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[english] Background: The rapid development in technology promotes the increasing use of electronic activity monitors to assess physical activity in large-scale epidemiological studies. Our aim was to explore and discuss both subjective and objective methods assessing physical activity.Methods: Based on a thorough literature search, major strengths and limitations of questionnaires and electronic activity monitors in assessing physical activity are elaborated and discussed, taking into consideration physical activity in all its complexity. Important research questions and the aim and scope of physical activity assessment for next-generation research are defined.Results: Questionnaires can provide details and background information of physical activity, including type of activity, and can identify the activity behaviour patterns that underlie measurable endpoints such as energy expenditure, cardiorespiratory fitness, muscular strength, or certain biomarkers. They can differentiate well between settings and enable retrospective assessment. Electronic activity monitors, on the other hand, are rapidly becoming better at assessing energy expenditure and are good at quantifying the amount and intensity of physical activity and sedentary behaviour. Both methods, however, also have their weaknesses. While questionnaires may not be accurate, due to recall bias or incomplete assessment of all activity domains, electronic activity monitors are not able to provide information about setting, exact type and mode of activity, and cannot recognize and reliably assess resistance exercise or activities with or without carrying weights.Conclusions: Since physical activity is multidimensional and complex, no single method is suitable to capture all aspects and domains. Both methods have their strengths and limitations and do not compete with each other, but should be seen as complementary tools that assess distinct aspects of physical activity. Studies should therefore rely on both methods to enable improved public health recommendations for this complex lifestyle factor.

Background/Objectives: Products from various parts of Crataegus species are traditionally applied as a cardiotonic. In Europe and the USA, mainly Crataegus monogyna Jacq. (Lindm.) and Crataegus laevigata (Poir.) DC (synonym Crataegus oxyacantha L.) are used, but worldwide, other Crataegus species are also used. Phytotherapeutic preparations with a standardised content of flavonoids and/or oligomeric procyanidins are commercially available. The products are generally considered as safe and are at most associated with minor and atypical adverse reactions. The aim of this study was to critically assess the information about the safety of Crataegus-containing products in humans. Methods: A scoping review of the literature about adverse reactions associated with Crataegus-containing products was performed. Next, individual case safety reports (ICSRs) were assessed, which were included in VigiBase (the World Health Organisation's global database of adverse event reports for medicines and vaccines) and in the database of the Netherlands Pharmacovigilance Centre Lareb. The findings are discussed in relation to the literature. Results: The scoping review yielded 23 clinical studies with single-herb and 14 with multi-herb preparations, from which only a few minor gastrointestinal and cardiac events had been reported. A total of 1527 reports from VigiBase, from 1970 to 2023, were analysed, as well as 13 reports from Lareb. The most frequently reported adverse reactions belonged to the system organ classes 'gastrointestinal disorders', 'skin and subcutaneous tissue disorders', 'general disorders and administration site conditions', 'cardiac disorders' or 'nervous system disorders'. In 277 reports of VigiBase, a single-herb product was the only suspect for causing the adverse reaction(s). Of these, 12.6% were graded as serious. Conclusions: The results of our study provide deeper insight in the adverse reaction profile of Crataegus-containing products and should contribute to their safe application in the treatment of less severe forms of cardiac failure. [ABSTRACT FROM AUTHOR]

Introduction: Air pollution from diesel combustion is linked in part to the generation of diesel exhaust particles (DEP). DEP exposure induces various processes, including inflammation and oxidative stress, which ultimately contribute to a decline in lung function. Cyclic AMP (cAMP) signaling is critical for lung homeostasis. The impact of DEP on cAMP signaling is largely unknown. Methods: We exposed human bronchial epithelial (BEAS-2B) cells to DEP for 24-72 h and evaluated mitochondrial bioenergetics, markers of oxidative stress and inflammation and the components of cAMP signaling. Mitochondrial bioenergetics was measured at 72 h to capture the potential and accumulative effects of prolonged DEP exposure on mitochondrial function. Results: DEP profoundly altered mitochondrial morphology and network integrity, reduced both basal and ATP-linked respiration as well as the glycolytic capacity of mitochondria. DEP exposure increased gene expression of oxidative stress and inflammation markers such as interleukin-8 and interleukin-6. DEP significantly affected mRNA levels of exchange protein directly activated by cAMP-1 and -2 (Epac1, Epac2), appeared to increase Epac1 protein, but left phospho-PKA levels unhanged. DEP exposure increased A-kinase anchoring protein 1, β2-adrenoceptor and prostanoid E receptor subtype 4 mRNA levels. Interestingly, DEP decreased mRNA levels of adenylyl cyclase 9 and reduced cAMP levels stimulated by forskolin (AC activator), fenoterol (β2-AR agonist) or PGE2 (EPR agonist). Discussion: Our findings suggest that DEP induces mitochondrial dysfunction, a process accompanied by oxidative stress and inflammation, and broadly dampens cAMP signaling. These epithelial responses may contribute to lung dysfunction induced by air pollution exposure. [ABSTRACT FROM AUTHOR]

In various neurodegenerative conditions, inflammation plays a significant role in disrupting the blood–brain barrier (BBB), contributing to disease progression. Nitric oxide (NO) emerges as a central regulator of vascular function, with a dual role in inflammation, acting as both a pro- and anti-inflammatory molecule. This study investigates the effects of the NO donor sodium nitroprusside (SNP) in protecting the BBB from lipopolysaccharide (LPS)-induced inflammation, using bEnd.3 endothelial cells as a model system. Additionally, Raw 264.7 macrophages were employed to assess the effects of LPS and SNP on their adhesion to a bEnd.3 cell monolayer. Our results show that LPS treatment induces oxidative stress, activates the JAK2/STAT3 pathway, and increases pro-inflammatory markers. SNP administration effectively mitigates ROS production and IL-6 expression, suggesting a potential anti-inflammatory role. However, SNP did not significantly alter the adhesion of Raw 264.7 cells to bEnd.3 cells induced by LPS, probably because it did not have any effect on ICAM-1 expression, although it reduced VCAM expression. Moreover, SNP did not prevent BBB disruption. This research provides new insights into the role of NO in BBB disruption induced by inflammation. [ABSTRACT FROM AUTHOR]

Interest in post‐traumatic growth (PTG) as a predictor of health‐related quality of life (HRQoL) is currently gaining attention. However, current evidence is still inconclusive on the nature of this relationship. The first objective of this study was to investigate the relationship between PTG and global HRQoL among cancer survivors. We further investigated the moderating role of fatigue in the association between PTG and global HRQoL. In the FiX study (Fatigue in Germany ‐ Examination of prevalence, severity, and state of screening and treatment) cancer‐related fatigue (EORTC QLQ‐FA12), PTG inventory and global HRQoL (EORTC QLQ‐C30) were assessed four years after cancer diagnosis in 1316 cancer‐free survivors (mean age = 67.28, SD = 11.05, 51.4% female). Multiple linear regression analysis and moderation analysis were performed. The results showed that PTG had a convex quadratic relationship with global HRQoL (p < 0.001). Contrary to our hypothesis, fatigue did not moderate the relationship between PTG (linear and quadratic terms) and global HRQoL, neither when considering the overall PTG score nor for any PTG subdimension. In conclusion, PTG has a convex quadratic relationship with long‐term global HRQoL that was not modified by persisting fatigue. Future statistical models investigating PTG and global HRQoL should take this non‐linear relationship into account. Aiming to increase PTG might contribute to, but is likely not sufficient for high levels of global HRQoL in cancer survivors in the long run. [ABSTRACT FROM AUTHOR]