Exercise has many benefits for physical and mental well-being. Metabolomics research has allowed scientists to study the impact of exercise on the body by analyzing metabolites released by tissues such as skeletal muscle, bone, and the liver. Endurance training increases mitochondrial content and oxidative enzymes, while resistance training increases muscle fiber and glycolytic enzymes. Acute endurance exercise affects amino acid metabolism, fat metabolism, cellular energy metabolism, and cofactor and vitamin metabolism. Subacute endurance exercise alters amino acid metabolism, lipid metabolism, and nucleotide metabolism. Chronic endurance exercise improves lipid metabolism and changes amino acid metabolism. Acute resistance exercise changes several metabolic pathways, including anaerobic processes and muscular strength. Chronic resistance exercise affects metabolic pathways, resulting in skeletal muscle adaptations. Combined endurance–resistance exercise alters lipid metabolism, carbohydrate metabolism, and amino acid metabolism, increasing anaerobic metabolic capacity and fatigue resistance. Studying exercise-induced metabolites is a growing field, and further research can uncover the underlying metabolic mechanisms and help tailor exercise programs for optimal health and performance.
The SARS-CoV-2 pandemic has posed global medical challenges due to its ability to affect multiple organ systems. Among the post-COVID-19 complications, multisystem inflammatory syndrome has emerged as a severe condition affecting both children (MIS-C) and adults (MIS-A). This review aims to compile and analyze published data to investigate clinical characteristics, laboratory findings, and outcomes of MIS post-COVID-19. A comprehensive search of various databases was conducted to identify studies reporting MIS-related complications in pediatric and adult populations post-COVID-19 infection. Screening, data extraction, and cross-checking were performed by two independent reviewers. Only 64 studies met our inclusion criteria, and compiled results revealed that cardiac complications were the predominant manifestation followed by gastrointestinal, hematologic, neurological, and mucocutaneous involvement. Laboratory findings consistently demonstrated elevated inflammatory markers including CRP, ferritin, D-dimer, and IL-6. Most patients required hospitalization, and many needed intensive care; treatment typically involved IVIG, corticosteroids, and biologic therapies. While most patients recovered, a subset experienced persistent complications. These findings highlight the importance of early recognition, multidisciplinary management, and structured follow-up for MIS. Future research is warranted to clarify the underlying mechanisms, risk factors, and long-term outcomes associated with MIS in post-COVID-19 patients.
As the primary cause of death for >90% of cancers, metastasis is the fourth and final stage of cancer during which cells gain the ability to leave their primary site, invade surrounding tissues, and disseminate to distant organs
Merkel cell carcinoma (MCC) is a rare and aggressive neuroendocrine cutaneous malignancy that commonly affects older individuals with a high mortality rate
Cancer cell plasticity is a phenomenon that allows cancer cells to change their phenotype in response to alterations in their microenvironment. This flexibility promotes tumor progression and facilitates the emergence of therapy-resistant cells. Plasticity of cancer stem cells is critical for their ability to help tumors overcome sensitivity to therapies and metastasize. Epigenetic modifications like DNA methylation, histone modifications, and acetylation lead to epithelial-mesenchymal transition (EMT) or dedifferentiation and contribute to tumor invasion and drug resistance. EMT is associated with the acquisition of more motile mesenchymal traits while dedifferentiation allows cells to switch to a less differentiated state, leading to the loss of original cell gene expression and phenotype, and the acquisition of a new phenotype, all in an attempt to favorably adapt to changing microenvironments, particularly when exposed to therapeutic agents. Therapeutic resistance can be overcome by targeting these pathways, and more precisely by countering the associated plasticity. This will require targeting not just the players: genes and other molecular markers/factors, but also the underlying epigenetic events. Transdifferentiation is yet another phenomenon that can potentially be exploited to overcome resistance by transforming tumor cells into a non-drug-resistant state. Understanding these mechanisms, particularly the complexity of interactions and epigenetic regulation, will hold the key to better cancer treatment and patient outcomes.