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C8H16Cl3NO2, monoclinic, P21 (no. 4), a = 9.1804(5), Å, b = 19.4133(10) Å, c = 13.9191(7) Å, β = 90.593(3)°, V = 2480.6(2) Å3, Z = 8, Rgt(F) = 0.0605, wRref(F2) = 0.1387, T = 296(2) K.

Legitimation of circular timber construction The sustainability principle requires that only as much wood is removed from the forest as will grow back in the same period. The annual harvest volume available for use in construction is therefore limited, also in view of the fact that other sectors of the economy are increasingly relying on the raw material. Accordingly, the aim is to maximise carbon storage as the sum of the carbon bound in the forest and the material use of wood. For the construction industry, this means maximising the longevity of building components by using wood as a resource in a circularly effective way. On the one hand, this paper presents the strategic approach to increasing the circularity of timber construction. On the other hand, the climate‐relevant proof of the necessity of circularly effective construction is provided and demonstrated using a dynamic balancing method. For this purpose, it is shown for resource consumption and global warming potential how circularly effective construction can be quantified in principle and in particular with wood. [ABSTRACT FROM AUTHOR]

Objective: Rheumatoid arthritis (RA) CD8+ T cells maintain their effector proinflammatory phenotype by changing their metabolism toward aerobic glycolysis. However, their massive energy and biosynthesis needs may require additional substrates other than glucose. Since systemic alterations in lipid metabolism have been reported in RA patients, we explored the role of fatty acid (FA) metabolism in CD8+ T cells to identify potential targets to curb their proinflammatory potential. Methods: The expression of FA metabolism–related genes was analyzed for total CD8+ T cells and CD8+ T cell subsets in the data of RA patients and healthy controls retrieved from the GEO database. Functional assays were performed using peripheral blood CD8+ T cells isolated from RA (n = 31), psoriatic arthritis (n = 26), and spondyloarthritis (n = 21) patients receiving different therapies (disease‐modifying antirheumatic drugs, biologics, and JAK inhibitors) and from healthy controls (n = 14). We quantified the expression of FA transporters, lipid uptake, intracellular FA content, cytokine production, activation, proliferation, and capacity to inhibit tumor cell growth, either with or without FA metabolism inhibitors. Results: The CD8+ T cell gene expression profile of FA metabolism–related genes was significantly different between untreated RA patients and healthy controls. RA patients who had a good clinical response after 6 months of methotrexate therapy had significantly increased expression of FA metabolism–related genes. Cell surface expression of the FA transporters FA binding protein 4 (FABP4) and G protein–coupled receptor 84 (GPR84) and FA uptake were higher in effector and memory CD8+ T cells from RA patients compared to those from healthy controls. In vitro blockade of FA metabolism significantly impaired CD8+ T cell effector functions. Conclusion: RA CD8+ T cells present an altered FA metabolism, which could provide potential therapeutic targets to control their proinflammatory profile, particularly therapies directed against the transport and oxidation of free FA. [ABSTRACT FROM AUTHOR]