Advances in understanding of dendritic cell in the pathogenesis of acute kidney injury

Acute kidney injury (AKI) is characterized by a rapid decline in renal function and is associated with a high morbidity and mortality rate. At present, the underlying mechanisms of AKI remain incompletely understood. Immune disorder is a prominent feature of AKI, and dendritic cells (DCs) play a pivotal role in orchestrating both innate and adaptive immune responses, including the induction of protective proinflammatory and tolerogenic immune reactions. Emerging evidence suggests that DCs play a critical role in the initiation and development of AKI. This paper aimed to conduct a comprehensive review and analysis of the role of DCs in the progression of AKI and elucidate the underlying molecular mechanism. The ultimate objective was to offer valuable insights and guidance for the treatment of AKI

Nanostructural origin of semiconductivity and large magnetoresistance in epitaxial NiCo\u3csub\u3e2\u3c/sub\u3eO\u3csub\u3e4\u3c/sub\u3e/Al\u3csub\u3e2\u3c/sub\u3eO\u3csub\u3e3\u3c/sub\u3e thin films

Despite low resistivity (~1 mΩ cm), metallic electrical transport has not been commonly observed in inverse spinel NiCo2O4, except in certain epitaxial thin films. Previous studies have stressed the effect of valence mixing and the degree of spinel inversion on the electrical conduction of NiCo2O4 films. In this work, we studied the effect of nanostructural disorder by comparing the NiCo2O4 epitaxial films grown on MgAl2O4 (1 1 1) and on Al2O3 (0 0 1) substrates. Although the optimal growth conditions are similar for the NiCo2O4 (1 1 1)/MgAl2O4 (1 1 1) and the NiCo2O4 (1 1 1)/Al2O3 (0 0 1) films, they show metallic and semiconducting electrical transport, respectively. Post-growth annealing decreases the resistivity of NiCo2O4 (1 1 1)/Al2O3 (0 0 1) films, but the annealed films are still semiconducting. While the semiconductivity and the large magnetoresistance in NiCo2O4 (1 1 1)/Al2O3 (0 0 1) films cannot be accounted for in terms of non-optimal valence mixing and spinel inversion, the presence of anti-phase boundaries between nano-sized crystallites, generated by the structural mismatch between NiCo2O4 and Al2O3, may explain all the experimental observations in this work. These results reveal nanostructural disorder as being another key factor for controlling the electrical transport of NiCo2O4, with potentially large magnetoresistance for spintronics applications

Liquid-Ammonia-Mediated Dyeing Process of Wool at a Lower Temperature

Liquid ammonia as a non-aqueous medium has many physical properties close to water, such as small molecular weight and strong permeability. It has been widely used for the ecological processing of cellulosic fibers to improve their luster, softness and dyeing properties. However, there are few reports on the dyeing of wool treated with liquid ammonia, especially at a lower temperature. Herein, a continuous liquid ammonia finishing machine was used to batch process wool followed by dyeing in a commonly-used wool dyeing machine. The results showed that many scale flakes and some cuticle cracking were seen on the fiber surface, and the disulfide bonds of cystine were broken down after liquid ammonia treatment, which promoted the diffusion of dyestuff into the fiber. Moreover, the uptakes and K/S value of wool dyed with Lanaset and Lanasol CE dyes were higher than the untreated wool, and the dyeing temperature could decrease to 85 °C, while the degree of fiber strength reduction merely decreased by 3–5%. Furthermore, for the reactive dyes, the dyeing temperature can reduce to 70 °C with the chemical auxiliaries Miralan LTD, while the degree of strength reduction decrease by 8–10%. Liquid ammonia treatment can be used for dyeing at a lower temperature than boiling temperature (100 °C), reduce energy consumption and reduce the degree of fiber strength reduction of wool. The method shows considerable to great value and is significant in providing a feasible approach for the industrial application of low-temperature dyeing technology

EGFR/MAPK signaling pathway acts as a potential therapeutic target for sulforaphane-rescued heart tube malformation induced by various concentrations of PhIP exposure

Background: 2-Amino-1-methyl-6-phenylimidazo [4,5-b] pyrimidine (PhIP) is a known carcinogen generated mainly from cooking meat and environmental pollutants. It is worth exploring the potential of natural small-molecule drugs to protect against adverse effects on embryonic development. Purpose: In this study, we investigated the potential toxicological effects of PhIP on embryonic heart tube formation and the effect of Sulforaphane (SFN) administration on the anti-toxicological effects of PhIP on embryonic cardiogenesis. Study design and methods: First, the chicken embryo model was used to investigate the different phenotypes of embryonic heart tubes induced by various concentrations of PhIP exposure. We also proved that SFN rescues PhIP-induced embryonic heart tube malformation. Second, immunofluorescence, western blot, Polymerase Chain Reaction (PCR) and flow cytometry experiments were employed to explore the mechanisms by which SFN protects cardiac cells from oxidative damage in the presence of PhIP. We used RNA-seq analysis, molecular docking, in situ hybridization, cellular thermal shift assay and solution nuclear magnetic resonance spectroscopy to explore whether SFN protects cardiogenesis through the EGFR/MAPK signaling pathway. Results: The study showed that PhIP might dose-dependently interfere with the C-looping heart tube (mild) or the fusion of a pair of bilateral endocardial tubes (severe) in chick embryos, while SFN administration prevented cardiac cells from oxidative damage in the presence of high-level PhIP. Furthermore, we found that excessive reactive oxygen species (ROS) production and subsequent apoptosis were not the principal mechanisms by which low-level PhIP induced malformation of heart tubes. This is due to PhIP-disturbed Mitogen-activated protein kinase (MAPK) signaling pathway could be corrected by SFN administration. Conclusions: This study provided novel insight that PhIP exposure could increase the risk of abnormalities in early cardiogenesis and that SFN could partially rescue various concentrations of PhIP-induced abnormal heart tube formation by targeting EGFR and mediating EGFR/MAPK signaling pathways