Sullivanbarnett0441

Correction for 'Utilization of a Pt(ii) di-yne chromophore incorporating a 2,2'-bipyridine-5,5'-diyl spacer as a chelate to synthesize a green and red emitting d-f-d heterotrinuclear complex' by Idris Juma Al-Busaidi et al., Dalton Trans., 2021, DOI 10.1039/d0dt04198j.Alcoholic liver diseases (ALDs) impose a substantial health burden on many countries. Bioactive peptides isolated from people, marine organisms, animals and plants have shown hepatoprotective effects on animal and hepatocyte models. In this study, an LO2 cell model of ethanol-induced liver injury in vitro was constructed. We investigated the hepatoprotective effects of the three-spot seahorse bioactive peptide (SBP) PAGPRGPA (Pro-Ala-Gly-Pro-Arg-Gly-Pro-Ala; 721.39 Da) and characterised the underlying metabolic pathways and biomarkers through a nontargeted metabolomics approach. We found that ethanol-induced oxidative stress impaired the cellular antioxidant system, leading to an imbalance in cellular homeostasis. However, SBP with a certain antioxidant activity inhibited reactive oxygen species (ROS) production, excessive intracellular Ca2+ level and abnormal apoptosis. JAK activation It also restored the superoxide dismutase (SOD) and glutathione (GSH) levels and attenuated ethanol-induced oxidative damage and inflammation. SBP suppressed the activation of mitogen-activated protein kinase (MAPK) in ethanol-stimulated LO2 cells. It also regulated the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) signalling pathway to protect LO2 cells from oxidative damage by promoting the expression of antioxidant enzymes, such as heme oxygenase-1 (HO-1). Furthermore, the metabolomics approach demonstrated nine different biomarkers and six metabolic pathways. In summary, the hepatoprotective mechanisms of SBP in vitro, which can be attributed to the upregulation of antioxidant substances and amino acid metabolism, attenuate ethanol-induced oxidative stress.Intestinal epithelial cells are the primary biological barriers for orally administrated nano-formulations and the delivered protein drugs. Thereinto, besides the cellular uptake, intracellular trafficking pathway and the related exocytosis are of great importance to the trans-epithelial transport of drug-loaded NPs. Herein, inspired by the physiological functions of Golgi apparatus for secreting proteins out of cells, Golgi localization-related amino acid l-cysteine (Cys) was modified on the surface of NPs to see whether and how this modification could guide the Golgi pathway-related transport and facilitate the exocytosis of drug-loaded NPs. Meanwhile, cell-penetrating peptide octa-arginine (R8) was co-modified to increase the cellular uptake. The proportion of R8 and Cys modification was explored to get the best effect of endocytosis and exocytosis of NPs. As a result, 25%R8 + 75%Cys NPs with most Cys modification showed efficient transcytosis with the highest transcytosis/endocytosis ratio (0.87). Interesng to facilitate the exocytosis of NPs, thus further improving the oral absorption of loaded protein drugs.Nonlinear photonic crystals are capable of highly efficient nonlinear wavefront manipulation, providing a promising platform for compact and large-scale integrated nonlinear devices. However, the current nonlinear encoding methods for nonlinear photonic crystals inherently require a number of disordered and complex microstructures, which are quite challenging in a real fabrication process. Herein we propose and experimentally demonstrate a nonlinear detour phase method for nonlinear wavefront manipulation in nonlinear photonic crystals. With the proposed method, the designed nonlinear detour phase hologram only requires a set of basic building blocks with simple shapes, which are easy to fabricate by using the femtosecond laser writing technique. The second-harmonic hologram is demonstrated by designing the nonlinear detour phase patterns, and the quasi-phase-matching scheme in the second-harmonic holographic imaging process is also discussed. This study conceptually extends the conventional detour phase method into the nonlinear regime, offering new possibilities for compact nonlinear micro-devices with multi-functions.A novel hybrid supramolecular system with near-infrared photon-excited energy transfer has been successfully constructed, relying on the assistance of upconversion nanoparticles in platinum(ii)-based supramolecular polymers. The resulting hybrid system is capable of displaying intriguing photo-switchable and sequential energy transfer features.Urban particulate matter (UPM), an air pollutant-absorbing toxic substance, can access alveoli, leading to pulmonary diseases. Studies have shown that the water-soluble components of UPM (WS-UPM), containing main toxic substances, can induce oxidative damage in lung cells. In this study, the UPM particle size and composition were detected via instrumental analysis. The isoflavones (biochanin A (BCA), formononetin and daidzein) from chickpeas possess biological antioxidant properties. The present study aimed to investigate the mechanism of the oxidative damage induced by WS-UPM, and the protective role of isoflavones in human alveolar basal epithelial cells. The antioxidant activity of BCA, formononetin and daidzein was investigated through the total reduction capacity, diphenylpicrylhydrazine radical (DPPH), superoxide radical, and hydroxyl radical scavenging capacity detection. We also established cell models in vitro to further explore the BCA-protective mechanism. BCA presented a significant protection, and increased the levels of antioxidant makers including superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). The effects were also reflected as the reduction of malondialdehyde (MDA) and nitric oxide (NO). Moreover, results obtained from RT-PCR and western blot techniques revealed that MEK5/ERK5 played an indispensable role in regulating the antioxidant effect of BCA, alleviating WS-UPM-induced lung injury. Furthermore, BCA mitigated WS-UPM-exposed damage through upregulating the Nrf2 signaling pathway to enhance the antioxidase expression downstream of Nrf2. In summary, our findings indicated that the WS-UPM-induced pulmonary disease was involved in oxidative stress and the MEK5/ERK5-Nrf2 signaling pathway, and BCA regulated the WS-UPM-induced lung damage via upregulation of the MEK5/ERK5-Nrf2 pathway.