An Analytical Mechanics Model for the Rotary Sliding Triboelectric Nanogenerator.

In recent years, global attention towards new energy has surged due to increasing energy demand and environmental concerns. Researchers have intensified their focus on new energy, leading to advancements in technologies like triboelectrification, which harnesses energy from the environment. The invention of the triboelectric nanogenerator (TENG) has led to new possibilities, with the rotary sliding TENG standing out for its superior performance. However, understanding its mechanical behavior remains a challenge, potentially leading to structural issues. This paper introduces a novel analytical mechanics model to analyze the mechanical performance of the stator of the rotary sliding TENG, offering a new analytical solution. The solution also presents an innovative approach to solving axisymmetric problems in elasticity theory since it challenges a traditional assumption that the stress function depends solely on the radial coordinate, proposing a new stress function to derive a more general solution, supplementing the classical approach in the theory of elasticity. Through the obtained solutions, the mechanical characteristics of the rotary sliding TENG during operation are analyzed. A clearer relationship between mechanical characteristics and electrical output is expected to provide a theoretical basis for the design of the rotary sliding TENG.

An Analytical Thermal Buckling Model for Semiconductor Chips on a Substrate.

Semiconductor chips on a substrate have a wide range of applications in electronic devices. However, environmental temperature changes may cause mechanical buckling of the chips, resulting in an urgent demand to develop analytical models to study this issue with high efficiency and accuracy such that safety designs can be sought. In this paper, the thermal buckling of chips on a substrate is considered as that of plates on a Winkler elastic foundation and is studied by the symplectic superposition method (SSM) within the symplectic space-based Hamiltonian system. The solution procedure starts by converting the original problem into two subproblems, which are solved by using the separation of variables and the symplectic eigenvector expansion. Through the equivalence between the original problem and the superposition of subproblems, the final analytical thermal buckling solutions are obtained. The SSM does not require any assumptions of solution forms, which is a distinctive advantage compared with traditional analytical methods. Comprehensive numerical results by the SSM for both buckling temperatures and mode shapes are presented and are well validated through comparison with those using the finite element method. With the solutions obtained, the effects of the moduli of elastic foundations and geometric parameters on critical buckling temperatures and buckling mode shapes are investigated.

A TGFBR2/SMAD2/DNMT1/miR-145 negative regulatory loop is responsible for LPS-induced sepsis.

The critical roles of TGFBR2/Smad2 signaling have been established in LPS-induced sepsis, however, the underlying mechanisms by which TGFBR2/Smad2 signaling was regulated in LPS-induced sepsis are still confused. Here, miRNA-based on RNA-sequencing dataset revealed that miR-145 was significantly decreased in human umbilical vein endothelial cells (HUVECs) following LPS treatment. Bioinformatics, luciferase reporter and RNA immune co-precipitation (RIP) assays showed that miR-145 could directly target TGFBR2 and thus inactivated TGFBR2/Smad2 axis. On the contrary, luciferase reporter and chromatin immunoprecipitation (ChIP) analysis showed that Smad2 could directly bind to DNA methyltransferase 1 (DNMT1), the upregulation of which led to miR-145 promoter hypermethylation and downregulation of miR-145 expression, conversely promoting TGFBR2 expression. Notably, knockdown of TGFBR2 partially rescued the inhibition on miR-145 expression induced by LPS treatment. Additionally, we found that knockdown of TGFBR2 or overexpression of miR-145 attenuated LPS-induced sepsis and prolonged the overall survival of septic mice. Furthermore, TGFBR2 overexpression abrogated miR-145 overexpression-mediated attenuation on LPS-induced sepsis. Our results demonstrate the TGFBR2/SMAD2/DNMT1/miR-145 negative regulatory loop is responsible for LPS-induced sepsis.