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For the trajectory tracking control problem of the omnidirectional mobile platform of Mecanum wheels, a strategy of double closed-loop control with model predictive control (MPC) and differential forward proportional plus integral plus derivative (PID) is proposed. The attitude control loop and velocity control loop are designed based on the kinematics characteristics of Mecanum wheels. The linear error model of the Mecanum wheels chassis is established by the attitude control loop, the quadratic objective function is designed, and the problem of path following is transformed into predictive control for the nonlinear model. In the velocity control loop, the differential forward PID controller is used to avoid the high-frequency disturbance to the system caused by frequent step changes of the input quantity, accelerate the convergence of the angular velocity of the Mecanum wheels, and enhance the stability of the system. Simulation experiments demonstrate that the controller designed in this study has better convergence speed and tracking accuracy than the commonly used trajectory algorithm, and it can provide good robustness to control the mobile platform of Mecanum wheels.

In the context of social governance innovation, the integration and sharing of information are studied through the construction of an information-sharing platform. The process of interpreting the evolution of new media information dissemination includes analyzing the characteristics and laws of information dissemination on various platforms. Based on the existing scale of public welfare charities, the kinetic evolution equation of the public welfare information dissemination model is established to describe the dissemination process of public welfare information and its influencing factors. The impact of media intervention on the final scale of public welfare information dissemination is analyzed using the collected Facebook dataset as the background, and it is found that the higher the media credibility is at t = 4, the public welfare information attracts media attention. After the release of public interest information, the immunity node began to show a gradual upward trend, reaching a maximum of 1.0. Indicating that after the media release of public interest information, the final scale of dissemination of public interest information increases.

The effect of stress on risk‐taking or risk‐averse behavior in decision‐making has been inconclusive in previous research, with few studies revealing the underlying neural mechanisms. This study employed event‐related potentials technique and combined a social cold pressor assessment test with a mental arithmetic task to induce stress responses, aiming to investigate the influence of exogenous stress on the risk decision‐making process. Stress induction results indicated that, in addition to raising heart rate and blood pressure, stress responses were accompanied by enhanced negative emotions, diminished positive emotions, and alterations in neural activity. The outcomes of risk decision‐making showed that stress did not significantly affect risk preference or time of choice but did reduce the feedback‐related negativity/reward positivity, with a particularly significant effect observed for large outcomes. Stress also altered the amplitude of the P3 component, with stress decreasing the P3 value for winning outcomes relative to losing outcomes. The study suggests that understanding how stress affects risk preference should consider the emotional valence induced by stress. Contrary to the reward sensitivity hypothesis, stress weakened reward sensitivity. Stress led to changes in the allocation of cognitive resources for outcome evaluation: compared to negative outcomes, stress reduced cognitive resources for positive outcomes, which might be related to the enhanced negative emotions induced by stress. The study highlights the importance of focusing on the subjective emotional experience induced by stress in future research on stress and risk decision‐making. We find that stress with negative emotions weakens reward sensitivity, which challenges the reward sensitivity hypothesis. Stress also modifies cognitive resource allocation for outcome evaluation: compared to negative outcomes, stress reduced cognitive resources for positive outcomes. This study underscores the significance of incorporating emotional experiences induced by stress into future investigations about stress and risk decision‐making. [ABSTRACT FROM AUTHOR]

Lung cancer (LC) is one of the malignancies with the highest incidence and mortality in the world, approximately 85% of which is non‐small cell lung cancer (NSCLC). Circular RNAs (circRNAs) exert multiple roles in NSCLC occurrence and development. The sequencing results in previous literature have illustrated that multiple circRNAs exhibit upregulation in NSCLC. We attempted to figure out which circRNA exerts an oncogenic role in NSLCL progression. RT‐qPCR evaluated circDHTKD1 level in NSCLC tissue specimens and cells. Reverse transcription as well as RNase R digestion assay evaluated circDHTKD1 circular characterization in NSCLC cells. FISH determined circDHTKD1 subcellular distribution in NSCLC cells. Loss‐ and gain‐of‐function assays clarified circDHTKD1 role in NSCLC cell growth, tumour growth and glycolysis. Bioinformatics and RIP and RNA pull‐down assessed association of circDHTKD1 with upstream molecule Eukaryotic initiation factor 4A‐III (EIF4A3) or downstream molecule phosphofructokinase‐1 liver type (PFKL) and insulin‐like growth factor 2 mRNA binding protein 2 (IGF2BP2) in NSCLC cells. Rescue assays assessed regulatory function of PFKL in circDHTKD1‐meidated NSCLC cellular phenotypes. CircDHTKD1 exhibited upregulation and stable circular nature in NSCLC cells. EIF4A3 upregulated circDHTKD1 in NSCLC cells. CircDHTKD1 exerted a promoting influence on NSCLC cell malignant phenotypes and tumour growth. CircDHTKD1 exerted a promoting influence on NSCLC glucose metabolism. CircDHTKD1 exerts a promoting influence on NSCLC glucose metabolism through PFKL upregulation. RIP and RNA pull‐down showed that circDHTKD1 could bind to IGF2BP, PFKL could bind to IGF2BP2, and circDHTKD1 promoted the binding of PFKL to IGF2BP2. In addition, RT‐qPCR showed that IGF2BP2 knockdown promoted PFKL mRNA degradation, suggesting that IGF2BP2 stabilized PFKL in NSCLC cells. CircDHTKD1 exhibits upregulation in NSCLC. We innovatively validate that EIF4A3‐triggered circDHTKD1 upregulation facilitates NSCLC glycolysis through recruiting m6A reader IGF2BP2 to stabilize PFKL, which may provide a new direction for seeking targeted therapy plans of NSCLC. [ABSTRACT FROM AUTHOR]

Uterine leiomyosarcoma (uLMS) is the most common subtype of uterine sarcomas. They have a poor prognosis with high rates of recurrence and metastasis. The five-year survival for uLMS patients is between 25 and 76%, with survival rates approaching 10–15% for patients with metastatic disease at the initial diagnosis. Accumulating evidence suggests that several biological pathways are involved in uLMS pathogenesis. Notably, drugs that block abnormal functions of these pathways remarkably improve survival in uLMS patients. However, due to chemotherapy resistance, there remains a need for novel drugs that can target these pathways effectively. In this review article, we provide an overview of the recent progress in ascertaining the biological functions and regulatory mechanisms in uLMS from the perspective of aberrant biological pathways, including DNA repair, immune checkpoint blockade, protein kinase and intracellular signaling pathways, and the hedgehog pathway. We review the emerging role of epigenetics and epitranscriptome in the pathogenesis of uLMS. In addition, we discuss serum markers, artificial intelligence (AI) combined with machine learning, shear wave elastography, current management and medical treatment options, and ongoing clinical trials for patients with uLMS. Comprehensive, integrated, and deeper insights into the pathobiology and underlying molecular mechanisms of uLMS will help develop novel strategies to treat patients with this aggressive tumor. [ABSTRACT FROM AUTHOR]