Covalent Organic Frameworks for Neuromorphic Devices.

Neuromorphic computing could enable the potential to break the inherent limitations of conventional von Neumann architectures, which has led to widespread research interest in developing novel neuromorphic memory devices, such as memristors and bioinspired artificial synaptic devices. Covalent organic frameworks (COFs), as crystalline porous polymers, have tailorable skeletons and pores, providing unique platforms for the interplay with photons, excitons, electrons, holes, ions, spins, and molecules. Such features encourage the rising research interest in COF materials in neuromorphic electronics. To develop high-performance COF-based neuromorphic memory devices, it is necessary to comprehensively understand materials, devices, and applications. Therefore, this Perspective focuses on discussing the use of COF materials for neuromorphic memory devices in terms of molecular design, thin-film processing, and neuromorphic applications. Finally, we provide an outlook for future directions and potential applications of COF-based neuromorphic electronics.

Polystyrene nanoplastics affect digestive function and growth in juvenile groupers.

Polystyrene nanoplastics (PS-NPs) can impair antioxidant, immune, and nervous system functions as well as growth and development in aquatic organisms. At present, however, little is known about the effects and underlying mechanisms of PS-NPs on the digestive system of marine fish. Here, we studied the effects of these plastics on the intestinal health and growth performance of juvenile orange-spotted groupers (Epinephelus coioides). Based on histopathological analysis, we found that the liver and intestines can uptake PS-NPs at exposure concentrations of 300 and 3000 µg/ml, respectively. After 14 d of exposure, the activities of digestive enzymes lipase (LPS), trypsin (TRS), and lysozyme (LZM) were reduced, indicating that PS-NPs negatively affected digestive function in juvenile groupers. The PS-NPs also altered microbial community composition, resulting in a decrease in diversity and simplification of network relationships in the intestinal microbiota, but a significant increase in certain harmful bacteria, especially Vibrio and Aliivibrio. In addition, community assembly changed from being driven primarily by deterministic processes (68.89% for control group) to stochastic processes (73.33% and 51.11% for 300 and 3000 µg/ml PS-NP exposure groups, respectively). Furthermore, the specific growth rate (SGR) of the juvenile orange-spotted groupers decreased significantly with increasing PS-NP exposure concentrations (0.158% ± 0.032%, 0.095% ± 0.020%, and 0.074% ± 0.016% for 0, 300, and 3000 µg/L PS-NP groups, respectively). These results suggest that marine PS-NPs are harmful to the digestive system of juvenile fish and highlight the importance of evaluating the long-term impact of NPs in reshaping marine populations.

Polystyrene nanoplastics alter virus replication in orange-spotted grouper (Epinephelus coioides) spleen and brain tissues and spleen cells.

Polystyrene nanoplastics (PS-NPs) are known to impair the function of the digestive system, intestinal flora, immune system, and nervous system of marine organisms. We tested whether PS-NPs influence viral infection of orange-spotted grouper (Epinephelus coioides). We found that grouper spleen (GS) cells took up PS-NPs at exposure concentrations of 5, 50, and 500 µg/mL and experienced cytotoxicity at 50 and 500 µg/mL concentrations. At 12 h after exposure to 50 µg/mL of PS-NPs, the replication of Singapore grouper iridovirus (SGIV) and red-spotted grouper nervous necrosis virus (RGNNV) increased in GS cells after their invasion. Juvenile fish exposed to 300 and 3000 µg/L of PS-NPs for 7 d showed PS-NPs uptake to the spleen and vacuole formation in brain tissue. Moreover, PS-NPs exposure accelerated SGIV replication in the spleen and RGNNV replication in the brain. PS-NP exposure also decreased the expression of toll-like receptor genes and interferon-related genes before and after virus invasion in vitro and in vivo, thus reducing the resistance of cells and tissues to viral replication. This is the first report that PS-NPs have toxic effects on GS cells and spleen and brain tissues, and it provides new insights into assessing the impact of PS-NPs on marine fish.

The ERß-CXCL19/CXCR4-NFκB pathway is critical in mediating the E2-induced inflammation response in the orange-spotted grouper (Epinephelus coioides).

The main physiological function of 17ß-estradiol (E2) in vertebrates is to regulate sexual development and reproduction. In fish, especially hermaphroditic fish, estrogen is often used to aid reproduction, but it also can trigger an inflammatory response. However, the molecular mechanism for this E2-induced inflammatory reaction is not clear. In this study, we found that the ERß-CXCL19/CXCR4-NFκB cascade regulated the E2-induced inflammatory response in the orange-spotted grouper (Epinephelus coioides). Strikingly, E2 treatment resulted in significantly high expression of inflammatory cytokines and induced phosphorylation and degradation of IκBα and translocation of NFκB subunit p65 to the nucleus in grouper spleen cells. However, the E2-induced inflammatory response could be prevented by the broad estrogen receptor (ER) ligand ICI 182,780. Moreover, the luciferase assay showed that E2 induced the inflammatory response by activating the promotor of chemokine CXCL19 through ERß1 and ERß2. Knockdown of CXCL19 blocked the E2-induced inflammatory response and NFκB nucleus translocation. Additionally, knockdown of chemokines CXCR4a and CXCR4b together, but not alone, blocked the E2-induced inflammatory response. The immunofluorescence assay and co-immunoprecipitation analysis showed that CXCL19 mediated the E2-induced inflammatory response by activating CXCR4a or CXCR4b. Taken together, these results showed that the ERß-CXCL19/CXCR4-NFκB pathway mediated the E2-induced inflammatory response in grouper. These findings are valuable for future comparative immunological studies and provide a theoretical basis for mitigating the adverse reactions that occur when using E2 to help fish reproduce.