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- Gärtner, Antje, et al.
(författare)
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Temperature and Tree Size Explain the Mean Time to Fall of Dead Standing Trees across Large Scales
- 2023
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Ingår i: Forests. - : MDPI. - 1999-4907. ; 14:5
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Tidskriftsartikel (refereegranskat)abstract
- AbstractDead standing trees (DSTs) generally decompose slower than wood in contact with the forest floor. In many regions, DSTs are being created at an increasing rate due to accelerating tree mortality caused by climate change. Therefore, factors determining DST fall are crucial for predicting dead wood turnover time but remain poorly constrained. Here, we conduct a re-analysis of published DST fall data to provide standardized information on the mean time to fall (MTF) of DSTs across biomes. We used multiple linear regression to test covariates considered important for DST fall, while controlling for mortality and management effects. DSTs of species killed by fire, insects and other causes stood on average for 48, 13 and 19 years, but MTF calculations were sensitive to how tree size was accounted for. Species’ MTFs differed significantly between DSTs killed by fire and other causes, between coniferous and broadleaved plant functional types (PFTs) and between managed and unmanaged sites, but management did not explain MTFs when we distinguished by mortality cause. Mean annual temperature (MAT) negatively affected MTFs, whereas larger tree size or being coniferous caused DSTs to stand longer. The most important explanatory variables were MAT and tree size, with minor contributions of management and plant functional type depending on mortality cause. Our results provide a basis to improve the representation of dead wood decomposition in carbon cycle assessments.
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| 2. |
- Gärtner, Manja, et al.
(författare)
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Decision-making traits and states as determinants of risky choices
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- We test the effects of dual processing differences in both individual traits and decision states on risk taking. In an experiment with a large representative sample (N = 1,832), we vary whether risky choices are induced to be based on either emotion or reason, while simultaneously measuring individual decision-making traits. Our results show that decision-making traits are strong and robust determinants of risk taking: a more intuitive trait is associated with more risk taking, while a more deliberative trait is associated with less risk taking. Experimentally induced states, on the other hand, have no effect on risk taking. A test of state-trait interactions shows that the association between an intuitive trait and risk taking becomes weaker in the emotion-inducing state and in the loss domain. In contrast, the association between a deliberative trait and risk taking is stable across states. These findings highlight the importance of considering state-trait interactions when using dual processing theories to predict individual differences in risk taking.
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| 3. |
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| 4. |
- Keller, Maria, et al.
(författare)
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Genome-wide DNA promoter methylation and transcriptome analysis in human adipose tissue unravels novel candidate genes for obesity
- 2017
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Ingår i: Molecular Metabolism. - : Elsevier BV. - 2212-8778. ; 6:1, s. 86-100
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Tidskriftsartikel (refereegranskat)abstract
- Objective/methods DNA methylation plays an important role in obesity and related metabolic complications. We examined genome-wide DNA promoter methylation along with mRNA profiles in paired samples of human subcutaneous adipose tissue (SAT) and omental visceral adipose tissue (OVAT) from non-obese vs. obese individuals. Results We identified negatively correlated methylation and expression of several obesity-associated genes in our discovery dataset and in silico replicated ETV6 in two independent cohorts. Further, we identified six adipose tissue depot-specific genes (HAND2, HOXC6, PPARG, SORBS2, CD36, and CLDN1). The effects were further supported in additional independent cohorts. Our top hits might play a role in adipogenesis and differentiation, obesity, lipid metabolism, and adipose tissue expandability. Finally, we show that in vitro methylation of SORBS2 directly represses gene expression. Conclusions Taken together, our data show distinct tissue specific epigenetic alterations which associate with obesity.
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| 5. |
- Lu, Yingchang, et al.
(författare)
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New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk
- 2016
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P<5 × 10(-8)), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk.
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| 7. |
- Wagner, Leona, et al.
(författare)
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Proteolytic degradation of neuropeptide Y (NPY) from head to toe: Identification of novel NPY-cleaving peptidases and potential drug interactions in CNS and Periphery.
- 2015
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Ingår i: Journal of Neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 135:5, s. 1019-1037
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Tidskriftsartikel (refereegranskat)abstract
- The bioactivity of neuropeptide Y (NPY) is either N-terminally modulated with respect to receptor-selectivity by dipeptidyl-peptidase 4 (DP4)-like enzymes or proteolytic degraded by neprilysin or meprins, thereby abrogating signal transduction. However, neither the subcellular nor the compartmental differentiation of these regulatory mechanisms is fully understood. Using mass spectrometry, selective inhibitors and histochemistry, studies across various cell types, body fluids and tissues revealed that most frequently DP4-like enzymes, aminopeptidases P (AmpP), secreted meprin-A (Mep-A) and cathepsin D (CTSD) rapidly hydrolyze NPY, depending on the cell type and tissue under study. Novel degradation of NPY by cathepsins B, D, L, G, S and tissue kallikrein could also be identified. Expression of DP4, CTSD, and Mep-A at the median eminence indicates that the bioactivity of NPY is regulated by peptidases at the interphase between the periphery and the CNS. Detailed ex vivo studies on human sera and CSF samples recognized CTSD as the major NPY-cleaving enzyme in the CSF, whereas an additional C-terminal truncation by angiotensin-converting enzyme (ACE) could be detected in serum. The latter finding hints to potential drug interaction between antidiabetic DP4 inhibitors and anti-hypertensive ACE inhibitors, while it ablates suspected hypertensive side-effects of only antidiabetic DP4-inhibitors application. This article is protected by copyright. All rights reserved.
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