth; and expression of insulin-like growth factor receptor 1 (IGF-1R), platelet-derived growth factor A (PDGFA), nerve growth factor (NGF), c-Jun N-terminal kinase 2 (JNk-2), and NF-κB in a human primary breast cancer cells and breast cancer cell line MDA-MB-231.</p> <p>Methods</p> <p>The cell lines cultured were divided into four groups: 1) control group, 2) UTI group, 3) TXT group, and 4) UTI+TXT group. The method of MTT essay, flow cytometry, and RT-PCR were used to detect cell proliferation, cell apoptosis, and expression of IGF-1R, PDGFA, NGF, NF-κB, JNk-2, respectively. The growth of xenografted tumor in nude mice was used to calculate the anti-tumor rate. Immunohistochemistry staining (SP) was used to detect the expression of IGF-1R, PDGFA, NGF, ki-67, caspase-3, JNk-2, and NF-κB.</p> <p>Results</p> <p>Proliferation of human breast cancer cells and MDA-MB-231 cell lines, and growth rate of xenografted tumor decreased in order of UTI+TXT > TXT > UTI > control, apoptosis increased in the order control < UTI < TXT < UTI+TXT. The gene expression and protein expression of IGF-1R, PDGFA, NGF, NF-κB and JNk-2 in breast cancer cells was inhibited by UTI and TXT.</p> <p>Conclusions</p> <p>UTI 1) inhibits the proliferation of human breast cancer cells and the growth of xenografted tumors, 2) induces cancer cell apoptosis, and 3) enhances the anti-tumor effect of TXT. This mechanism might be related to decreasing signal transduction of JNk-2 and NF-κB, and then expression of IGF-1R, PDGFA, NGF.</p

Bright solitons in spin-orbit-coupled Bose-Einstein condensates

We study bright solitons in a Bose-Einstein condensate with a spin-orbit coupling that has been realized experimentally. Both stationary bright solitons and moving bright solitons are found. The stationary bright solitons are the ground states and possess well-defined spin-parity, a symmetry involving both spatial and spin degrees of freedom; these solitons are real valued but not positive definite, and the number of their nodes depends on the strength of spin-orbit coupling. For the moving bright solitons, their shapes are found to change with velocity due to the lack of Galilean invariance in the system