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- Armesto, N., et al.
(författare)
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Heavy-ion collisions at the LHC-Last call for predictions
- 2008
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Ingår i: Journal of Physics G. - : IOP Publishing. - 0954-3899 .- 1361-6471. ; 35:5, s. 054001-
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Forskningsöversikt (refereegranskat)abstract
- This writeup is a compilation of the predictions for the forthcoming Heavy Ion Program at the Large Hadron Collider, as presented at the CERN Theory Institute 'Heavy Ion Collisions at the LHC - Last Call for Predictions', held from 14th May to 10th June 2007.
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- D'Hoore, A., et al.
(författare)
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COMPRES : a prospective postmarketing evaluation of the compression anastomosis ring CAR 27/ColonRing
- 2015
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Ingår i: Colorectal Disease. - : Wiley. - 1462-8910 .- 1463-1318. ; 17:6, s. 522-529
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Tidskriftsartikel (refereegranskat)abstract
- AimPreclinical studies have suggested that nitinol-based compression anastomosis might be a viable solution to anastomotic leak following low anterior resection. A prospective multicentre open label study was therefore designed to evaluate the performance of the ColonRing in (low) colorectal anastomosis. MethodThe primary outcome measure was anastomotic leakage. Patients were recruited at 13 different colorectal surgical units in Europe, the United States and Israel. Institutional review board approval was obtained. ResultsBetween 21 March 2010 and 3 August 2011, 266 patients completed the study protocol. The overall anastomotic leakage rate was 5.3% for all anastomoses, including a rate of 3.1% for low anastomoses. Septic anastomotic complications occurred in 8.3% of all anastomoses and 8.2% of low anastomoses. ConclusionNitinol compression anastomosis is safe, effective and easy to use and may offer an advantage for low colorectal anastomosis. A prospective randomized trial comparing ColonRing with conventional stapling is needed.
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- Lipoma, Lucrecia, et al.
(författare)
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No general support for functional diversity enhancing resilience across terrestrial plant communities
- 2024
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Ingår i: Global Ecology and Biogeography. - : John Wiley & Sons. - 1466-822X .- 1466-8238.
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Forskningsöversikt (refereegranskat)abstract
- Aim: Understanding the mechanisms promoting resilience in plant communities is crucial in times of increasing disturbance and global environmental change. Here, we present the first meta-analysis evaluating the relationship between functional diversity and resilience of plant communities. Specifically, we tested whether the resilience of plant communities is positively correlated with interspecific trait variation (following the niche complementarity hypothesis) and the dominance of acquisitive and small-size species (following the mass ratio hypothesis), and for the context-dependent effects of ecological and methodological differences across studies.Location: Global.Time Period: 2004–2021.Major Taxa Studied: Vascular plants.Methods: We compiled a dataset of 69 independent sites from 26 studies that have quantified resilience. For each site, we calculated functional diversity indices based on the floristic composition and functional traits of the plant community (obtained from the TRY database) which we correlated with resilience of biomass and floristic composition. After transforming correlation coefficients to Fisher's Z-scores, we conducted a hierarchical meta-analysis, using a multilevel random-effects model that accounted for the non-independence of multiple effect sizes and the effects of ecological and methodological moderators. Results: In general, we found no positive functional diversity–resilience relationships of grand mean effect sizes. In contrast to our expectations, we encountered a negative relationship between resilience and trait variety, especially in woody ecosystems, whereas there was a positive relationship between resilience and the dominance of acquisitive species in herbaceous ecosystems. Finally, the functional diversity–resilience relationships were strongly affected by both ecological (biome and disturbance properties) and methodological (temporal scale, study design and resilience metric) characteristics. Main Conclusions: We rejected our hypothesis of a general positive functional diversity–resilience relationship. In addition to strong context dependency, we propose that idiosyncratic effects of single resident species present in the communities before the disturbances and biological legacies could play major roles in the resilience of terrestrial plant communities.
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- Ruppert, Philip M. M., et al.
(författare)
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Fasting induces ANGPTL4 and reduces LPL activity in human adipose tissue
- 2020
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Ingår i: Molecular Metabolism. - : Elsevier. - 2212-8778. ; 40
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Studies in mice have shown that the decrease in lipoprotein lipase (LPL) activity in adipose tissue upon fasting is mediated by induction of the inhibitor ANGPTL4. Here, we aimed to validate this concept in humans by determining the effect of a prolonged fast on ANGPTL4 and LPL gene and protein expression in human subcutaneous adipose tissue.Methods: Twenty-three volunteers ate a standardized meal at 18.00 h and fasted until 20.00 h the next day. Blood was drawn and periumbilical adipose tissue biopsies were collected 2 h and 26 h after the meal.Results: Consistent with previous mouse data, LPL activity in human adipose tissue was significantly decreased by fasting (−60%), concurrent with increased ANGPTL4 mRNA (+90%) and decreased ANGPTL8 mRNA (−94%). ANGPTL4 protein levels in adipose tissue were also significantly increased by fasting (+46%), whereas LPL mRNA and protein levels remained unchanged. In agreement with the adipose tissue data, plasma ANGPTL4 levels increased upon fasting (+100%), whereas plasma ANGPTL8 decreased (−79%). Insulin, levels of which significantly decreased upon fasting, downregulated ANGPTL4 mRNA and protein in primary human adipocytes. By contrast, cortisol, levels of which significantly increased upon fasting, upregulated ANGPTL4 mRNA and protein in primary human adipocytes as did fatty acids.Conclusion: ANGPTL4 levels in human adipose tissue are increased by fasting, likely via increased plasma cortisol and free fatty acids and decreased plasma insulin, resulting in decreased LPL activity.
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- Villard, Eric, et al.
(författare)
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A genome-wide association study identifies two loci associated with heart failure due to dilated cardiomyopathy
- 2011
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 32:9, s. 1065-1076
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Dilated cardiomyopathy (DCM) is a major cause of heart failure with a high familial recurrence risk. So far, the genetics of DCM remains largely unresolved. We conducted the first genome-wide association study (GWAS) to identify loci contributing to sporadic DCM.Methods and results: One thousand one hundred and seventy-nine DCM patients and 1108 controls contributed to the discovery phase. Pools of DNA stratified on disease status, population, age, and gender were constituted and used for testing association of DCM with 517 382 single nucleotide polymorphisms (SNPs). Three DCM-associated SNPs were confirmed by individual genotyping (P < 5.0 10−7), and two of them, rs10927875 and rs2234962, were replicated in independent samples (1165 DCM patients and 1302 controls), with P-values of 0.002 and 0.009, respectively. rs10927875 maps to a region on chromosome 1p36.13 which encompasses several genes among which HSPB7 has been formerly suggested to be implicated in DCM. The second identified locus involves rs2234962, a non-synonymous SNP (c.T757C, p. C151R) located within the sequence of BAG3 on chromosome 10q26. To assess whether coding mutations of BAG3 might cause monogenic forms of the disease, we sequenced BAG3 exons in 168 independent index cases diagnosed with familial DCM and identified four truncating and two missense mutations. Each mutation was heterozygous, present in all genotyped relatives affected by the disease and absent in a control group of 347 healthy individuals, strongly suggesting that these mutations are causing the disease.Conclusion: This GWAS identified two loci involved in sporadic DCM, one of them probably implicates BAG3. Our results show that rare mutations in BAG3 contribute to monogenic forms of the disease, while common variant(s) in the same gene are implicated in sporadic DCM.
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- Vlacil, AK, et al.
(författare)
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Deficiency of Nucleotide-binding oligomerization domain-containing proteins (NOD) 1 and 2 reduces atherosclerosis
- 2020
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Ingår i: Basic research in cardiology. - : Springer Science and Business Media LLC. - 1435-1803 .- 0300-8428. ; 115:4, s. 47-
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Tidskriftsartikel (refereegranskat)abstract
- Atherosclerosis is crucially fueled by inflammatory pathways including pattern recognition receptor (PRR)-related signaling of the innate immune system. Currently, the impact of the cytoplasmic PRRs nucleotide-binding oligomerization domain-containing protein (NOD) 1 and 2 is incompletely characterized. We, therefore, generated Nod1/Nod2 double knockout mice on a low-density lipoprotein receptor (Ldlr)-deficient background (= Ldlr−/−Nod1/2−/−) which were subsequently analyzed regarding experimental atherosclerosis, lipid metabolism, insulin resistance and gut microbiota composition. Compared to Ldlr−/− mice, Ldlr−/−Nod1/2−/− mice showed reduced plasma lipids and increased hepatic expression of the scavenger receptor LDL receptor-related protein 1 after feeding a high-fat diet for 12 weeks. Furthermore, intestinal cholesterol and its bacterial degradation product coprostanol were elevated in Ldlr−/−Nod1/2−/− mice, correlating with the increased abundance of Eubacterium coprostanoligenes as assessed by 3rd generation sequencing of the gut microbiota. Atherosclerotic plaques of Ldlr−/−Nod1/2−/− mice exhibited less lipid deposition and macrophage accumulation. Moreover, macrophages from Ldlr−/−Nod1/2−/− mice showed higher expression of the cholesterol efflux transporters Abca1 and Abcg1 and accordingly reduced foam cell formation. Deficiency of Nod1 and Nod2 led to reduced plaque lipid deposition and inflammatory cell infiltration in atherosclerotic plaques. This might be explained by diminished plasma lipid levels and foam cell formation due to altered expression of key regulators of the hepatic cholesterol pathway as well as differential intestinal cholesterol metabolism and microbiota composition.
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- Yin, Wenguang, et al.
(författare)
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An essential function for autocrine hedgehog signaling in epithelial proliferation and differentiation in the trachea
- 2022
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Ingår i: Development. - : The Company of Biologists. - 0950-1991 .- 1477-9129. ; 149:3
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Tidskriftsartikel (refereegranskat)abstract
- The tracheal epithelium is a primary target for pulmonary diseases as it provides a conduit for air flow between the environment and the lung lobes. The cellular and molecular mechanisms underlying airway epithelial cell proliferation and differentiation remain poorly understood. Hedgehog (HH) signaling orchestrates communication between epithelial and mesenchymal cells in the lung, where it modulates stromal cell proliferation, differentiation and signaling back to the epithelium. Here, we reveal a previously unreported autocrine function of HH signaling in airway epithelial cells. Epithelial cell depletion of the ligand sonic hedgehog (SHH) or its effector smoothened (SMO) causes defects in both epithelial cell proliferation and differentiation. In cultured primary human airway epithelial cells, HH signaling inhibition also hampers cell proliferation and differentiation. Epithelial HH function is mediated, at least in part, through transcriptional activation, as HH signaling inhibition leads to downregulation of cell type-specific transcription factor genes in both the mouse trachea and human airway epithelial cells. These results provide new insights into the role of HH signaling in epithelial cell proliferation and differentiation during airway development.
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