| 1. |
- Chew, Yilen Gomez Maqueo, et al.
(författare)
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Luminosity Discrepancy in the Equal-Mass, Pre-Main-Sequence Eclipsing Binary Par 1802 : Non-Coevality or Tidal Heating?
- 2012
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Ingår i: Astrophysical Journal. - 0004-637X .- 1538-4357. ; 745:1, s. 58-
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Tidskriftsartikel (refereegranskat)abstract
- Parenago 1802, a member of the similar to 1 Myr Orion Nebula Cluster, is a double-lined, detached eclipsing binary in a 4.674 day orbit, with equal-mass components (M-2/M-1 = 0.985 +/- 0.029). Here we present extensive VI(C)JHK(S) light curves (LCs) spanning similar to 15 yr, as well as a Keck/High Resolution Echelle Spectrometer (HIRES) optical spectrum. The LCs evince a third light source that is variable with a period of 0.73 days, and is also manifested in the high-resolution spectrum, strongly indicating the presence of a third star in the system, probably a rapidly rotating Classical T Tauri star. We incorporate this third light into our radial velocity and LC modeling of the eclipsing pair, measuring accurate masses (M-1 = 0.391 +/- 0.032 and M-2 = 0.385 +/- 0.032 M-circle dot), radii (R-1 = 1.73 +/- 0.02 and R-2 = 1.62 +/- 0.02 R-circle dot), and temperature ratio (T-eff,T-1/T-eff,T-2 = 1.0924 +/- 0.0017). Thus, the radii of the eclipsing stars differ by 6.9% +/- 0.8%, the temperatures differ by 9.2% +/- 0.2%, and consequently the luminosities differ by 62% +/- 3%, despite having masses equal to within 3%. This could be indicative of an age difference of similar to 3 x 10(5) yr between the two eclipsing stars, perhaps a vestige of the binary formation history. We find that the eclipsing pair is in an orbit that has not yet fully circularized, e = 0.0166 +/- 0.003. In addition, we measure the rotation rate of the eclipsing stars to be 4.629 +/- 0.006 days; they rotate slightly faster than their 4.674 day orbit. The non-zero eccentricity and super-synchronous rotation suggest that the eclipsing pair should be tidally interacting, so we calculate the tidal history of the system according to different tidal evolution theories. We find that tidal heating effects can explain the observed luminosity difference of the eclipsing pair, providing an alternative to the previously suggested age difference.
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| 2. |
- Hess, Timo, et al.
(författare)
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Dissecting the genetic heterogeneity of gastric cancer
- 2023
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Ingår i: EBioMedicine. - : Elsevier. - 2352-3964. ; 92
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Tidskriftsartikel (refereegranskat)abstract
- Background: Gastric cancer (GC) is clinically heterogenous according to location (cardia/non-cardia) and histopathology (diffuse/intestinal). We aimed to characterize the genetic risk architecture of GC according to its subtypes. Another aim was to examine whether cardia GC and oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett's oesophagus (BO), which are all located at the gastro-oesophageal junction (GOJ), share polygenic risk architecture.Methods: We did a meta-analysis of ten European genome-wide association studies (GWAS) of GC and its subtypes. All patients had a histopathologically confirmed diagnosis of gastric adenocarcinoma. For the identification of risk genes among GWAS loci we did a transcriptome-wide association study (TWAS) and expression quantitative trait locus (eQTL) study from gastric corpus and antrum mucosa. To test whether cardia GC and OAC/BO share genetic aetiology we also used a European GWAS sample with OAC/BO.Findings: Our GWAS consisting of 5816 patients and 10,999 controls highlights the genetic heterogeneity of GC according to its subtypes. We newly identified two and replicated five GC risk loci, all of them with subtype-specific association. The gastric transcriptome data consisting of 361 corpus and 342 antrum mucosa samples revealed that an upregulated expression of MUC1, ANKRD50, PTGER4, and PSCA are plausible GC-pathomechanisms at four GWAS loci. At another risk locus, we found that the blood-group 0 exerts protective effects for non-cardia and diffuse GC, while blood-group A increases risk for both GC subtypes. Furthermore, our GWAS on cardia GC and OAC/BO (10,279 patients, 16,527 controls) showed that both cancer entities share genetic aetiology at the polygenic level and identified two new risk loci on the single-marker level.Interpretation: Our findings show that the pathophysiology of GC is genetically heterogenous according to location and histopathology. Moreover, our findings point to common molecular mechanisms underlying cardia GC and OAC/BO.
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| 3. |
- Park, Julien H., et al.
(författare)
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The motor system is exceptionally vulnerable to absence of the ubiquitously expressed superoxide dismutase-1
- 2023
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Ingår i: Brain Communications. - : Oxford University Press. - 2632-1297. ; 5:1
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Tidskriftsartikel (refereegranskat)abstract
- Superoxide dismutase-1 is a ubiquitously expressed antioxidant enzyme. Mutations in SOD1 can cause amyotrophic lateral sclerosis, probably via a toxic gain-of-function involving protein aggregation and prion-like mechanisms. Recently, homozygosity for loss-of-function mutations in SOD1 has been reported in patients presenting with infantile-onset motor neuron disease. We explored the bodily effects of superoxide dismutase-1 enzymatic deficiency in eight children homozygous for the p.C112Wfs∗11 truncating mutation. In addition to physical and imaging examinations, we collected blood, urine and skin fibroblast samples. We used a comprehensive panel of clinically established analyses to assess organ function and analysed oxidative stress markers, antioxidant compounds, and the characteristics of the mutant Superoxide dismutase-1. From around 8 months of age, all patients exhibited progressive signs of both upper and lower motor neuron dysfunction, cerebellar, brain stem, and frontal lobe atrophy and elevated plasma neurofilament concentration indicating ongoing axonal damage. The disease progression seemed to slow down over the following years. The p.C112Wfs∗11 gene product is unstable, rapidly degraded and no aggregates were found in fibroblast. Most laboratory tests indicated normal organ integrity and only a few modest deviations were found. The patients displayed anaemia with shortened survival of erythrocytes containing decreased levels of reduced glutathione. A variety of other antioxidants and oxidant damage markers were within normal range. In conclusion, non-neuronal organs in humans show a remarkable tolerance to absence of Superoxide dismutase-1 enzymatic activity. The study highlights the enigmatic specific vulnerability of the motor system to both gain-of-function mutations in SOD1 and loss of the enzyme as in the here depicted infantile superoxide dismutase-1 deficiency syndrome.
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