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Based on the linear regression algorithm, this paper uses the basic linear regression algorithm and the kernel linear regression algorithm to construct the relationship model between academic input and academic achievement based on linear regression and to determine the independent variables, dependent variables and control variables in the model. The engineering students of East China Normal University are selected as the research object, the research instrument is determined, the research index is determined according to the survey, and the research hypothesis is proposed, and then the research and analysis design of the impact of academic input on academic achievement is completed. Using reliability and validity to test the validity of the questionnaire, the initial data of the study can be obtained by distributing the questionnaire, and correlation analysis and regression analysis are used to carry out an empirical study of academic input and academic achievement based on linear regression. The results show that the correlation coefficient between academic input and academic achievement of master’s degree students is R=0.892 and R2=0.792, indicating that the predictive variance of academic input on academic achievement is 89.2%. The effects of the dimensions under the academic input on the social adjustment dimension under the academic achievement were, in descending order, as follows: active cooperation > teacher-student interaction > educational enrichment > academic challenge > campus support. This study comprehensively analyzes the impact of academic engagement on academic achievement, and colleges and universities should change the test of students’ ability to memorize knowledge and skills to the test of students’ ability to analyze and solve problems by applying what they have learned.

Pathological hyperphosphorylation and aggregation of microtubule‐associated Tau protein contribute to Alzheimer's Disease (AD) and other related tauopathies. Currently, no cure exists for Alzheimer's Disease. Aptamers offer significant potential as next‐generation therapeutics in biotechnology and the treatment of neurological disorders. Traditional aptamer selection methods for Tau protein focus on binding affinity rather than interference with pathological Tau. In this study, we developed a new selection strategy to enrich DNA aptamers that bind to surviving monomeric Tau protein under conditions that would typically promote Tau aggregation. Employing this approach, we identified a set of aptamer candidates. Notably, BW1c demonstrates a high binding affinity (Kd=6.6 nM) to Tau protein and effectively inhibits arachidonic acid (AA)‐induced Tau protein oligomerization and aggregation. Additionally, it inhibits GSK3β‐mediated Tau hyperphosphorylation in cell‐free systems and okadaic acid‐mediated Tau hyperphosphorylation in cellular milieu. Lastly, retro‐orbital injection of BW1c tau aptamer shows the ability to cross the blood brain barrier and gain access to neuronal cell body. Through further refinement and development, these Tau aptamers may pave the way for a first‐in‐class neurotherapeutic to mitigate tauopathy‐associated neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

Piezoelectric actuators can offer micro/nano-level precision actuating ability and have been employed in different applications. For the piezoelectric actuating systems, the output actuating performance is affected not only by the internal non-smooth hysteresis but also by the operating load and the excitation frequency. To improve the actuating precision, predicting the nonlinear behaviour of the piezoelectric actuating system is essential for effective designs of control approaches. In this paper, a modified rate-dependent Prandtl–Ishlinskii model is presented to explore the coupling effects analytically between the internal hysteresis and the operating frequency with the external loads and predict the output behaviour of the piezoelectric actuating system accurately. The proposed modelling method is testified on a piezoelectric actuating platform under broad ranges of excitation frequencies (1–80 Hz) and external loads (0–0.5 kg), and the comparison results using the rate-dependent Prandtl–Ishlinskii (RDPI) model are also provided to prove the precision of the proposed method. Combining with the modified RDPI model, a guaranteeing preselected tracking controller is developed to ensure the output performance, and a set of tracking experiments under different frequencies with load is performed. The experimental results compared with PID control performance validate the effectiveness of the proposed prescribed performance control method and its high actuating performance against the adverse effects from the external hysteresis nonlinearities and external loads. [ABSTRACT FROM AUTHOR]

Pathological hyperphosphorylation and aggregation of microtubule-associated Tau protein contribute to Alzheimer's Disease (AD) and other related tauopathies. Currently, no cure exists for Alzheimer's Disease. Aptamers offer significant potential as next-generation therapeutics in biotechnology and the treatment of neurological disorders. Traditional aptamer selection methods for Tau protein focus on binding affinity rather than interference with pathological Tau. In this study, we developed a new selection strategy to enrich DNA aptamers that bind to surviving monomeric Tau protein under conditions that would typically promote Tau aggregation. Employing this approach, we identified a set of aptamer candidates. Notably, BW1c demonstrates a high binding affinity (K d =6.6 nM) to Tau protein and effectively inhibits arachidonic acid (AA)-induced Tau protein oligomerization and aggregation. Additionally, it inhibits GSK3β-mediated Tau hyperphosphorylation in cell-free systems and okadaic acid-mediated Tau hyperphosphorylation in cellular milieu. Lastly, retro-orbital injection of BW1c tau aptamer shows the ability to cross the blood brain barrier and gain access to neuronal cell body. Through further refinement and development, these Tau aptamers may pave the way for a first-in-class neurotherapeutic to mitigate tauopathy-associated neurodegenerative disorders., (© 2024 The Authors. Angewandte Chemie International Edition published by Wiley-VCH GmbH.)

Objective: To summarize the effect of cartilage progenitor cells (CPCs) and microRNA-140 (miR-140) on the repair of osteoarthritic cartilage injury, and analyze their clinical prospects., Methods: The recent researches regarding the CPCs, miR-140, and repair of cartilage in osteoarthritis (OA) disease were extensively reviewed and summarized., Results: CPCs possess the characteristics of self-proliferation, expression of stem cell markers, and multi-lineage differentiation potential, and their chondrogenic ability is superior to other tissues-derived mesenchymal stem cells. CPCs are closely related to the development of OA, but the autonomic activation and chondrogenic ability of CPCs around the osteoarthritic cartilage lesion cannot meet the requirements of complete cartilage repair. miR-140 specifically express in cartilage, and has the potential to activate CPCs by inhibiting key molecules of Notch signaling pathway and enhance its chondrogenic ability, thus promoting the repair of osteoarthritic cartilage injury. Intra-articular delivery of drugs is one of the main methods of OA treatment, although intra-articular injection of miR-140 has a significant inhibitory effect on cartilage degeneration in rats, it also exhibit some limitations such as non-targeted aggregation, low bioavailability, and rapid clearance. So it is a good application prospect to construct a carrier with good safety, cartilage targeting, and high-efficiency for miR-140 based on articular cartilage characteristics. In addition, CPCs are mainly dispersed in the cartilage surface, while OA cartilage injury also begins from this layer, it is therefore essential to emphasize early intervention of OA., Conclusion: miR-140 has the potential to activate CPCs and promote the repair of cartilage injury in early OA, and it is of great clinical significance to further explore the role of miR-140 in OA etiology and to develop new OA treatment strategies based on miR-140.