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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.

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]

Cancer‐related fatigue is a frequent, burdensome and often insufficiently treated symptom. A more targeted treatment of fatigue is urgently needed. Therefore, we examined biomarkers and clinical factors to identify fatigue subtypes with potentially different pathophysiologies. The study population comprised disease‐free breast cancer survivors of a German population‐based case‐control study who were re‐assessed on average 6 (FU1, n = 1871) and 11 years (FU2, n = 1295) after diagnosis. At FU1 and FU2, we assessed fatigue with the 20‐item multidimensional Fatigue Assessment Questionnaire and further factors by structured telephone‐interviews. Serum samples collected at FU1 were analyzed for IL‐1ß, IL‐2, IL‐4, IL‐6, IL‐10, TNF‐a, GM‐CSF, IL‐5, VEGF‐A, SAA, CRP, VCAM‐1, ICAM‐1, leptin, adiponectin and resistin. Exploratory cluster analyses among survivors with fatigue at FU1 and no history of depression yielded three clusters (CL1, CL2 and CL3). CL1 (n = 195) on average had high levels of TNF‐α, IL1‐β, IL‐6, resistin, VEGF‐A and GM‐CSF, and showed high BMI and pain levels. Fatigue in CL1 manifested rather in physical dimensions. Contrarily, CL2 (n = 78) was characterized by high leptin level and had highest cognitive fatigue. CL3 (n = 318) did not show any prominent characteristics. Fatigued survivors with a history of depression (n = 214) had significantly higher physical, emotional and cognitive fatigue and showed significantly less amelioration of fatigue from FU1 to FU2 than survivors without depression. In conclusion, from the broad phenotype "cancer‐related fatigue" we were able to delineate subgroups characterized by biomarkers or history of depression. Future investigations may take these subtypes into account, ultimately enabling a better targeted therapy of fatigue. [ABSTRACT FROM AUTHOR]

Polythiophene‐based conjugated polyelectrolytes (CPE) are attracting increasing attention as sensor or interface materials in chemistry and biology. While cationic polythiophenes are better understood, limited structural information is available on their anionic counterparts. Limited access to well‐defined polymers has made the study of structure‐property relationships difficult and clear correlations have remained elusive. By combining controlled Kumada catalyst transfer polymerization with a polymer‐analog substitution, regioregular and narrowly distributed poly(6‐(thiophen‐3‐yl)hexane‐1‐sulfonate)s (PTHS) with tailored chain length are prepared. Analysis of their aqueous solution structures by small‐angle neutron scattering (SANS) revealed a cylindrical conformation for all polymers tested, with a length close to the contour length of the polymer chains, while the estimated radii remain too small (<1.5 nm) for extensive π‐stacking of the chains. The latter is particularly interesting as the longest polymer exhibits a concentration‐independent structured absorption typical of crystalline polythiophenes. Increasing the ionic strength of the solution diminishes these features as the Coulomb repulsion between the charged repeat units is shielded, allowing the polymer to adopt a more coiled conformation. The extended π‐conjugation, therefore, appears to be a key parameter for these unique optical features, which are not present in the corresponding cationic polythiophenes. [ABSTRACT FROM AUTHOR]