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Simple Summary: Cancer-related fatigue is a prevalent symptom, with a significant impact on the daily lives of those affected. While physical exercise has demonstrated effectiveness in reducing the intensity and duration of fatigue, the literature still lacks sufficient evidence on the physiological mechanisms explaining this impact. This conceptual review aimed to provide an overview of the evidence regarding the effect of acute exercise on peripheral and neuronal inflammation, immune function, and the neuroendocrine system in the context of cancer. We aim to integrate these pathways into a conceptual model that can serve as a starting point for further research into the physiological mechanisms linking exercise and cancer-related fatigue. Cancer-related fatigue (CRF) is a prevalent and persistent issue affecting cancer patients, with a broad impact on their quality of life even years after treatment completion. The precise mechanisms underlying CRF remain elusive, yet its multifaceted nature involves emotional, physical, and cognitive dimensions. The absence of effective medical treatments has prompted researchers to explore integrative models for potential insights. Notably, physical exercise emerges as a promising strategy for managing CRF and related symptoms, as studies showed a reduction in CRF ranging from 19% to 40%. Current recommendations highlight aerobic training at moderate intensity as beneficial, although questions about a dose–response relationship and the importance of exercise intensity persist. Despite the positive impact of exercise on CRF, the underlying mechanisms remain elusive. This review aims to provide a theoretical model explaining how aerobic exercise may alleviate CRF. Focusing on acute exercise effects, this review delves into the potential influence on peripheral and neural inflammation, immune function dysregulation, and neuroendocrine system disruptions. The objective is to enhance our understanding of the intricate relationship between exercise and CRF, ultimately paving the way for tailored interventions and potential pharmacological treatments for individuals unable to engage in physical exercise. [ABSTRACT FROM AUTHOR]

An explicit compatibility condition formula is presented for the Eulerian left Cauchy–Green deformation tensor field. It is shown to be the appropriate finite‐strain counterpart of Saint‐Venant's compatibility condition. The difference between the Eulerian problem and the Lagrangian one is highlighted. [ABSTRACT FROM AUTHOR]

Background: Growing evidence supports that receptor for advanced glycation end products (RAGE) and glyoxalase-1 (GLO-1) are implicated in the pathophysiology of Alzheimer's disease (AD). Extracellular vesicles (EVs) are nanovesicles secreted by almost all cell types, contribute to cellular communication, and are implicated in AD pathology. Recently, EVs are considered as promising tools to identify reliable biomarkers in AD.Objective: The aim of our study was to determine the levels of RAGE and GLO-1 in circulating EVs from mild cognitive impairment (MCI) and AD patients and to analyze their correlation with the clinical Mini-Mental State Examination and Montreal Cognitive Assessment scores. We have studied the possibility that neuronal cells could release and transfer GLO-1 through EVs.Methods: RAGE and GLO-1 levels were measured in circulating EVs, respectively, by Luminex assay and western blot. Released-EVs from SK-N-SH neuronal cells were isolated and GLO-1 levels were determined by western blot.Results: Our data showed higher levels of RAGE in EVs from late AD patients while GLO-1 levels in EVs from early AD were lower as compared to control and MCI patients. Interestingly, levels of RAGE and GLO-1 in EVs were correlated with the cognitive scores regardless of age. For the first time, we demonstrated that GLO-1 was released from neuronal cells through EVs.Conclusion: Although more samples will be needed, our preliminary results support the use of peripheral EVs cargo as new tools for the discovery of peripheral AD biomarkers. [ABSTRACT FROM AUTHOR]

It is a long-lasting task to understand heat conduction phenomena beyond Fourier. Besides the low-temperature experiments on extremely pure crystals, it has turned out recently that heterogeneous materials with macro-scale size can also show thermal effects that cannot be modeled by the Fourier equation. This is called over-diffusive propagation, different from low-temperature observations, and is found in numerous samples made from metal foam, rocks, and composites. The measured temperature history is indeed similar to what Fourier's law predicts but the usual evaluation cannot provide reliable thermal parameters. This paper is a report on our experiments on several rock types, each type having multiple samples with different thicknesses. We show that size-dependent thermal behavior can occur for both Fourier and non-Fourier situations. Moreover, based on the present experimental data, we find an empirical relation between the Fourier and non-Fourier parameters, which may be helpful in later experiments to develop a more robust and reliable evaluation procedure. [ABSTRACT FROM AUTHOR]

Rocks exhibit beyond-Hookean, delayed and damped elastic, behaviour (creep, relaxation etc.). In many cases, the Poynting-Thomson-Zener (PTZ) rheological model proves to describe these phenomena successfully. A forecast of the PTZ model is that the dynamic elasticity coefficients are larger than the static (slow-limit) counterparts. This prediction has recently been confirmed on a large variety of rock types. Correspondingly, according to the model, the speed of wave propagation depends on frequency, the high-frequency limit being larger than the low-frequency limit. This frequency dependence can have a considerable influence on the evaluation of various wave-based measurement methods of rock mechanics. As experience shows, commercial finite element softwares are not able to properly describe wave propagation, even for the Hooke model and simple specimen geometries, the seminal numerical artefacts being instability, dissipation error and dispersion error, respectively. This has motivated research on developing reliable numerical methods, which amalgamate beneficial properties of symplectic schemes, their thermodynamically consistent generalization (including contact geometry), and spacetime aspects. The present work reports on new results obtained by such a numerical scheme, on wave propagation according to the PTZ model, in one space dimension. The simulation outcomes coincide nicely with the theoretically obtained phase velocity prediction. [ABSTRACT FROM AUTHOR]

The internal variable methodology of non-equilibrium thermodynamics, with a symmetric tensorial internal variable, provides an important rheological model family for solids, the so-called Kluitenberg–Verhás model family [Cs. Asszonyi et al., Contin. Mech. Thermodyn. 27, 2015]. This model family is distinguished not only by theoretical aspects but also on experimental grounds (see [Cs. Asszonyi et al., Period. Polytech., Civ. Eng. 60, 2016] for plastics and [W. Lin et al., Rock Engineering in Difficult Ground Conditions (Soft Rock and Karst), Proceedings of Eurock'09, 2009; K. Matsuki, K. Takeuchi, Int. J. Rock Mech. Min. Sci. Geomech. Abstr. 30, 1993; K. Matsuki, Int. J. Rock Mech. Min. Sci. 45, 2008] for rocks). In this article, we present and discuss how the internal variable formulation of the Kluitenberg–Verhás model family can be presented in the non-equilibrium thermodynamical framework GENERIC (General Equation for the Non-Equilibrium Reversible–Irreversible Coupling) [H. C. Öttinger, Beyond Equilibrium Thermodynamics, 2005; M. Grmela, J. Non-Newton. Fluid Mech. 165, 2010; M. Grmela, H. C. Öttinger, Phys. Rev. E 56, 1997; H. C. Öttinger, M. Grmela, Phys. Rev. E 56, 1997], for the benefit of both thermodynamical methodologies and promising practical applications. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a progressive neurodegenerative disorder, where neuroinflammation and immune cells are key pathological factors. Recently, it was suggested a possible association between AD and human herpesvirus 6 (HHV-6) infection. Since we recently observed that multiple sclerosis patients with KIR2DL2 expression on natural killer (NK) cells are more susceptible to herpesvirus infection, we tested the possible implication of KIR/HLA genetic for HHV-6A infection. We identified, for the first time, a possible implication of a specific KIR/HLA subset in AD. The combination KIR2DS2/KIR2DL2/C1 correlated with a lower MMSEDi score, representative of a severe AD status and an increased susceptibility to HHV-6A infection. Therefore, the results seem to converge on the hypothesis that herpesvirus infection might play a role in AD. If this hypothesis finds experimental confirmation, a new therapeutic strategy, modulating KIR2DL2 expression on NK cells, for AD might be envisaged. [ABSTRACT FROM AUTHOR]

Senile amyloid plaques are one of the main hallmarks of Alzheimer's disease (AD). They correspond to insoluble deposits of amyloid-β peptides (Aβ) and are responsible for the inflammatory response and neurodegeneration that lead to loss of memory. Recent data suggest that Aβ possess antimicrobial and anti-viral activity in vitro. Here, we have used cocultures of neuroglioma (H4) and glioblastoma (U118-MG) cells as a minimal in vitro model to investigate whether Aβ is produced by neuroglioma cells and whether this could result in protective anti-viral activity against HSV-1 infection. Results showed that H4 cells secreted Aβ42 in response to HSV-1 challenge and that U118-MG cells could rapidly internalize Aβ42. Production of pro-inflammatory cytokines TNFα and IL-1β by H4 and U118-MG cells occurred under basal conditions but infection of the cells with HSV-1 did not significantly upregulate production. Both cell lines produced low levels of IFNα. However, extraneous Aβ42 induced strong production of these cytokines. A combination of Aβ42 and HSV-1 induced production of pro-inflammatory cytokines TNFα and IL-1β, and IFNα in the cell lines. The reported anti-viral protection of Aβ42 was revealed in transfer experiments involving conditioned medium (CM) of HSV-1-infected H4 cells. CM conferred Aβ-dependent protection against HSV-1 replication in de novo cultures of H4 cells challenged with HSV-1. Type 1 interferons did not play a role in these assays. Our data established that H4 neuroglioma cells produced Aβ42 in response to HSV-1 infection thus inhibiting secondary replication. This mechanism may play a role in the etiology of AD. [ABSTRACT FROM AUTHOR]

AP@LZ is an electronic organiser that was designed to support the day-to-day activities of persons with Alzheimer's disease. To assess the potential of this technology, three participants (NI, JB, RD) were approached to take part in the study. They benefited from a structured cognitive intervention to learn how to operate AP@LZ; the intervention included the following learning stages: Acquisition, Application and Adaptation. Pre- and post-intervention measures were collected. NI, for whom a longitudinal study was conducted, still continued to use AP@LZ 24 months post-intervention. JB and RD also showed a gradual improvement in their performance throughout the intervention phase (sessions 1 to 19 for JB: performance increased from 50 to 100%; sessions 1 to 25 for RD: from 56 to 89%). The results of the use of AP@LZ in activities of daily living suggest that the application was beneficial for three persons with Alzheimer's disease whose profiles differed notably (age, cognitive and social profiles). Thus, results indicate that they were all able to learn how to operate AP@LZ's functions and to use them in their activities of daily living. Cognitive intervention appears to play an important role for the promotion of learning and adoption of such technology. [ABSTRACT FROM AUTHOR]