OBJECTIVE Ischemic stroke remains a significant cause of death and disability in industrialized nations. Janus tyrosine kinase (JAK) and signal transducer and activator of transcription (STAT) of the JAK2/STAT3 pathway play important roles in the downstream signal pathway regulation of ischemic stroke-related inflammatory neuronal damage. Recently, microRNAs (miRNAs) have emerged as major regulators in cerebral ischemic injury; therefore, the authors aimed to investigate the underlying molecular mechanism between miRNAs and ischemic stroke, which may provide potential therapeutic targets for ischemic stroke. METHODS The JAK2- and JAK3-related miRNA (miR-135, miR-216a, and miR-433) expression levels were detected by real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blot analysis in both oxygen-glucose deprivation (OGD)-treated primary cultured neuronal cells and mouse brain with middle cerebral artery occlusion (MCAO)-induced ischemic stroke. The miR-135, miR-216a, and miR-433 were determined by bioinformatics analysis that may target JAK2, and miR-216a was further confirmed by 3' untranslated region (3'UTR) dual-luciferase assay. The study further detected cell apoptosis, the level of lactate dehydrogenase, and inflammatory mediators (inducible nitric oxide synthase [iNOS], matrix metalloproteinase-9 [MMP-9], tumor necrosis factor-α [TNF-α], and interleukin-1β [IL-1β]) after cells were transfected with miR-NC (miRNA negative control) or miR-216a mimics and subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) damage with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, annexin V-FITC/PI, Western blots, and enzyme-linked immunosorbent assay detection. Furthermore, neurological deficit detection and neurological behavior grading were performed to determine the infarction area and neurological deficits. RESULTS JAK2 showed its highest level while miR-216a showed its lowest level at day 1 after ischemic reperfusion. However, miR-135 and miR-433 had no obvious change during the process. The luciferase assay data further confirmed that miR-216a can directly target the 3'UTR of JAK2, and overexpression of miR-216a repressed JAK2 protein levels in OGD/R-treated neuronal cells as well as in the MCAO model ischemic region. In addition, overexpression of miR-216a mitigated cell apoptosis both in vitro and in vivo, which was consistent with the effect of knockdown of JAK2. Furthermore, the study found that miR-216a obviously inhibited the inflammatory mediators after OGD/R, including inflammatory enzymes (iNOS and MMP-9) and cytokines (TNF-α and IL-1β). Upregulating miR-216a levels reduced ischemic infarction and improved neurological deficit. CONCLUSIONS These findings suggest that upregulation of miR-216a, which targets JAK2, could induce neuroprotection against ischemic injury in vitro and in vivo, which provides a potential therapeutic target for ischemic stroke.

In this paper, for the problems of low convergence rate and getting trapped in local optima easily, the average path similarity (APS) was proposed to present the optimization maturity by analyzing the relationship between parameters of local pheromone updating and global pheromone updating, as well as the optimizing capacity and convergence rate. Furthermore, the coefficients of pheromone updating adaptively were adjusted to improve the convergence rate and prevent the algorithm from getting stuck in local optima. The adaptive ACS has been applied to optimize several benchmark TSP instances. The solution quality and convergence rate of the algorithm were compared comprehensively with conventional ACS to verify the validity and the effectiveness.

An ergonomics optimization method of human-product contact surface design based on stochastic finite element was described. The shape of the contact surface between user and the product is the most complex content in product morphology design. Thinking of the individual needs of users, the stochastic finite element method was used to simulate the shape of product surface to meet the randomness of design variables, and the genetic algorithm was used to search the optimal surface solutions. And then a case of the seat back surface design of a driver chair was studied. The optimization results showed that the maximum pressure of the surface was decreased and the structure's reliability were guaranteed. The effectiveness of this ergonomics optimization method was verified.

The ability to understand human emotions is desirable for the computer in many applications recently. Recording and recognizing physiological signals of emotion has become an increasingly important field of research in affective computing and human computer interaction. For the problem of feature redundancy of physiological signals-based emotion recognition and low efficiency of traditional feature reduction algorithms on great sample data, this paper proposed an improved adaptive genetic algorithm (IAGA) to solve the problem of emotion feature selection, and then presented a weighted kNN classifier (wkNN) to classify features by making full use of emotion sample information. We demonstrated a case study of emotion recognition application and verified the algorithm's validity by the analysis of experimental simulation data and the comparison of several recognition methods.

For the problem of feature redundancy of emotion recognition based on multi-channel physiological signals and low efficiency of traditional feature reduction algorithms on great sample data, a new chaotic particle swarm optimization algorithm (TM-CPSO) was proposed to solve the problem of emotion feature selection by combining tent map based chaos search mechanism and improved particle swarm optimization algorithm. The problem of falling into local minimum can be avoided by mapping the search process to the recursive procedure of the chaotic orbit. The recognition rate and efficiency was increased and the algorithm's validity was verified through the analysis of experimental simulation data and the comparison of several recognition methods.