| 1. |
- Wei, Weigang, et al.
(författare)
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Urban background noise mapping : The general model
- 2014
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Ingår i: Acta Acoustica united with Acustica. - 1610-1928 .- 1861-9959. ; 100:6, s. 1098-1111
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Tidskriftsartikel (refereegranskat)abstract
- Surveys show that inhabitants of dwellings exposed to high noise levels benefit from having access to a quiet side. However, current practice in noise prediction often underestimates the noise levels at a shielded façade. Multiple reflections between façades in street canyons and inner yards are commonly neglected and façades are approximated as perfectly flat surfaces yielding only specular reflection. In addition, sources at distances much larger than normally taken into account in noise maps might still contribute significantly. Since one of the main reasons for this is computational burden, an efficient engineering model for the diffraction of the sound over the roof tops is proposed, which considers multiple reflections, variation in building height, canyon width, façade roughness and different roof shapes. The model is fitted on an extensive set of full-wave numerical calculations of canyon-to-canyon sound propagation with configurations matching the distribution of streets and building geometries in a typical historically grown European city. This model allows calculating the background noise in the shielded areas of a city, which could then efficiently be used to improve existing noise mapping calculations. The model was validated by comparison to long-term measurements at 9 building façades whereof 3 were at inner yards in the city of Ghent, Belgium. At shielded façades, a strong improvement in prediction accuracy is obtained.
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| 2. |
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| 3. |
- Parpura, Vladimir, et al.
(författare)
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Glial cells in (patho)physiology.
- 2012
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Ingår i: Journal of neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 121:1, s. 4-27
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Forskningsöversikt (refereegranskat)abstract
- Neuroglial cells define brain homeostasis and mount defense against pathological insults. Astroglia regulate neurogenesis and development of brain circuits. In the adult brain, astrocytes enter into intimate dynamic relationship with neurons, especially at synaptic sites where they functionally form the tripartite synapse. At these sites, astrocytes regulate ion and neurotransmitter homeostasis, metabolically support neurons and monitor synaptic activity; one of the readouts of the latter manifests in astrocytic intracellular Ca(2+) signals. This form of astrocytic excitability can lead to release of chemical transmitters via Ca(2+) -dependent exocytosis. Once in the extracellular space, gliotransmitters can modulate synaptic plasticity and cause changes in behavior. Besides these physiological tasks, astrocytes are fundamental for progression and outcome of neurological diseases. In Alzheimer's disease, for example, astrocytes may contribute to the etiology of this disorder. Highly lethal glial-derived tumors use signaling trickery to coerce normal brain cells to assist tumor invasiveness. This review not only sheds new light on the brain operation in health and disease, but also points to many unknowns.
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| 4. |
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| 5. |
- lambert, matt
(författare)
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An Everyday Chat About David Chatt
- 2022
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Ingår i: Surface Design Journal. - New Mexico, U.S. - 0197-4483. ; 46:4, s. 18-23
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Schmidt, Tobias T, et al.
(författare)
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Alterations in cellular metabolism triggered by URA7 or GLN3 inactivation cause imbalanced dNTP pools and increased mutagenesis
- 2017
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 114:22, s. E4442-E4451
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Tidskriftsartikel (refereegranskat)abstract
- Eukaryotic DNA replication fidelity relies on the concerted action of DNA polymerase nucleotide selectivity, proofreading activity, and DNA mismatch repair (MMR). Nucleotide selectivity and proofreading are affected by the balance and concentration of deoxyribonucleotide (dNTP) pools, which are strictly regulated by ribonucleotide reductase (RNR). Mutations preventing DNA polymerase proofreading activity or MMR function cause mutator phenotypes and consequently increased cancer susceptibility. To identify genes not previously linked to high-fidelity DNA replication, we conducted a genome-wide screen in Saccharomyces cerevisiae using DNA polymerase active-site mutants as a "sensitized mutator background." Among the genes identified in our screen, three metabolism-related genes (GLN3, URA7, and SHM2) have not been previously associated to the suppression of mutations. Loss of either the transcription factor Gln3 or inactivation of the CTP synthetase Ura7 both resulted in the activation of the DNA damage response and imbalanced dNTP pools. Importantly, these dNTP imbalances are strongly mutagenic in genetic backgrounds where DNA polymerase function or MMR activity is partially compromised. Previous reports have shown that dNTP pool imbalances can be caused by mutations altering the allosteric regulation of enzymes involved in dNTP biosynthesis (e.g., RNR or dCMP deaminase). Here, we provide evidence that mutations affecting genes involved in RNR substrate production can cause dNTP imbalances, which cannot be compensated by RNR or other enzymatic activities. Moreover, Gln3 inactivation links nutrient deprivation to increased mutagenesis. Our results suggest that similar genetic interactions could drive mutator phenotypes in cancer cells.
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