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In this paper, an analytical expression for describing propagation properties of twisted Gaussian Schell model array (TGSMA) beams through turbulent biological tissues is derived based on the extended Huygens Fresnel integral. With the help of the formulae, properties of the rotation and mergence for the TGSMA beams in turbulent biological tissues are researched in detail. It is found that the TGSMA beams go through the distinct mergence period in the far field besides phenomena of abruption and rotation in the near field, and turbulent biological tissues play a dominated role in mergence of the TGSMA beams. These novel results may be helpful in optical trapping.

Compressed air energy storage (CAES) technology has attracted growing attention because of the demand for load shifting and electricity cost reduction in energy‐intensive industries. To increase the round‐trip efficiency and energy storage density and simplify the structure of advanced adiabatic CAES (AA‐CAES) systems, a waste heat‐assisted CAES (WH‐CAES) design integrating a tube‐in‐tube thermal energy storage unit and an organic Rankine cycle (ORC) is described herein. Thermodynamic models of the proposed WH‐CAES system are established, and the effects of waste heat temperature, ratio of compression ratios, ratio of expansion ratios, and air storage cavern pressure on the performance of different systems, including AA‐CAES and WH‐CAES with and without ORC, are investigated. The results show that when the waste heat temperature is 500 °C, the input work of the compressors reaches its minimum value at a ratio of compression ratios of 1.14, and the optimal ratio of expansion ratios is 0.39. Under these optimal operating conditions, compared with the AA‐CAES system, the round‐trip storage efficiency, energy storage density, and system energy efficiency of the WH‐CAES system can be increased significantly. The findings validate the potential of the proposed WH‐CAES system. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is the most common joint disease. Currently there are no effective methods that simultaneously prevent joint degeneration and reduce pain1. Although limited evidence suggests the existence of voltage-gated sodium channels (VGSCs) in chondrocytes2, their expression and function in chondrocytes and in OA remain essentially unknown. Here we identify Nav1.7 as an OA-associated VGSC and demonstrate that human OA chondrocytes express functional Nav1.7 channels, with a density of 0.1 to 0.15 channels per µm2 and 350 to 525 channels per cell. Serial genetic ablation of Nav1.7 in multiple mouse models demonstrates that Nav1.7 expressed in dorsal root ganglia neurons is involved in pain, whereas Nav1.7 in chondrocytes regulates OA progression. Pharmacological blockade of Nav1.7 with selective or clinically used pan-Nav channel blockers significantly ameliorates the progression of structural joint damage, and reduces OA pain behaviour. Mechanistically, Nav1.7 blockers regulate intracellular Ca2+ signalling and the chondrocyte secretome, which in turn affects chondrocyte biology and OA progression. Identification of Nav1.7 as a novel chondrocyte-expressed, OA-associated channel uncovers a dual target for the development of disease-modifying and non-opioid pain relief treatment for OA.The voltage-gated sodium channel Nav1.7 has a dual role in osteoarthritis—in chondrocytes, it promotes joint damage, and in dorsal root ganglia neurons, it increases pain transmission. [ABSTRACT FROM AUTHOR]

TNFR1 and TNFR2 have received prominent attention because of their dominance in the pathogenesis of inflammation and autoimmunity. TNFR1 has been extensively studied and primarily mediates inflammation. TNFR2 remains far less studied, although emerging evidence demonstrates that TNFR2 plays an antiinflammatory and immunoregulatory role in various conditions and diseases. Herein, we report that TNFR2 regulates macrophage polarization, a highly dynamic process controlled by largely unidentified intracellular regulators. Using biochemical copurification and mass spectrometry approaches, we isolated the signaling molecule 14-3-3[epsilon] as a component of TNFR2 complexes in response to progranulin stimulation in macrophages. In addition, 14-3-3[epsilon] was essential for TNFR2 signaling-mediated regulation of macrophage polarization and switch. Both global and myeloid-specific deletion of 14-3-3[epsilon] resulted in exacerbated inflammatory arthritis and counteracted the protective effects of progranulin-mediated TNFR2 activation against inflammation and autoimmunity. TNFR2/14-3-3[epsilon] signaled through PI3K/Akt/mTOR to restrict NF-[kappa]B activation while simultaneously stimulating C/EBP[beta] activation, thereby instructing macrophage plasticity. Collectively, this study identifies 14-3-3[epsilon] as a previously unrecognized vital component of the TNFR2 receptor complex and provides new insights into the TNFR2 signaling, particularly its role in macrophage polarization with therapeutic implications for various inflammatory and autoimmune diseases with activation of the TNFR2/14-3-3[epsilon] antiinflammatory pathway., Introduction Rheumatoid arthritis (RA) is a common chronic autoimmune condition characterized by inflammatory joint disease (1), resulting from protracted inflammation of the synovial membrane. Macrophages are a major subset of [...]