Mouse Anti-Human FAS Hybridoma [ivGbtN49]

Deadlock-free scheduling and control is critical for optimizing the performance of flexible assembly systems (FASs). Based on the Petri net models of FASs, this paper integrates a deadlock prevention policy with local search and develops a novel deadlock-free scheduling algorithm. A solution of the scheduling problem is coded as a chromosome representation that is a permutation with repetition of parts. By using the deadlock prevention policy, a repairing algorithm (RA) is developed to repair unfeasible chromosomes. A perturbation strategy based on estimation of distribution algorithm is developed to escape from local optima. Moreover, to improve population diversity, an acceptance criterion (AC) based on Pareto dominance is proposed. The chromosome representation, RA, perturbation strategy, and AC together support the cooperative aspect of local search for scheduling problems strongly.

Fat deposition in skeletal muscle is an important aspect of improving meat quality. Isoflavones can promote animal anabolism, but whether and how they regulate muscle fat deposition remain largely unclear. In this study, we explored the role and corresponding molecular mechanism of one of the major isoflavones, daidzein, in fat deposition in C2C12 myoblast cells. In the absence of fatty acids (FAs), daidzein did not promote triglyceride synthesis and lipid droplet formation in cells but increased sterol regulatory element-binding protein 1c (SREBP-1c) expression and maturation. In the presence of FAs, daidzein enhanced FAs-induced fat deposition and the SREBP-1c signaling. Daidzein promoted FAs-induced nuclear factor kappa B1 (NF kappa B1) phosphorylation and activated the SREBP-1c signaling in a PI3K-dependent manner. G protein-coupled receptor 30 (GPR30) knockdown but not estrogen receptor alpha (ER alpha) knockdown blocked the stimulation of daidzein on the PI3K-NF kappa B1-SREBP-1c signaling pathway, while both knockdown did not affect the stimulation of FAs on this signaling. qRT-PCR and ChIP-qPCR further detected that daidzein stimulated NF kappa B1-targeted SREBP-1c transcription. Daidzein did not affect ER alpha expression in cells, but it stimulated GPR30 expression and cytoplasmic localization. These results reveal that daidzein promotes FAs-induced fat deposition through the GPR30 signaling in C2C12 myoblast cells.