| 1. |
- Kehoe, Laura, et al.
(author)
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Make EU trade with Brazil sustainable
- 2019
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In: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 364:6438, s. 341-
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Journal article (other academic/artistic)
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- Conlon, Thomas M, et al.
(author)
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Inhibition of LTβR signalling activates WNT-induced regeneration in lung
- 2020
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In: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 588:7836, s. 151-156
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Journal article (peer-reviewed)abstract
- Lymphotoxin β-receptor (LTβR) signalling promotes lymphoid neogenesis and the development of tertiary lymphoid structures1,2, which are associated with severe chronic inflammatory diseases that span several organ systems3-6. How LTβR signalling drives chronic tissue damage particularly in the lung, the mechanism(s) that regulate this process, and whether LTβR blockade might be of therapeutic value have remained unclear. Here we demonstrate increased expression of LTβR ligands in adaptive and innate immune cells, enhanced non-canonical NF-κB signalling, and enriched LTβR target gene expression in lung epithelial cells from patients with smoking-associated chronic obstructive pulmonary disease (COPD) and from mice chronically exposed to cigarette smoke. Therapeutic inhibition of LTβR signalling in young and aged mice disrupted smoking-related inducible bronchus-associated lymphoid tissue, induced regeneration of lung tissue, and reverted airway fibrosis and systemic muscle wasting. Mechanistically, blockade of LTβR signalling dampened epithelial non-canonical activation of NF-κB, reduced TGFβ signalling in airways, and induced regeneration by preventing epithelial cell death and activating WNT/β-catenin signalling in alveolar epithelial progenitor cells. These findings suggest that inhibition of LTβR signalling represents a viable therapeutic option that combines prevention of tertiary lymphoid structures1 and inhibition of apoptosis with tissue-regenerative strategies.
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| 5. |
- D'Humières, Benoit, et al.
(author)
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The C3PO project : A laser communication system concept for small satellites
- 2017
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In: Proceedings of SPIE - The International Society for Optical Engineering. - : SPIE. - 9781510606333
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Conference paper (peer-reviewed)abstract
- The satellite market is shifting towards smaller (micro and nanosatellites), lowered mass and increased performance platforms. Nanosatellites and picosatellites have been used for a number of new, innovative and unique payloads and missions. This trend requires new concepts for a reduced size, a better performance/weight ratio and a reduction of onboard power consumption. In this context, disruptive technologies, such as laser-optical communication systems, are opening new possibilities. This paper presents the C3PO1 system, "advanced Concept for laser uplink/ downlink CommuniCation with sPace Objects", and the first results of the development of its key technologies. This project targets the design of a communications system that uses a ground-based laser to illuminate a satellite, and a Modulating Retro-Reflector (MRR) to return a beam of light modulated by data to the ground. This enables a downlink, without a laser source on the satellite. This architecture suits well to small satellite applications so as high data rates are potentially provided with very low board mass. C3PO project aims to achieve data rates of 1Gbit/s between LEO satellites and Earth with a communication payload mass of less than 1kilogram. In this paper, results of the initial experiments and demonstration of the key technologies will be shown.
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| 6. |
- Franzmeier, Nicolai, 1989, et al.
(author)
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Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease.
- 2024
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In: Nature communications. - 2041-1723. ; 15:1
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Journal article (peer-reviewed)abstract
- In Alzheimer's disease, amyloid-beta (Aβ) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote tau spreading. Aβ induces aberrant synaptic activity, manifesting in increases in the presynaptic growth-associated protein 43 (GAP-43), which is closely involved in synaptic activity and plasticity. We therefore tested whether Aβ-related GAP-43 increases, as a marker of synaptic changes, drive tau spreading in 93 patients across the aging and Alzheimer's spectrum with available CSF GAP-43, amyloid-PET and longitudinal tau-PET assessments. We found that (1) higher GAP-43 was associated with faster Aβ-related tau accumulation, specifically in brain regions connected closest to subject-specific tau epicenters and (2) that higher GAP-43 strengthened the association between Aβ and connectivity-associated tau spread. This suggests that GAP-43-related synaptic changes are linked to faster Aβ-related tau spread across connected regions and that synapses could be key targets for preventing tau spreading in Alzheimer's disease.
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| 7. |
- Malpetti, Maura, et al.
(author)
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Neuroinflammation Parallels 18F-PI-2620 Positron Emission Tomography Patterns in Primary 4-Repeat Tauopathies
- 2024
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In: MOVEMENT DISORDERS. - 0885-3185 .- 1531-8257.
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Journal article (peer-reviewed)abstract
- Background Preclinical, postmortem, and positron emission tomography (PET) imaging studies have pointed to neuroinflammation as a key pathophysiological hallmark in primary 4-repeat (4R) tauopathies and its role in accelerating disease progression. Objective We tested whether microglial activation (1) progresses in similar spatial patterns as the primary pathology tau spreads across interconnected brain regions, and (2) whether the degree of microglial activation parallels tau pathology spreading. Methods We examined in vivo associations between tau aggregation and microglial activation in 31 patients with clinically diagnosed 4R tauopathies, using 18F-PI-2620 PET and 18F-GE180 (translocator protein [TSPO]) PET. We determined tau epicenters, defined as subcortical brain regions with highest tau PET signal, and assessed the connectivity of tau epicenters to cortical regions of interest using a 3-T resting-state functional magnetic resonance imaging template derived from age-matched healthy elderly controls. Results In 4R tauopathy patients, we found that higher regional tau PET covaries with elevated TSPO-PET across brain regions that are functionally connected to each other (beta = 0.414, P < 0.001). Microglial activation follows similar distribution patterns as tau and distributes primarily across brain regions strongly connected to patient-specific tau epicenters (beta = -0.594, P < 0.001). In these regions, microglial activation spatially parallels tau distribution detectable with 18F-PI-2620 PET. Conclusions Our findings indicate that the spatial expansion of microglial activation parallels tau distribution across brain regions that are functionally connected to each other, suggesting that tau and inflammation are closely interrelated in patients with 4R tauopathies. The combination of in vivo tau and inflammatory biomarkers could therefore support the development of immunomodulatory strategies for disease-modifying treatments in these conditions.
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| 10. |
- Quax, Tessa E. F., et al.
(author)
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Differential Translation Tunes Uneven Production of Operon-Encoded Proteins
- 2013
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In: Cell Reports. - : Elsevier BV. - 2211-1247. ; 4:5, s. 938-944
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Journal article (peer-reviewed)abstract
- Clustering of functionally related genes in operons allows for coregulated gene expression in prokaryotes. This is advantageous when equal amounts of gene products are required. Production of protein complexes with an uneven stoichiometry, however, requires tuning mechanisms to generate subunits in appropriate relative quantities. Using comparative genomic analysis, we show that differential translation is a key determinant of modulated expression of genes clustered in operons and that codon bias generally is the best in silico indicator of unequal protein production. Variable ribosome density profiles of polycistronic transcripts correlate strongly with differential translation patterns. In addition, we provide experimental evidence that de novo initiation of translation can occur at intercistronic sites, allowing for differential translation of any gene irrespective of its position on a polycistronic messenger. Thus, modulation of translation efficiency appears to be a universal mode of control in bacteria and archaea that allows for differential production of operon-encoded proteins.
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