BACKGROUND Older adults have the highest sedentary time across all age groups, and only a small portion is meeting the minimum recommendations for weekly physical activity. Little research to date has looked at how changes in one of these behaviours influences the other. AIM To assess changes in 24-h movement behaviours (sedentary time, light intensity physical activity (LPA), moderate-vigorous PA (MVPA) and sleep) over three consecutive days, following acute bouts of exercise of varying intensity in older adults. METHODS Participants (n = 28, 69.7 ± 6.5 years) completed a maximal exercise test and the following exercise protocols in random order moderate continuous exercise (MOD), high-intensity interval exercise (HI) and sprint interval exercise (SPRT). A thigh-worn device (ActivPAL™) was used to measure movement behaviours at baseline and the 3 days following each exercise session. RESULTS Repeated measures analysis of variance indicated that compared to baseline, participants decreased MVPA in the 3 days following all exercise sessions and decreased LPA following HI and SPRT (p  less then  0.05). Over half of the sample had clinically meaningful increases in sedentary time (30 min/day) in the days following exercise participation. DISCUSSION Older adults who compensate for exercise participation by reducing physical activity and increasing sedentary time in subsequent days may require behavioural counseling to ensure that incidental and recreational physical activities are not reduced. CONCLUSION It appears that older adults compensate for acute exercise by decreasing MVPA and LPA, and increasing sedentary time in the days following exercise.  https://www.selleckchem.com/products/camostat-mesilate-foy-305.html  Future research is needed to determine whether compensation persists with regular engagement.Experimental tumor modeling has long supported the discovery of fundamental mechanisms of tumorigenesis and tumor progression, as well as provided platforms for the development of novel therapies. Still, the attrition rates observed today in clinical translation could be, in part, mitigated by more accurate recapitulation of environmental cues in research and preclinical models. The increasing understanding of the decisive role that tumor microenvironmental cues play in the outcome of drug response urges its integration in preclinical tumor models. In this chapter we review recent developments concerning in vitro and ex vivo approaches.The zebrafish larvae have emerged as a powerful model for studying tumorigenesis in vivo, with remarkable conservation with mammals in genetics, molecular and cell biology. Zebrafish tumor models bear the significant advantages of optical clarity in comparison to that in the mammalian models, allowing noninvasive investigation of the tumor cell and its microenvironment at single-cell resolution. Here we review recent progressions in the field of zebrafish models of solid tumor diseases in two main categories the genetically engineered tumor models in which all cells in the tumor microenvironment are zebrafish cells, and xenograft tumor models in which the tumor microenvironment is composed of zebrafish cells and cells from other species. Notably, the zebrafish patient-derived xenograft (zPDX) models can be used for personalized drug assessment on primary tumor biopsies, including the pancreatic cancer. For the future studies, a series of high throughput drug screenings on the library of transgenic zebrafish models of solid tumor are expected to provide systematic database of oncogenic mutation, cell-of-origin, and leading compounds; and the humanization of zebrafish in genetics and cellular composition will make it more practical hosts for zPDX modeling. Together, zebrafish tumor model systems are unique and convenient in vivo platforms, with great potential to serve as valuable tools for cancer researches.This chapter provides a brief overview of the methods to study and modulate the metabolic phenotype of the tumor microenvironment, including own research work to demonstrate the impact that metabolic shifts in the host have on cancer. Firstly, we briefly discuss the relevance of using animal models to address this topic, and also the importance of acknowledging that animals have diverse metabolic phenotypes according to species, and even with strain, age or sex. We also present original data to highlight the impact that changes in metabolic phenotype of the microenvironment have on tumor progression. Using an acute leukemia mouse xenograft model and high-fat diet we show that a shift in the host metabolic phenotype, induced by high-fat feeding, significantly impacts on tumor progression. The mechanism through which this occurs involves a direct effect of the increased levels of circulating lipoproteins in both tumor and non-neoplastic cells.Cancers are complex tissues composed by genetically altered cancer cells and stromal elements such as inflammatory/immune cells, fibroblasts, endothelial cells and pericytes, neuronal cells, and a non-cellular component, the extracellular matrix. The complex network of interactions and crosstalk established between cancer cells and the supportig cellular and non-cellular components of the microenvironment are of extreme importance for tumor initiation and progression, strongly impacting the course and the outcome of the disease. Therefore, a better understanding of the tumorigenic processes implies the combined study of the cancer cell and the biologic, chemical and mechanic constituents of the tumor microenvironment, as their concerted action plays a major role in the carcinogenic pathway and is a key determinant of the efficacy of anti-cancer treatments. The use of animal models (e.g. Mouse, Zebrafish and Drosophila) to study cancer has greatly impacted our understanding of the processes governing initiation, progression and metastasis and allowed the discovery and pre-clinical validation of novel cancer treatments as it allows to recreate tumor development in a more pathophysiologic environment.Altered metabolism is one of the key hallmarks of cancer. The development of sensitive, reproducible and robust bioanalytical tools such as Nuclear Magnetic Resonance Spectroscopy and Mass Spectrometry techniques offers numerous opportunities for cancer metabolism research, and provides additional and exciting avenues in cancer diagnosis, prognosis and for the development of more effective and personalized treatments. In this chapter, we introduce the current state of the art of metabolomics and metabolic phenotyping approaches in cancer research and clinical diagnostics.