The host immune system is highly compromised in case of viral infections and relapses are very common. The capacity of the virus to destroy the host cell by liberating its own DNA or RNA and replicating inside the host cell poses challenges in the development of antiviral therapeutics. In recent years, many new technologies have been explored for diagnosis, prevention, and treatment of viral infections. Nanotechnology has emerged as one of the most promising technologies on account of its ability to deal with viral diseases in an effective manner, addressing the limitations of traditional antiviral medicines. It has not only helped us to overcome problems related to solubility and toxicity of drugs, but also imparted unique properties to drugs, which in turn has increased their potency and selectivity toward viral cells against the host cells. The initial part of the paper focuses on some important proteins of influenza, Ebola, HIV, herpes, Zika, dengue, and corona virus and those of the host cells important for their entry and replication into the host cells. This is followed by different types of nanomaterials which have served as delivery vehicles for the antiviral drugs. It includes various lipid-based, polymer-based, lipid-polymer hybrid-based, carbon-based, inorganic metal-based, surface-modified, and stimuli-sensitive nanomaterials and their application in antiviral therapeutics. The authors also highlight newer promising treatment approaches like nanotraps, nanorobots, nanobubbles, nanofibers, nanodiamonds, nanovaccines, and mathematical modeling for the future. The paper has been updated with the recent developments in nanotechnology-based approaches in view of the ongoing pandemic of COVID-19.Graphical abstract.Advancing age, female sex, recent prior fracture and falls, and specific comorbidities and medications contribute to imminent (within 1-2 years) risk of fracture in Medicare enrollees. Clinician awareness of these risk factors and their dynamic nature may lead to improved osteoporosis care for elderly patients. The burden of osteoporotic fracture disproportionately affects the elderly. Growing awareness that fracture risk can change substantially over time underscores the need to understand risk factors for imminent (within 1-2years) fracture. This study assessed predictors of imminent risk of fracture in the US Medicare population. Administrative claims data from a random sample of Medicare beneficiaries were analyzed for patients aged ≥ 67years on January 1, 2011 (index date), with continuous coverage between January 1, 2009 and March 31, 2011, excluding patients with non-melanoma cancer or Paget's disease. Incident osteoporotic fractures were identified during 12 and 24months post-index. Potential predidications contribute to imminent risk of fracture in elderly patients. Demographics and factors including fall/fracture history, comorbidities, and medications contribute to imminent risk of fracture in elderly patients.Pathological remodelling of the myocardium, including inflammation, fibrosis and hypertrophy, in response to acute or chronic injury is central in the development and progression of heart failure (HF). While both resident and infiltrating cardiac cells are implicated in these pathophysiological processes, recent evidence has suggested that endothelial cells (ECs) may be the principal cell type responsible for orchestrating pathological changes in the failing heart. Epigenetic modification of nucleic acids, including DNA, and more recently RNA, by methylation is essential for physiological development due to their critical regulation of cellular gene expression. As accumulating evidence has highlighted altered patterns of DNA and RNA methylation in HF at both the global and individual gene levels, much effort has been directed towards defining the precise role of such cell-specific epigenetic changes in the context of HF. Considering the increasingly apparent crucial role that ECs play in cardiac homeostasis and disease, this article will specifically focus on nucleic acid methylation (both DNA and RNA) in the failing heart, emphasising the key influence of these epigenetic mechanisms in governing EC function. This review summarises current understanding of DNA and RNA methylation alterations in HF, along with their specific role in regulating EC function in response to stress (e.g. hyperglycaemia, hypoxia). Improved appreciation of this important research area will aid in further implicating dysfunctional ECs in HF pathogenesis, whilst informing development of EC-targeted strategies and advancing potential translation of epigenetic-based therapies for specific targeting of pathological cardiac remodelling in HF. The signaling pathways of tropomyosin-related kinase B (TrkB) receptor play a pivotal role in axonal sprouting, proliferation of dendritic arbor, synaptic plasticity, and neuronal differentiation. https://www.selleckchem.com/products/fatostatin.html of BDNF and TrkB receptor were reduced in patients with Alzheimer's disease (AD). The activation of TrkB signaling pathways is a potential strategy for AD therapies. #link# We intended to identify potential TrkB agonists to activate the neuroprotective signaling to alleviate the pathological features of AD mice. Both of the Aβ-deteriorated hippocampal primary neurons and mouse models were generated and showed AD characteristics. We first investigated 12 potential TrkB agonists with primary hippocampal neurons of mice. Both 7,8-DHF and LMDS-1 were identified to have better effect than the other compounds on dendritic arborization of the neurons and were further applied to the Aβ-injected mouse model. The short-term cognitive behavior and pathology in the mice were improved by LMDS-1. Further investigation indicated that LMDS-1 activated the TrkB through phosphorylation at Y516 rather than Y816. In addition, the ERK but not CaMKII or Akt was activated in the mouse hippocampus with LMDS-1 administration. LMDS-1 treatment also upregulated CREB and BDNF while downregulated the GSK3β active form and tau phosphorylation. This study suggests that LMDS-1 upregulates the expression of BDNF and ameliorates the early-phase phenotypes of the AD-like mice through the pTrkB (Y516)-ERK-CREB pathway. In addition, LMDS-1 has better effect than 7,8-DHF in ameliorating the behavioral and pathological features of AD-like mice. This study suggests that LMDS-1 upregulates the expression of BDNF and ameliorates the early-phase phenotypes of the AD-like mice through the pTrkB (Y516)-ERK-CREB pathway. In addition, LMDS-1 has better effect than 7,8-DHF in ameliorating the behavioral and pathological features of AD-like mice.