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Sökning: WFRF:(Sommer Felix)

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1.
  • Parseus, Ava, et al. (författare)
  • Microbiota-induced obesity requires farnesoid X receptor
  • 2017
  • Ingår i: Gut. - : BMJ. - 0017-5749 .- 1468-3288. ; 66:3, s. 429-437
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective The gut microbiota has been implicated as an environmental factor that modulates obesity, and recent evidence suggests that microbiota-mediated changes in bile acid profiles and signalling through the bile acid nuclear receptor farnesoid X receptor (FXR) contribute to impaired host metabolism. Here we investigated if the gut microbiota modulates obesity and associated phenotypes through FXR. Design We fed germ-free (GF) and conventionally raised (CONV-R) wild-type and Fxr(-/-) mice a high-fat diet (HFD) for 10 weeks. We monitored weight gain and glucose metabolism and analysed the gut microbiota and bile acid composition, beta-cell mass, accumulation of macrophages in adipose tissue, liver steatosis, and expression of target genes in adipose tissue and liver. We also transferred the microbiota of wild-type and Fxr(-) deficient mice to GF wild-type mice. Results The gut microbiota promoted weight gain and hepatic steatosis in an FXR-dependent manner, and the bile acid profiles and composition of faecal microbiota differed between Fxr(-/-) and wild-type mice. The obese phenotype in colonised wild-type mice was associated with increased beta-cell mass, increased adipose inflammation, increased steatosis and expression of genes involved in lipid uptake. By transferring the caecal microbiota from HFD-fed Fxr(-/-) and wild-type mice into GF mice, we showed that the obesity phenotype was transferable. Conclusions Our results indicate that the gut microbiota promotes diet-induced obesity and associated phenotypes through FXR, and that FXR may contribute to increased adiposity by altering the microbiota composition.
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2.
  • Silberzahn, Raphael, et al. (författare)
  • Many analysts, one dataset : Making transparent how variations in analytical choices affect results
  • 2018
  • Ingår i: Advances in Methods and Practices in Psychological Science. - : Sage Publications. - 2515-2459 .- 2515-2467. ; 1:3, s. 337-356
  • Tidskriftsartikel (refereegranskat)abstract
    • Twenty-nine teams involving 61 analysts used the same dataset to address the same research question: whether soccer referees are more likely to give red cards to dark skin toned players than light skin toned players. Analytic approaches varied widely across teams, and estimated effect sizes ranged from 0.89 to 2.93 in odds ratio units, with a median of 1.31. Twenty teams (69%) found a statistically significant positive effect and nine teams (31%) observed a non-significant relationship. Overall 29 differentanalyses used 21 unique combinations of covariates. We found that neither analysts' prior beliefs about the effect, nor their level of expertise, nor peer-reviewed quality of analysis readily explained variation in analysis outcomes. This suggests that significant variation in the results of analyses of complex data may be difficult to avoid, even by experts with honest intentions. Crowdsourcing data analysis, a strategy by which numerous research teams are recruited to simultaneously investigate the same research question, makes transparent how defensible, yet subjective analytic choices influence research results.
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3.
  • Sommer, Felix, et al. (författare)
  • Site-specific programming of the host epithelial transcriptome by the gut microbiota
  • 2015
  • Ingår i: Genome Biology. - : Springer Science and Business Media LLC. - 1465-6906 .- 1474-760X. ; 16
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The intestinal epithelium separates us from the microbiota but also interacts with it and thus affects host immune status and physiology. Previous studies investigated microbiota-induced responses in the gut using intact tissues or unfractionated epithelial cells, thereby limiting conclusions about regional differences in the epithelium. Here, we sought to investigate microbiota-induced transcriptional responses in specific fractions of intestinal epithelial cells. To this end, we used microarray analysis of laser capture microdissection (LCM)-harvested ileal and colonic tip and crypt epithelial fractions from germ-free and conventionally raised mice and from mice during the time course of colonization. Results: We found that about 10% of the host's transcriptome was microbially regulated, mainly including genes annotated with functions in immunity, cell proliferation, and metabolism. The microbial impact on host gene expression was highly site specific, as epithelial responses to the microbiota differed between cell fractions. Specific transcriptional regulators were enriched in each fraction. In general, the gut microbiota induced a more rapid response in the colon than in the ileum. Conclusions: Our study indicates that the microbiota engage different regulatory networks to alter host gene expression in a particular niche. Understanding host-microbiota interactions on a cellular level may facilitate signaling pathways that contribute to health and disease and thus provide new therapeutic strategies. RAMS GD, 1963, LABORATORY INVESTIGATION, V12, P355
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4.
  • Dupont, A., et al. (författare)
  • Age-Dependent Susceptibility to Enteropathogenic Escherichia coli (EPEC) Infection in Mice
  • 2016
  • Ingår i: Plos Pathogens. - : Public Library of Science (PLoS). - 1553-7366 .- 1553-7374. ; 12:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Enteropathogenic Escherichia coli (EPEC) represents a major causative agent of infant diarrhea associated with significant morbidity and mortality in developing countries. Although studied extensively in vitro, the investigation of the host-pathogen interaction in vivo has been hampered by the lack of a suitable small animal model. Using RT-PCR and global transcriptome analysis, high throughput 16S rDNA sequencing as well as immunofluorescence and electron microscopy, we characterize the EPEC-host interaction following oral challenge of newborn mice. Spontaneous colonization of the small intestine and colon of neonate mice that lasted until weaning was observed. Intimate attachment to the epithelial plasma membrane and microcolony formation were visualized only in the presence of a functional bundle forming pili (BFP) and type III secretion system (T3SS). Similarly, a T3SS-dependent EPEC-induced innate immune response, mediated via MyD88, TLR5 and TLR9 led to the induction of a distinct set of genes in infected intestinal epithelial cells. Infection-induced alterations of the microbiota composition remained restricted to the postnatal period. Although EPEC colonized the adult intestine in the absence of a competing microbiota, no microcolonies were observed at the small intestinal epithelium. Here, we introduce the first suitable mouse infection model and describe an age-dependent, virulence factor-dependent attachment of EPEC to enterocytes in vivo.
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5.
  • Friedrich, Jana, et al. (författare)
  • Investigating hypoxia in aquatic environments: diverse approaches to addressing a complex phenomenon
  • 2014
  • Ingår i: Biogeosciences. - : Copernicus GmbH. - 1726-4170 .- 1726-4189. ; 11, s. 1215-1259
  • Tidskriftsartikel (refereegranskat)abstract
    • In this paper we provide an overview of new knowledge on oxygen depletion (hypoxia) and related phenomena in aquatic systems resulting from the EU-FP7 project HYPOX (“In situ monitoring of oxygen depletion in hypoxic ecosystems of coastal and open seas, and landlocked water bodies”, www.hypox.net). In view of the anticipated oxygen loss in aquatic systems due to eutrophication and climate change, HYPOX was set up to improve capacities to monitor hypoxia as well as to understand its causes and consequences. Temporal dynamics and spatial patterns of hypoxia were analyzed in field studies in various aquatic environments, including the Baltic Sea, the Black Sea, Scottish and Scandinavian fjords, Ionian Sea lagoons and embayments, and Swiss lakes. Examples of episodic and rapid (hours) occurrences of hypoxia, as well as seasonal changes in bottom-water oxygenation in stratified systems, are discussed. Geologically driven hypoxia caused by gas seepage is demonstrated. Using novel technologies, temporal and spatial patterns of watercolumn oxygenation, from basin-scale seasonal patterns to meter-scale sub-micromolar oxygen distributions, were resolved. Existing multidecadal monitoring data were used to demonstrate the imprint of climate change and eutrophication on long-term oxygen distributions. Organic and inorganic proxies were used to extend investigations on past oxygen conditions to centennial and even longer timescales that cannot be resolved by monitoring. The effects of hypoxia on faunal communities and biogeochemical processes were also addressed in the project. An investigation of benthic fauna is presented as an example of hypoxia-devastated benthic communities that slowly recover upon a reduction in eutrophication in a system where naturally occurring hypoxia overlaps with anthropogenic hypoxia. Biogeochemical investigations reveal that oxygen intrusions have a strong effect on the microbially mediated redox cycling of elements. Observations and modeling studies of the sediments demonstrate the effect of seasonally changing oxygen conditions on benthic mineralization pathways and fluxes. Data quality and access are crucial in hypoxia research. Technical issues are therefore also addressed, including the availability of suitable sensor technology to resolve the gradual changes in bottom-water oxygen in marine systems that can be expected as a result of climate change. Using cabled observatories as examples, we show how the benefit of continuous oxygen monitoring can be maximized by adopting proper quality control. Finally, we discuss strategies for state-of-the-art data archiving and dissemination in compliance with global standards, and how ocean observations can contribute to global earth observation attempts.
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6.
  • Fuchs, B., et al. (författare)
  • Regulation of Polyp-to-Jellyfish Transition in Aurelia aurita
  • 2014
  • Ingår i: Current Biology. - : Elsevier BV. - 0960-9822. ; 24:3, s. 263-273
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The life cycle of scyphozoan cnidarians alternates between sessile asexual polyps and pelagic medusa. Transition from one life form to another is triggered by environmental signals, but the molecular cascades involved in the drastic morphological and physiological changes remain unknown. Results: We show in the moon jelly Aurelia aurita that the molecular machinery controlling transition of the sessile polyp into a free-swimming jellyfish consists of two parts. One is conserved and relies on retinoic acid signaling. The second, novel part is based on secreted proteins that are strongly upregulated prior to metamorphosis in response to the seasonal temperature changes. One of these proteins functions as a temperature-sensitive "timer" and encodes the precursor of the strobilation hormone of Aurelia. Conclusions: Our findings uncover the molecule framework controlling the polyp-to-jellyfish transition in a basal metazoan and provide insights into the evolution of complex life cycles in the animal kingdom.
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7.
  • Fulde, M., et al. (författare)
  • Neonatal selection by Toll-like receptor 5 influences long-term gut microbiota composition
  • 2018
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 560:7719
  • Tidskriftsartikel (refereegranskat)abstract
    • Alterations in enteric microbiota are associated with several highly prevalent immune-mediated and metabolic diseases(1-3), and experiments involving faecal transplants have indicated that such alterations have a causal role in at least some such conditions(4-6). The postnatal period is particularly critical for the development of microbiota composition, host-microbe interactions and immune homeostasis(7-9). However, the underlying molecular mechanisms of this neonatal priming period have not been defined. Here we report the identification of a host-mediated regulatory circuit of bacterial colonization that acts solely during the early neonatal period but influences life-long microbiota composition. We demonstrate age-dependent expression of the flagellin receptor Toll-like receptor 5 (TLR5) in the gut epithelium of neonate mice. Using competitive colonization experiments, we demonstrate that epithelial TLR5-mediated REG3 gamma production is critical for the counter-selection of colonizing flagellated bacteria. Comparative microbiota transfer experiments in neonate and adult wild-type and Tlr5-deficient germ-free mice reveal that neonatal TLR5 expression strongly influences the composition of the microbiota throughout life. Thus, the beneficial microbiota in the adult host is shaped during early infancy. This might explain why environmental factors that disturb the establishment of the microbiota during early life can affect immune homeostasis and health in adulthood.
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8.
  • Graham, Jesse R., et al. (författare)
  • The pipeline project: Pre-publication independent replications of a single laboratory's research pipeline
  • 2016
  • Ingår i: Journal of Experimental Social Psychology. - : Elsevier. - 1096-0465 .- 0022-1031. ; 66, s. 55-67
  • Tidskriftsartikel (refereegranskat)abstract
    • This crowdsourced project introduces a collaborative approach to improving the reproducibility of scientific research, in which findings are replicated in qualified independent laboratories before (rather than after) they are published. Our goal is to establish a non-adversarial replication process with highly informative final results. To illustrate the Pre-Publication Independent Replication (PPIR) approach, 25 research groups conducted replications of all ten moral judgment effects which the last author and his collaborators had “in the pipeline” as of August 2014. Six findings replicated according to all replication criteria, one finding replicated but with a significantly smaller effect size than the original, one finding replicated consistently in the original culture but not outside of it, and two findings failed to find support. In total, 40% of the original findings failed at least one major replication criterion. Potential ways to implement and incentivize pre-publication independent replication on a large scale are discussed.
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9.
  • Grunddal, K. V., et al. (författare)
  • Neurotensin Is Coexpressed, Coreleased, and Acts Together With GLP-1 and PYY in Enteroendocrine Control of Metabolism
  • 2016
  • Ingår i: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 157:1, s. 176-194
  • Tidskriftsartikel (refereegranskat)abstract
    • The 2 gut hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are well known to be coexpressed, costored, and released together to coact in the control of key metabolic target organs. However, recently, it became clear that several other gut hormones can be coexpressed in the intestinal-specific lineage of enteroendocrine cells. Here, we focus on the anatomical and functional consequences of the coexpression of neurotensin with GLP-1 and PYY in the distal small intestine. Fluorescence-activated cell sorting analysis, laser capture, and triple staining demonstrated that GLP-1 cells in the crypts become increasingly multihormonal, ie, coexpressing PYY and neurotensin as they move up the villus. Proglucagon promoter and pertussis toxin receptor-driven cell ablation and reappearance studies indicated that although all the cells die, the GLP-1 cells reappear more quickly than PYY- and neurotensin-positive cells. High-resolution confocal fluorescence microscopy demonstrated that neurotensin is stored in secretory granules distinct from GLP-1 and PYY storing granules. Nevertheless, the 3 peptides were cosecreted from both perfused small intestines and colonic crypt cultures in response to a series of metabolite, neuropeptide, and hormonal stimuli. Importantly, neurotensin acts synergistically, ie, more than additively together with GLP-1 and PYY to decrease palatable food intake and inhibit gastric emptying, but affects glucose homeostasis in a more complex manner. Thus, neurotensin is a major gut hormone deeply integrated with GLP-1 and PYY, which should be taken into account when exploiting the enteroendocrine regulation of metabolism pharmacologically.
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10.
  • Ihne-Schubert, Sandra Michaela, et al. (författare)
  • Cardio-Hepatic Interaction in Cardiac Amyloidosis
  • 2024
  • Ingår i: Journal of Clinical Medicine. - 2077-0383. ; 13:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Congestion is associated with poor prognosis in cardiac amyloidosis (CA). The cardio-hepatic interaction and the prognostic impact of secondary liver affection by cardiac congestion in CA are poorly understood and require further characterisation. Methods: Participants of the amyloidosis cohort study AmyKoS at the Interdisciplinary Amyloidosis Centre of Northern Bavaria with proven transthyretin (ATTR-CA) and light chain CA (AL-CA) underwent serial work-up including laboratory tests, echocardiography, and in-depth hepatic assessment by vibration-controlled transient elastography (VCTE) and 13C-methacetin breath test. Results: In total, 74 patients with AL-CA (n = 17), ATTR-CA (n = 26) and the controls (n = 31) were analysed. ATTR-CA patients showed decreased microsomal liver function expressed by maximal percentage of dose rate (PDRpeak) related to hepatic congestion. Reduced PDRpeak in AL-CA could result from altered pharmacokinetics due to changed hepatic blood flow. Liver stiffness as a combined surrogate of chronic liver damage and congestion was identified as a predictor of all-cause mortality. Statistical modelling of the cardio-hepatic interaction revealed septum thickness, NT-proBNP and PDRpeak as predictors of liver stiffness in both CA subtypes; dilatation of liver veins and the fibrosis score FIB-4 were only significant for ATTR-CA. Conclusions: Non-invasive methods allow us to characterise CA-associated hepatic pathophysiology. Liver stiffness might be promising for risk stratification in CA.
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11.
  • Jakobsson, Hedvig E, et al. (författare)
  • The composition of the gut microbiota shapes the colon mucus barrier.
  • 2015
  • Ingår i: EMBO reports. - : EMBO. - 1469-3178 .- 1469-221X. ; 16, s. 164-177
  • Tidskriftsartikel (refereegranskat)abstract
    • Two C57BL/6 mice colonies maintained in two rooms of the same specific pathogen-free (SPF) facility were found to have different gut microbiota and a mucus phenotype that was specific for each colony. The thickness and growth of the colon mucus were similar in the two colonies. However, one colony had mucus that was impenetrable to bacteria or beads the size of bacteria-which is comparable to what we observed in free-living wild mice-whereas the other colony had an inner mucus layer penetrable to bacteria and beads. The different properties of the mucus depended on the microbiota, as they were transmissible by transfer of caecal microbiota to germ-free mice. Mice with an impenetrable mucus layer had increased amounts of Erysipelotrichi, whereas mice with a penetrable mucus layer had higher levels of Proteobacteria and TM7 bacteria in the distal colon mucus. Thus, our study shows that bacteria and their community structure affect mucus barrier properties in ways that can have implications for health and disease. It also highlights that genetically identical animals housed in the same facility can have rather distinct microbiotas and barrier structures.
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12.
  • Pan, W. H., et al. (författare)
  • Exposure to the gut microbiota drives distinct methylome and transcriptome changes in intestinal epithelial cells during postnatal development
  • 2018
  • Ingår i: Genome Medicine. - : Springer Science and Business Media LLC. - 1756-994X. ; 10
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The interplay of epigenetic processes and the intestinal microbiota may play an important role in intestinal development and homeostasis. Previous studies have established that the microbiota regulates a large proportion of the intestinal epithelial transcriptome in the adult host, but microbial effects on DNA methylation and gene expression during early postnatal development are still poorly understood. Here, we sought to investigate the microbial effects on DNA methylation and the transcriptome of intestinal epithelial cells (IECs) during postnatal development. Methods: We collected IECs from the small intestine of each of five 1-, 4-and 12 to 16-week-old mice representing the infant, juvenile, and adult states, raised either in the presence or absence of a microbiota. The DNA methylation profile was determined using reduced representation bisulfite sequencing (RRBS) and the epithelial transcriptome by RNA sequencing using paired samples from each individual mouse to analyze the link between microbiota, gene expression, and DNA methylation. Results: We found that microbiota-dependent and -independent processes act together to shape the postnatal development of the transcriptome and DNA methylation signatures of IECs. The bacterial effect on the transcriptome increased over time, whereas most microbiota-dependent DNA methylation differences were detected already early after birth. Microbiota-responsive transcripts could be attributed to stage-specific cellular programs during postnatal development and regulated gene sets involved primarily immune pathways and metabolic processes. Integrated analysis of the methylome and transcriptome data identified 126 genomic loci at which coupled differential DNA methylation and RNA transcription were associated with the presence of intestinal microbiota. We validated a subset of differentially expressed and methylated genes in an independent mouse cohort, indicating the existence of microbiota-dependent " functional" methylation sites which may impact on long-term gene expression signatures in IECs. Conclusions: Our study represents the first genome-wide analysis of microbiota-mediated effects on maturation of DNA methylation signatures and the transcriptional program of IECs after birth. It indicates that the gut microbiota dynamically modulates large portions of the epithelial transcriptome during postnatal development, but targets only a subset of microbially responsive genes through their DNA methylation status.
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13.
  • Sommer, Felix, et al. (författare)
  • Altered mucus glycosylation in core 1 O-glycan-deficient mice affects microbiota composition and intestinal architecture.
  • 2014
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 9:1
  • Tidskriftsartikel (refereegranskat)abstract
    • A functional mucus layer is a key requirement for gastrointestinal health as it serves as a barrier against bacterial invasion and subsequent inflammation. Recent findings suggest that mucus composition may pose an important selection pressure on the gut microbiota and that altered mucus thickness or properties such as glycosylation lead to intestinal inflammation dependent on bacteria. Here we used TM-IEC C1galt (-/-) mice, which carry an inducible deficiency of core 1-derived O-glycans in intestinal epithelial cells, to investigate the effects of mucus glycosylation on susceptibility to intestinal inflammation, gut microbial ecology and host physiology. We found that TM-IEC C1galt (-/-) mice did not develop spontaneous colitis, but they were more susceptible to dextran sodium sulphate-induced colitis. Furthermore, loss of core 1-derived O-glycans induced inverse shifts in the abundance of the phyla Bacteroidetes and Firmicutes. We also found that mucus glycosylation impacts intestinal architecture as TM-IEC C1galt(-/-) mice had an elongated gastrointestinal tract with deeper ileal crypts, a small increase in the number of proliferative epithelial cells and thicker circular muscle layers in both the ileum and colon. Alterations in the length of the gastrointestinal tract were partly dependent on the microbiota. Thus, the mucus layer plays a role in the regulation of gut microbiota composition, balancing intestinal inflammation, and affects gut architecture.
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14.
  • Sommer, Felix, et al. (författare)
  • Know your neighbor: Microbiota and host epithelial cells interact locally to control intestinal function and physiology
  • 2016
  • Ingår i: Bioessays. - : Wiley. - 0265-9247. ; 38:5, s. 455-464
  • Tidskriftsartikel (refereegranskat)abstract
    • Interactions between the host and its associated microbiota differ spatially and the local cross talk determines organ function and physiology. Animals and their organs are not uniform but contain several functional and cellular compartments and gradients. In the intestinal tract, different parts of the gut carry out different functions, tissue structure varies accordingly, epithelial cells are differentially distributed and gradients exist for several physicochemical parameters such as nutrients, pH, or oxygen. Consequently, the microbiota composition also differs along the length of the gut, but also between lumen and mucosa of the same intestinal segment, and even along the crypt-villus axis in the epithelium. Thus, host-microbiota interactions are highly site-specific and the local cross talk determines intestinal function and physiology. Here we review recent advances in our understanding of site-specific host-microbiota interactions and discuss their functional relevance for host physiology. RAMS GD, 1963, LABORATORY INVESTIGATION, V12, P355
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15.
  • Sommer, Felix, et al. (författare)
  • The gut microbiota engages different signaling pathways to induce Duox2 expression in the ileum and colon epithelium
  • 2015
  • Ingår i: Mucosal Immunology. - : Elsevier BV. - 1933-0219. ; 8:2, s. 372-379
  • Tidskriftsartikel (refereegranskat)abstract
    • The epithelium is a first line of defense against microorganisms in the gut. Reactive oxygen species (ROS) have an important role in controlling the normal gut microbiota and pathogenic bacteria. Dual oxidase 2 (DUOX2) is an important source of hydrogen peroxide in the small and large intestine, and the gut microbiota induces Duox2 expression. Here, we investigated the microbial regulation of Duox2 expression. We found that Duox2 was expressed by intestinal epithelial cells mainly in the tip of the epithelium. Duox2 expression wasstrongly induced by the presence of a normal microbiota in mice, but not when germ-free mice were colonized with various commensal bacteria. Duox2 expression was more rapidly induced by the gut microbiota in the colon than in the ileum. Furthermore, we showed that regulation of Duox2 expression in the ileum involved TIR-domain-containing adaptor protein including interferon-beta (TRIF) and canonical nuclear factor-kappa B p50/p65 signaling, whereas regulation of Duox2 expression in the colon involved MyD88 and the p38 pathway. Collectively, these data indicate that the gut microbiota uses two distinct signaling pathways to induce Duox2 expression in the ileum and colon epithelium.
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16.
  • Sommer, Felix, et al. (författare)
  • The gut microbiota--masters of host development and physiology.
  • 2013
  • Ingår i: Nature reviews. Microbiology. - : Springer Science and Business Media LLC. - 1740-1534 .- 1740-1526. ; 11:4, s. 227-38
  • Tidskriftsartikel (refereegranskat)abstract
    • Establishing and maintaining beneficial interactions between the host and its associated microbiota are key requirements for host health. Although the gut microbiota has previously been studied in the context of inflammatory diseases, it has recently become clear that this microbial community has a beneficial role during normal homeostasis, modulating the host's immune system as well as influencing host development and physiology, including organ development and morphogenesis, and host metabolism. The underlying molecular mechanisms of host-microorganism interactions remain largely unknown, but recent studies have begun to identify the key signalling pathways of the cross-species homeostatic regulation between the gut microbiota and its host.
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17.
  • Sommer, Felix, et al. (författare)
  • The Gut Microbiota Modulates Energy Metabolism in the Hibernating Brown Bear Ursus arctos
  • 2016
  • Ingår i: Cell Reports. - Cambridge, USA : Elsevier BV. - 2211-1247. ; 14:7, s. 1655-1661
  • Tidskriftsartikel (refereegranskat)abstract
    • Hibernation is an adaptation that helps many animals to conserve energy during food shortage in winter. Brown bears double their fat depots during summer and use these stored lipids during hibernation. Although bears seasonally become obese, they remain metabolically healthy. We analyzed the microbiota of free-ranging brown bears during their active phase and hibernation. Compared to the active phase, hibernation microbiota had reduced diversity, reduced levels of Firmicutes and Actinobacteria, and increased levels of Bacteroidetes. Several metabolites involved in lipid metabolism, including triglycerides, cholesterol, and bile acids, were also affected by hibernation. Transplantation of the bear microbiota from summer and winter to germ-free mice transferred some of the seasonal metabolic features and demonstrated that the summer microbiota promoted adiposity without impairing glucose tolerance, suggesting that seasonal variation in the microbiota may contribute to host energy metabolism in the hibernating brown bear.
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18.
  • Washburn, Anthony N., et al. (författare)
  • Data from a pre-publication independent replication initiative examining ten moral judgement effects
  • 2016
  • Ingår i: Scientific Data. - : Nature Research (part of Springer Nature): Fully open access journals / Nature Publishing Group. - 2052-4463. ; 3
  • Tidskriftsartikel (refereegranskat)abstract
    • We present the data from a crowdsourced project seeking to replicate findings in  independent laboratories before (rather than after) they are published. In this Pre-Publication Independent Replication (PPIR) initiative, 25 research groups attempted to replicate 10 moral judgment effects from a single laboratory's research pipeline of unpublished findings. The 10 effects were investigated using online/lab surveys containing psychological manipulations (vignettes) followed by questionnaires.
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19.
  • 2017
  • swepub:Mat__t
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