| 1. |
- Nadolny, Jakub, et al.
(författare)
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Main Sequence to Starburst Transitioning Galaxies : Gamma-Ray Burst Hosts at z ∼ 2
- 2023
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Ingår i: Astrophysical Journal. - 0004-637X .- 1538-4357. ; 952:2
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Tidskriftsartikel (refereegranskat)abstract
- Star-forming galaxies populate a main sequence (MS), a well-defined relation between stellar mass (M*) and star formation rate (SFR). Starburst (SB) galaxies lie significantly above the relation, whereas quenched galaxies lie below the sequence. In order to study the evolution of galaxies on the SFR–M* plane and its connection to the gas content, we use the fact that recent episodes of star formation can be pinpointed by the existence of gamma-ray bursts (GRBs). Here we present sensitive [C i] nondetections of z ∼ 2 ultraluminous infrared (ULIRG) GRB host galaxies. We find that our GRB hosts have similar molecular masses to those of other ULIRGs. However, unlike other ULIRGs, the GRB hosts are located at the MS or only a factor of a few above it. Hence, our GRB hosts are caught in the transition toward the SB phase. This is further supported by the estimated depletion times, which are similar to those of other transitioning galaxies. The GRB hosts are [C i]-dark galaxies, defined as having a [C i]/CO temperature brightness ratio of <0.1. Such a low [C i]/CO ratio has been found in high-density environments (nH > 104 cm−3) where CO is shielded from photodissociation, leading to underabundances of [C i]. This is consistent with the merger process that is indeed suggested for our GRB hosts by their morphologies.
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| 2. |
- Zaniew, Marcin, et al.
(författare)
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Long-term renal outcome in children with OCRL mutations : Retrospective analysis of a large international cohort
- 2018
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Ingår i: Nephrology Dialysis Transplantation. - : Oxford University Press (OUP). - 0931-0509 .- 1460-2385. ; 33:1, s. 85-94
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Tidskriftsartikel (refereegranskat)abstract
- Background. Lowe syndrome (LS) and Dent-2 disease (DD2) are disorders associated with mutations in the OCRL gene and characterized by progressive chronic kidney disease (CKD). Here, we aimed to investigate the long-term renal outcome and identify potential determinants of CKD and its progression in children with these tubulopathies. Methods. Retrospective analyses were conducted of clinical and genetic data in a cohort of 106 boys (LS: 88 and DD2: 18). For genotype-phenotype analysis, we grouped mutations according to their type and localization. To investigate progression of CKD we used survival analysis by Kaplan-Meier method using stage 3 CKD as the end-point. Results. Median estimated glomerular filtration rate (eGFR) was lower in the LS group compared with DD2 (58.8 versus 87.4 mL/min/1.73 m2, P < 0.01). CKD stage II-V was found in 82% of patients, of these 58% and 28% had moderate-to-severe CKD in LS and DD2, respectively. Three patients (3%), all with LS, developed stage 5 of CKD. Survival analysis showed that LS was also associated with a faster CKD progression than DD2 (P < 0.01). On multivariate analysis, eGFR was dependent only on age (b0.46, P < 0.001). Localization, but not type of mutations, tended to correlate with eGFR. There was also no significant association between presence of nephrocalcinosis, hypercalciuria, proteinuria and number of adverse clinical events and CKD. Conclusions. CKD is commonly found in children with OCRL mutations. CKD progression was strongly related to the underlying diagnosis but did not associate with clinical parameters, such as nephrocalcinosis or proteinuria.
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