We report the discovery of two new Galactic candidate luminous blue variable (LBV) stars via detection of circular shells (typical of confirmed and candidate LBVs) and follow-up spectroscopy of their central stars. The shells were detected at 22 mu m in the archival data of the Mid-Infrared All Sky Survey carried out with the Wide-field Infrared Survey Explorer (WISE). Follow-up optical spectroscopy of the central stars of the shells conducted with the renewed Southern African Large Telescope (SALT) showed that their spectra are very similar to those of the well-known LBVs P Cygni and AG Car, and the recently discovered candidate LBV MN112, which implies the LBV classification for these stars as well. The LBV classification of both stars is supported by detection of their significant photometric variability: one of them brightened in the R and I bands by 0.68 +/- 0.10 and 0.61 +/- 0.04 mag, respectively, during the last 1318 years, while the second one (known as Hen 3-1383) varies its B, V, R, I and Ks brightnesses by similar or equal to 0.50.9 mag on time-scales from 10 d to decades. We also found significant changes in the spectrum of Hen 3-1383 on a time-scale of similar or equal to 3 months, which provides additional support for the LBV classification of this star. Further spectrophotometric monitoring of both stars is required to firmly prove their LBV status. We discuss a connection between the location of massive stars in the field and their fast rotation, and suggest that the LBV activity of the newly discovered candidate LBVs might be directly related to their possible runaway status.
A considerable fraction of the central stars of planetary nebulae (CSPNe) are hydrogen-deficient. Almost all of these H-deficient central stars (CSs) display spectra with strong carbon and helium lines. Most of them exhibit emission-line spectra resembling those of massive WC stars. Therefore these stars are classed as CSPNe of spectral type [WC]. Recently, quantitative spectral analysis of two emission-line CSs, PB 8 and IC 4663, revealed that these stars do not belong to the [WC] class. Instead PB 8 has been classified as [WN/WC] type and IC 4663 as [WN] type. In this work we report the spectroscopic identification of another rare [WN] star, the CS of Abell 48. We performed a spectral analysis of Abell 48 with the Potsdam Wolf-Rayet (PoWR) models for expanding atmospheres. We find that the expanding atmosphere of Abell 48 is mainly composed of helium (85 per cent by mass), hydrogen (10 per cent) and nitrogen (5 per cent). The residual hydrogen and the enhanced nitrogen abundance make this object different from the other [WN] star IC 4663. We discuss the possible origin of this atmospheric composition.
Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.
Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.