Adhesion Energy-Assisted Low Contact Thermal Resistance Epoxy Resin-Based Composite.

Although intense efforts have been devoted to the development of thermally conductive epoxy resin composites, most previous works ignore the importance of the contact thermal resistance between epoxy resin composites and mating surfaces. Here, we report on epoxy resin/hexagonal boron nitride (h-BN) composites, which show low contact thermal resistance with the contacting surface by tuning adhesion energy. We found that adhesion energy increases with increasing the ratio of soybean-based epoxy resin/amino silicone oil and h-BN contents. The adhesion energy has a negative correlation with the contact thermal resistance; that is, enhancing the adhesion energy will lead to reduced contact thermal resistance. The contact thermal conductance increases with the h-BN contents and is low to 0.025 mm2·K/W for the epoxy resin/60 wt % h-BN composites, which is consistent with the theoretically calculated value. By investigating the wettability and chain dynamics of the epoxy resin/h-BN composites, we confirm that the low contact thermal resistance stems from the increased intermolecular interaction between the epoxy resin chains. The present study provides a practical approach for the development of epoxy resin composites with enhanced thermal conductivity and reduced contact thermal resistance, aiming for effective thermal management of electronics.

p53 suppresses the inflammatory response following respiratory syncytial virus infection by inhibiting TLR2.

-Respiratory syncytial virus (RSV) is a pivotal virus leading to acute lower respiratory tract infections in children under 5 years old. This study aimed to explore the correlation between p53 and Toll-like receptors (TLRs) post RSV infection. p53 levels exhibited a substantial decrease in nasopharyngeal aspirates (NPAs) from infants with RSV infection compared to control group. Manipulating p53 expression had no significant impact on RSV replication or interferon signaling pathway. Suppression of p53 expression led to heightened inflammation following RSV infection in A549 cells or airways of BALB/c mice. while stabilizing p53 expression using Nutlin-3a mitigated the inflammatory response in A549 cells. Additionally, Inhibiting p53 expression significantly increased Toll-like receptor 2 (TLR2) expression in RSV-infected epithelial cells and BALB/c mice. Furthermore, the TLR2 inhibitor, C29, effectively reduced inflammation mediated by p53 in A549 cells. Collectively, our results indicate that p53 modulates the inflammatory response after RSV infection through TLR2.

Targeted therapy in glomerular diseases.

Targeted therapy has emerged as a more precise approach to treat glomerular diseases, focusing on specific molecular or cellular processes that contribute to disease development or progression. This approach complements or replaces traditional immunosuppressive therapy, optimizes supportive care, and provides a more personalized treatment strategy. In this review, we summarize the evolving understanding of pathogenic mechanisms in immune-mediated glomerular diseases and the developing targeted therapies based on these mechanisms. We begin by discussing pan-B-cell depletion, anti-CD20 rituximab, and targeting B-cell survival signaling through the BAFF/APRIL pathway. We also exam specific plasma cell depletion with anti-CD38 antibody. We then shift our focus to complement activation in glomerular diseases, which is involved in antibody-mediated glomerular diseases, such as IgA nephropathy, membranous nephropathy, ANCA-associated vasculitis, and lupus nephritis. Non-antibody-mediated complement activation occurs in glomerular diseases, including C3 glomerulopathy, complement-mediated atypical hemolytic uremic syndrome, and focal segmental glomerulosclerosis. We discuss specific inhibition of terminal, lectin, and alternative pathways in different glomerular diseases. Finally, we summarize current clinical trials targeting the final pathways of various glomerular diseases, including kidney fibrosis. We conclude that targeted therapy based on individualized pathogenesis should be the future of treating glomerular diseases.

Evolution of the complete photonic bandgap of two-dimensional photonic crystal.

In this paper, the complete photonic bandgap (CPBG) of two-dimensional photonic crystals (PCs), which are formed by a square array of solid or hollow dielectric rods connected with dielectric veins, are numerically investigated using the plane wave expansion method. It is clearly demonstrated how the CPBG evolves as the pattern of veins or the type of rods changes. An optimal structure with an ultralarge CPBG is found, whose CPBG reaches Δω=0.22374 (2πc/a), which is larger than those reported in literatures. The proposed structure seems to have promising applications due to its ultralarge CPBG and large fabrication tolerance.