The depletion in the acetylcholinesterase (AChE) level reveals altered neurotransmission in brain cells. Resultant cellular degeneration was also observed in the radiation-exposed hippocampus. Conclusively, the present study revealed that microwave radiation induces oxidative stress, depleted redox status, and causes DNA damage with the subsequent reduction in working memory in a time-dependent manner. This study provides insight over the associative reciprocity between redox status, cellular degeneration and reduced cholinergic activity, which presumably leads to the behavioral alterations following mobile emitted electromagnetic radiation. V.Promoting healthy endothelialization of the tissue-engineered vascular grafts is of great importance in preventing the occurrence of undesired post-implantation complications including neointimal hyperplasia, late thrombosis, and neoatherosclerosis. Previous researches have demonstrated the crucial role of scaffold topography or stiffness in modulating the behavior of the monolayer endothelial cells (ECs). However, effects of the stiffness of scaffolds with anisotropic topography on ECs with in vivo like oriented morphology has received little attention.  https://www.selleckchem.com/  In this study, aligned fibrous substrates (AFSs) with tunable stiffness (14.68∼2141.72 MPa), similar to the range of stiffness of the healthy and diseased subendothelial matrix, were used to investigate the effects of fiber stiffness on ECs' attachment, orientation, proliferation, function, remodeling and dysfunction. The results demonstrate that stiffness of the AFSs, capable of providing topographical cues, is a crucial endothelium-protective microenvironmental factor by maintaining stable and quiescent endothelium with in vivo like orientation and strong cell-cell junctions. Stiffer AFSs exacerbated the disruption of endothelium integrity, the occurrence of endothelial-to-mesenchymal transition (EndMT), and the inflammation-induced activation in the endothelial monolayer. This study provides new insights into the understanding on how the stiffness of biomimicking anisotropic substrate regulates the structural and functional integrity of the in vivo like endothelial monolayer, and offers essential designing parameters in engineering biomimicking small-diameter vascular grafts for the regeneration of viable blood vessels. Bioactivatable polymer nanoparticles (NPs) have attracted considerable attention as a prospective cancer therapy. Herein, we describe bioactivatable reactive oxygen species (ROS)-sensitive prodrug NPs designed to elicit spatiotemporally controlled, phototriggered chemo-photodynamic therapy. First, an effective anticancer agent, doxorubicin (DOX), was conjugated to poly(ethylene glycol) (PEG) via an ROS-responsive degradable thioketal (TK) linker. The resulting amphiphilic PEG-DOX conjugate (PEG-TK-DOX) self-assembled into a bioactivatable ROS-responsive NP system could efficiently encapsulate a hydrophobic photodynamic therapy (PDT) agent, pheophorbide A (PhA), with good colloidal stability and unimodal size distribution. Second, after the selective retention of NPs in the tumor, the site-specific release of DOX and PhA was spatiotemporally controlled, initially by endogenous ROS and subsequently by exogenous ROS produced during PDT. The locoregional treatment not only photoactivates PhA molecules to generate cytotoxic ROS but also triggers an ROS cascade, which accelerates the release of DOX and PhA via the ROS-mediated structural destruction of NPs, resulting in an enhanced anticancer therapeutic effect. This prodrug-NP system may function as an effective nanomedicine platform, working synergistically to maximize the efficacy of the combination of chemotherapy and photodynamic therapy with a remote-controlled release mechanism. The history of carotenoid research as this progressed from chemistry to biochemistry and biology is outlined. Proposed roles of carotenoids in eye health, as antioxidants, and in protection against cancer and other degenerative diseases, as well as stimulatory effects on the immune system and metabolism are covered. Proposed biological actions must be consistent with the chemistry of carotenoids in the largely aqueous biological systems, which may differ from the known chemistry of carotenoids in organic solvents. In particular, carotenoids tend to form aggregates. The effects of this aggregation and of other molecular interactions in vivo are likely to be crucial to biological activity. These perspectives of the chemistry of carotenoids and carotenoid free radicals are examined and the need for carotenoid samples used in experimental work to be pure and free from breakdown products and pro-oxidant peroxides is emphasised. This article is part of a Special Issue entitled Carotenoids recent advances in cell and molecular biology edited by Johannes von Lintig and Loredana Quadro. V.Viral myocarditis (VMC) is a type of inflammation affecting myocardial cells caused by viral infection and has been an important cause of dilated cardiomyopathy (DCM) worldwide. Type B3 coxsackievirus (CVB3), a non-enveloped positive-strand RNA virus of the Enterovirus genus, is one of most common agent of viral myocarditis. Till now, effective treatments for VMC are lacking due to lack of drugs or vaccine. Lithium chloride (LiCl) is applied in the clinical management of manic depressive disorders. Accumulating evidence have demonstrated that LiCl, also as an effective antiviral drug, exhibited antiviral effects for specific viruses. However, there are few reports of evaluating LiCl's antiviral effect in mice model. Here, we investigated the inhibitory influence of LiCl on the CVB3 replication in vitro and in vivo and the development of CVB3-induced VMC. We found that LiCl significantly suppressed CVB3 replication in HeLa via inhibiting virus-induced cell apoptosis. Moreover, LiCl treatment in vivo obviously inhibited virus replication within the myocardium and alleviated CVB3-induced acute myocarditis. Collectively, our data demonstrated that LiCl inhibited CVB3 replication and negatively regulated virus-triggered inflammatory responses. Our finding further expands the antiviral targets of LiCl and provides an alternative agent for viral myocarditis.