Recent advances in technology are expected to increase our current understanding of neuroscience. Nanotechnology and nanomaterials can alter and control neural functionality in both in vitro and in vivo experimental setups. The intersection between neuroscience and nanoscience may generate long-term neural interfaces adapted at the molecular level. Owing to their intrinsic physicochemical characteristics, gold nanostructures (GNSs) have received much attention in neuroscience, especially for combined diagnostic and therapeutic (theragnostic) purposes. GNSs have been successfully employed to stimulate and monitor neurophysiological signals. Hence, GNSs could provide a promising solution for the regeneration and recovery of neural tissue, novel neuroprotective strategies, and integrated implantable materials. This review covers the broad range of neurological applications of GNS-based materials to improve clinical diagnosis and therapy. Sub-topics include neurotoxicity, targeted delivery of therapeutics to the central nervous system (CNS), neurochemical sensing, neuromodulation, neuroimaging, neurotherapy, tissue engineering, and neural regeneration. It focuses on core concepts of GNSs in neurology, to circumvent the limitations and significant obstacles of innovative approaches in neurobiology and neurochemistry, including theragnostics. We will discuss recent advances in the use of GNSs to overcome current bottlenecks and tackle technical and conceptual challenges.

Overall process of stem cell derivation and isolation, as well as microfluidic stem cell culture and neural tissue engineering.

Nanotechnology could provide a new complementary approach to treat coronary artery disease (CAD) which is now one of the biggest killers in the Western world. The course of events, which leads to atherosclerosis and CAD, involves many biological factors and cellular disease processes which may be mitigated by therapeutic methods enhanced by nanotechnology. Nanoparticles can provide a variety of delivery systems for cargoes such as drugs and genes that can address many problems within the arteries. In order to improve the performance of current stents, nanotechnology provides different nanomaterial coatings, in addition to controlled-release nanocarriers, to prevent in-stent restenosis. Nanotechnology can increase the efficiency of drugs, improve local and systematic delivery to atherosclerotic plaques and reduce the inflammatory or angiogenic response after intravascular intervention. Nanocarriers have potential for delivery of imaging and diagnostic agents to precisely targeted destinations. This review ...

Interleukin 4 (IL4) and interleukin 13 (IL13) are closely related cytokines that have been classically attributed to type II immunity, namely, differentiation of T-helper 2 (T_H2) cells and alternative activation of macrophages. Although the role of IL4/13 has been well described in various contexts such as defense against helminth parasites, pathogenesis of allergic disease, and several models of wound healing, relatively little is known about the role of IL4/13 in the heart following injury. Emerging literature has identified various roles for IL4/13 in animal models of cardiac regeneration as well as in the adult mammalian heart following myocardial injury. Notably, although IL4 and IL13 signal to hematopoietic cell types following myocardial infarction (MI) to promote wound healing phenotypes, there is substantial evidence that these cytokines can signal directly to non-hematopoietic cell types in the heart during development, homeostasis, and following injury. Comprehensive understanding of the molecular and cellular actions of IL4/13 in the heart is still lacking, but overall evidence to date suggests that activation of these cytokines results in beneficial outcomes with respect to cardiac repair. Here, we aim to comprehensively review the role of IL4 and IL13 and their prospective mechanisms in cardiac regeneration and repair.

Here, we investigate the potential of epidermal growth factor receptor (EGFR) inhibition to prevent vascular calcification, a leading indicator of and contributor to cardiovascular morbidity and mortality. EGFR interacts and affects the trafficking of the plasma membrane scaffolding protein caveolin-1. Previous studies reported a key role for caveolin-1 in the development of specialized extracellular vesicles that mediate vascular calcification; however, no role of EGFR has been reported. We demonstrated that EGFR inhibition modulates caveolin-1 trafficking and hinders calcifying extracellular vesicle formation, which prevents vascular calcification. Given that EGFR inhibitors are clinically approved for other indications, this may represent a novel therapeutic strategy for vascular calcification.