| 1. |
-
The Seventeenth Data Release of the Sloan Digital Sky Surveys : Complete Release of MaNGA, MaStar, and APOGEE-2 Data
- 2022
-
In: Astrophysical Journal Supplement Series. - : Institute of Physics (IOP). - 0067-0049 .- 1538-4365. ; 259:2
-
Journal article (peer-reviewed)abstract
- This paper documents the seventeenth data release (DR17) from the Sloan Digital Sky Surveys; the fifth and final release from the fourth phase (SDSS-IV). DR17 contains the complete release of the Mapping Nearby Galaxies at Apache Point Observatory (MaNGA) survey, which reached its goal of surveying over 10,000 nearby galaxies. The complete release of the MaNGA Stellar Library accompanies this data, providing observations of almost 30,000 stars through the MaNGA instrument during bright time. DR17 also contains the complete release of the Apache Point Observatory Galactic Evolution Experiment 2 survey that publicly releases infrared spectra of over 650,000 stars. The main sample from the Extended Baryon Oscillation Spectroscopic Survey (eBOSS), as well as the subsurvey Time Domain Spectroscopic Survey data were fully released in DR16. New single-fiber optical spectroscopy released in DR17 is from the SPectroscipic IDentification of ERosita Survey subsurvey and the eBOSS-RM program. Along with the primary data sets, DR17 includes 25 new or updated value-added catalogs. This paper concludes the release of SDSS-IV survey data. SDSS continues into its fifth phase with observations already underway for the Milky Way Mapper, Local Volume Mapper, and Black Hole Mapper surveys.
|
|
| 2. |
- Holleboom, Adriaan G, et al.
(author)
-
Heterozygosity for a Loss-of-Function Mutation in GALNT2 Improves Plasma Triglyceride Clearance in Man
- 2011
-
In: Cell Metabolism. - : Elsevier. - 1550-4131 .- 1932-7420. ; 14:6, s. 811-8
-
Journal article (peer-reviewed)abstract
- Genome-wide association studies have identified GALNT2 as a candidate gene in lipid metabolism, but it is not known how the encoded enzyme ppGalNAc-T2, which contributes to the initiation of mucin-type O-linked glycosylation, mediates this effect. In two probands with elevated plasma high-density lipoprotein cholesterol and reduced triglycerides, we identified a mutation in GALNT2. It is shown that carriers have improved postprandial triglyceride clearance, which is likely attributable to attenuated glycosylation of apolipoprotein (apo) C-III, as observed in their plasma. This protein inhibits lipoprotein lipase (LPL), which hydrolyses plasma triglycerides. We show that an apoC-III-based peptide is a substrate for ppGalNAc-T2 while its glycosylation by the mutant enzyme is impaired. In addition, neuraminidase treatment of apoC-III which removes the sialic acids from its glycan chain decreases its potential to inhibit LPL. Combined, these data suggest that ppGalNAc-T2 can affect lipid metabolism through apoC-III glycosylation, thereby establishing GALNT2 as a lipid-modifying gene.
|
|
| 3. |
- Cornelissen, Johannes H C, et al.
(author)
-
Global negative vegetation feedback to climate warming responses of leaf litter decomposition rates in cold biomes
- 2007
-
In: Ecology Letters. - : Wiley. - 1461-023X .- 1461-0248. ; 10:7, s. 619-627
-
Journal article (peer-reviewed)abstract
- Whether climate change will turn cold biomes from large long-term carbon sinks into sources is hotly debated because of the great potential for ecosystem-mediated feedbacks to global climate. Critical are the direction, magnitude and generality of climate responses of plant litter decomposition. Here, we present the first quantitative analysis of the major climate-change-related drivers of litter decomposition rates in cold northern biomes worldwide.Leaf litters collected from the predominant species in 33 global change manipulation experiments in circum-arctic-alpine ecosystems were incubated simultaneously in two contrasting arctic life zones. We demonstrate that longer-term, large-scale changes to leaf litter decomposition will be driven primarily by both direct warming effects and concomitant shifts in plant growth form composition, with a much smaller role for changes in litter quality within species. Specifically, the ongoing warming-induced expansion of shrubs with recalcitrant leaf litter across cold biomes would constitute a negative feedback to global warming. Depending on the strength of other (previously reported) positive feedbacks of shrub expansion on soil carbon turnover, this may partly counteract direct warming enhancement of litter decomposition.
|
|
| 4. |
- Cornwell, William K., et al.
(author)
-
Plant species traits are the predominant control on litter decomposition rates within biomes worldwide
- 2008
-
In: Ecology Letters. - : Wiley. - 1461-023X .- 1461-0248. ; 11:10, s. 1065-1071
-
Journal article (peer-reviewed)abstract
- Worldwide decomposition rates depend both on climate and the legacy of plant functional traits as litter quality. To quantify the degree to which functional differentiation among species affects their litter decomposition rates, we brought together leaf trait and litter mass loss data for 818 species from 66 decomposition experiments on six continents. We show that: (i) the magnitude of species-driven differences is much larger than previously thought and greater than climate-driven variation; (ii) the decomposability of a species' litter is consistently correlated with that species' ecological strategy within different ecosystems globally, representing a new connection between whole plant carbon strategy and biogeochemical cycling. This connection between plant strategies and decomposability is crucial for both understanding vegetation-soil feedbacks, and for improving forecasts of the global carbon cycle.
|
|
| 5. |
- Dahl, Maria, et al.
(author)
-
Correction of pathology in mice displaying Gaucher disease type 1 by a clinically-applicable lentiviral vector
- 2021
-
In: Molecular Therapy - Methods and Clinical Development. - : Elsevier BV. - 2329-0501. ; 20, s. 312-323
-
Journal article (peer-reviewed)abstract
- This study evaluates a clinically applicable lentiviral vector for treatment of Gaucher disease type 1. Hematopoietic stem cells transduced with the vector and transplanted into a mouse model successfully halted or reversed pathology. These data were used as proof-of-concept for regulatory filing enabling the commencement of an international phase 1/2 clinical trial.
|
|
| 6. |
- Marques, André R A, et al.
(author)
-
Glucosylated cholesterol in mammalian cells and tissues: formation and degradation by multiple cellular β-glucosidases.
- 2016
-
In: Journal of Lipid Research. - 1539-7262. ; 57, s. 451-463
-
Journal article (peer-reviewed)abstract
- The membrane lipid glucosylceramide (GlcCer) is continuously formed and degraded. Cells express two GlcCer-degrading β-glucosidases, GBA and GBA2, located in and outside the lysosome, respectively. Here we demonstrate that through transglucosylation both GBA and GBA2 are able to catalyze in vitro the transfer of glucosyl-moieties from GlcCer to cholesterol, and vice versa. Furthermore, the natural occurrence of 1-O-cholesteryl-β-D-glucopyranoside (GlcChol) in mouse tissues and human plasma is demonstrated using LC-MS/MS and 13C6-labelled GlcChol as internal standard. In cells the inhibition of GBA increases GlcChol, whereas inhibition of GBA2 decreases glucosylated sterol. Similarly, in GBA2-deficient mice GlcChol is reduced. Depletion of GlcCer by inhibition of GlcCer synthase decreases GlcChol in cells and likewise in plasma of inhibitor-treated Gaucher disease patients. In tissues of mice with Niemann-Pick type C, a condition characterized by intralysosomal accumulation of cholesterol, marked elevations in GlcChol occur as well. When lysosomal accumulation of cholesterol is induced in cultured cells, GlcChol is formed via lysosomal GBA. This illustrates that reversible transglucosylation reactions are highly dependent on local availability of suitable acceptors. In conclusion, mammalian tissues contain GlcChol formed by transglucosylation through β-glucosidases using GlcCer as donor. Our findings reveal a novel metabolic function for GlcCer.
|
|
| 7. |
- Pavlova, Elena V., et al.
(author)
-
Inhibition of UDP-glucosylceramide synthase in mice prevents Gaucher disease-associated B-cell malignancy
- 2015
-
In: Journal of Pathology. - : Wiley. - 0022-3417. ; 235:1, s. 113-124
-
Journal article (peer-reviewed)abstract
- Clonal B-cell proliferation is a frequent manifestation of Gaucher disease-a sphingolipidosis associated with a high risk of multiple myeloma and non-Hodgkin lymphoma. Gaucher disease is caused by genetic deficiency of acid -glucosidase, the natural substrates of which (-d-glucosylceramide and -d-glucosylsphingosine) accumulate, principally in macrophages. Mice with inducible deficiency of -glucosidase [Gba(tm1Karl/tm1Karl)Tg(MX1-cre)1Cgn/0] serve as an authentic model of human Gaucher disease; we have recently reported clonal B-cell proliferation accompanied by monoclonal serum paraproteins and cognate tumours in these animals. To explore the relationship between B-cell malignancy and the biochemical defect, we treated Gaucher mice with eliglustat tartrate (GENZ 112638), a potent and selective inhibitor of the first committed step in glycosphingolipid biosynthesis. Twenty-two Gaucher mice received 300mg/kg of GENZ 112638 daily for 3-10 months from 6 weeks of age. Plasma concentrations of -d-glucosylceramide and the unacylated glycosphingolipid, -d-glucosylsphingosine, declined. After administration of GENZ 112638 to Gaucher mice for 3-10 months, serum paraproteins were not detected and there was a striking reduction in the malignant lymphoproliferation: neither lymphomas nor plasmacytomas were found in animals that had received the investigational agent. In contrast, 14 out of 60 Gaucher mice without GENZ 112638 treatment developed these tumours; monoclonal paraproteins were detected in plasma from 18 of the 44 age-matched mice with Gaucher disease that had not received GENZ 112638. Long-term inhibition of glycosphingolipid biosynthesis suppresses the development of spontaneous B-cell lymphoma and myeloma in Gaucher mice. Copyright (c) 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
|
|
| 8. |
- Hicks Pries, Caitlin E., et al.
(author)
-
Decadal warming causes a consistent and persistent shift from heterotrophic to autotrophic respiration in contrasting permafrost ecosystems
- 2015
-
In: Global Change Biology. - : Wiley. - 1354-1013 .- 1365-2486. ; 21:12, s. 4508-4519
-
Journal article (peer-reviewed)abstract
- Soil carbon in permafrost ecosystems has the potential to become a major positive feedback to climate change if permafrost thaw increases heterotrophic decomposition. However, warming can also stimulate autotrophic production leading to increased ecosystem carbon storage-a negative climate change feedback. Few studies partitioning ecosystem respiration examine decadal warming effects or compare responses among ecosystems. Here, we first examined how 11 years of warming during different seasons affected autotrophic and heterotrophic respiration in a bryophyte-dominated peatland in Abisko, Sweden. We used natural abundance radiocarbon to partition ecosystem respiration into autotrophic respiration, associated with production, and heterotrophic decomposition. Summertime warming decreased the age of carbon respired by the ecosystem due to increased proportional contributions from autotrophic and young soil respiration and decreased proportional contributions from old soil. Summertime warming's large effect was due to not only warmer air temperatures during the growing season, but also to warmer deep soils year-round. Second, we compared ecosystem respiration responses between two contrasting ecosystems, the Abisko peatland and a tussock-dominated tundra in Healy, Alaska. Each ecosystem had two different timescales of warming (<5years and over a decade). Despite the Abisko peatland having greater ecosystem respiration and larger contributions from heterotrophic respiration than the Healy tundra, both systems responded consistently to short- and long-term warming with increased respiration, increased autotrophic contributions to ecosystem respiration, and increased ratios of autotrophic to heterotrophic respiration. We did not detect an increase in old soil carbon losses with warming at either site. If increased autotrophic respiration is balanced by increased primary production, as is the case in the Healy tundra, warming will not cause these ecosystems to become growing season carbon sources. Warming instead causes a persistent shift from heterotrophic to more autotrophic control of the growing season carbon cycle in these carbon-rich permafrost ecosystems.
|
|
| 9. |
- Keuper, Frida, et al.
(author)
-
A race for space? : How Sphagnum fuscumstabilizes vegetation composition during long-termclimate manipulations
- 2011
-
In: Global Change Biology. - : Blackwell. - 1354-1013 .- 1365-2486. ; 17:6, s. 2162-2171
-
Journal article (peer-reviewed)abstract
- Strong climate warming is predicted at higher latitudes this century, with potentially major consequences forproductivity and carbon sequestration. Although northern peatlands contain one-third of the world’s soil organiccarbon, little is known about the long-term responses to experimental climate change of vascular plant communities inthese Sphagnum-dominated ecosystems.We aimed to see how long-term experimental climate manipulations, relevantto different predicted future climate scenarios, affect total vascular plant abundance and species composition whenthe community is dominated by mosses. During 8 years, we investigated how the vascular plant community of aSphagnum fuscum-dominated subarctic peat bog responded to six experimental climate regimes, including factorialcombinations of summer as well as spring warming and a thicker snow cover. Vascular plant species composition inour peat bog was more stable than is typically observed in (sub)arctic experiments: neither changes in total vascularplant abundance, nor in individual species abundances, Shannon’s diversity or evenness were found in response tothe climate manipulations. For three key species (Empetrum hermaphroditum, Betula nana and S. fuscum) we alsomeasured whether the treatments had a sustained effect on plant length growth responses and how these responsesinteracted. Contrasting with the stability at the community level, both key shrubs and the peatmoss showed sustainedpositive growth responses at the plant level to the climate treatments. However, a higher percentage of mossencroachedE. hermaphroditum shoots and a lack of change in B. nana net shrub height indicated encroachment byS. fuscum, resulting in long-term stability of the vascular community composition: in a warmer world, vascular speciesof subarctic peat bogs appear to just keep pace with growing Sphagnum in their race for space. Our findings contributeto general ecological theory by demonstrating that community resistance to environmental changes does notnecessarily mean inertia in vegetation response.
|
|
| 10. |
- Serra-Vinardell, Jenny, et al.
(author)
-
Selective chaperone effect of aminocyclitol derivatives on G202R and other mutant glucocerebrosidases causing Gaucher disease
- 2014
-
In: International Journal of Biochemistry and Cell Biology. - : Elsevier BV. - 1357-2725 .- 1878-5875. ; 54, s. 245-254
-
Journal article (peer-reviewed)abstract
- Gaucher disease is an autosomal recessive lysosomal disorder characterized by the accumulation of glucosylceramide as a result of a deficiency of the enzyme glucocerebrosidase. Several competitive glucocerebrosidase inhibitors are able to act as pharmacological chaperones for an efficient rescue of the mutated, misfolded forms of the enzyme. Along this line, we report in this work on the ability of several aminocyclitols to increase the residual glucocerebrosidase activity in patient fibroblasts with different genotypes. Some of the compounds were slightly active on fibroblasts bearing some mutations, including the highly prevalent N370S mutation. All compounds were highly active as enzyme activity enhancers on fibroblasts from Gaucher disease patients containing the G202R mutation. Moreover, using the novel tagged sphingolipid omega-azidosphingosine, a reduction in the tagged glucosylceramide accumulation was also observed for selected aminocyclitols. Attempts to explain the activity impairment observed in glucocerebrosidase bearing the G202R mutation by comparative molecular dynamic studies on wild type and the G202R mutated proteins (free and isofagomine-bound, in both cases) were unsuccessful. Under the simulation conditions used, no clear effect of the G202R mutation neither over the global structure of the protein nor on the loops that constitute the glucocerebrosidase active site was observed. Since the G202R residue is located on the protein surface, altered protein-membrane or protein-protein interactions could account for the observed differences. In conclusion, we have tested novel compounds that have shown some chaperone effect on particular glucocerebrosidase mutant enzymes, supporting the enhancement therapy as an alternative approach for Gaucher disease. (C) 2014 Elsevier Ltd. All rights reserved.
|
|
