The supergiant B[e] star LHA 115-S 18 - binary and/or luminous blue variable?

Context. The mechanism by which supergiant (sg)B[e] stars support cool, dense dusty discs/tori and their physical relationship with other evolved, massive stars such as luminous blue variables is uncertain. Aims. In order to investigate both issues we have analysed the long term behaviour of the canonical sgB[e] star LHA 115-S 18. Methods. We employed the OGLE II-IV lightcurve to search for (a-)periodic variability and supplemented these data with new and historic spectroscopy. Results. In contrast to historical expectations for sgB[e] stars, S18 is both photometrically and spectroscopically highly variable. The lightcurve is characterised by rapid aperiodic ` aring' throughout the 16 years of observations. Changes in the high excitation emission line component of the spectrum imply evolution in the stellar temperature - as expected for luminous blue variables - although somewhat surprisingly, spectroscopic and photometric variability appears not to be correlated. Characterised by emission in low excitation metallic species, the cool circumstellar torus appears largely unaffected by this behaviour. Finally, in conjunction with intense, highly variable He ii emission, X-ray emission implies the presence of an unseen binary companion. Conclusions. S18 provides observational support for the putative physical association of (a subset of) sgB[e] stars and luminous blue variables. Given the nature of the circumstellar environment of S18 and that luminous blue variables have been suggested as SN progenitors, it is tempting to draw a parallel to the progenitors of SN1987A and SN2009ip. Moreover the likely binary nature of S18 strengthens the possibility that the dusty discs/tori that characterise sgB[e] stars are the result of binary-driven mass-loss; consequently such stars may provide a window on the short lived phase of mass-transfer in massive compact binaries.

Puerto Rico and Greece: A Tale of two defaults in a monetary union. CEPS High-Level Brief. 18 June 2015, Update 30 June 2015

It is widely argued that the problems of Greece in the eurozone derive not only from mistakes made by successive Greek governments, but from deep-seated problems with the design of the euro area. The euro area is judged to be incomplete because it does not have any fiscal shock absorbers, nor a federal transfer system, and, according to many, it has imposed senseless austerity on the country. The US, by contrast, is often held up as an example of a complete monetary union in this type of problem could not arise. However, the working of the US is much less perfect than it appears from afar. The ‘genuine’ economic and monetary union, which undoubtedly exists in the US, also has problems in dealing with low-performing states in terms of productivity and governance. Puerto Rico exemplifies these difficulties and shows that in such an integrated area similar problems, including a fiscal crisis can arise. Both Puerto Rico and Greece are very special and extreme cases within their respective unions, but the strength of a system can be measured by how it deals with these cases.

Ferroportin Disease (Haemochromatosis-type IV): a case report

Introdution: Haemochromatosis-type IV, the ferroportin disease, is characterized by an autosomal-dominant transmission and early iron accumulation in macrophages. It is caused by mutations in the transmembrane iron exporter protein ferroportin1 (SLC40A1 gene). In form A (classic), ferroportin loss of function mutants are unable to export iron from cells leading to cellular iron accumulation with decreased availability of iron for serum transferrin (TS). We present a Portuguese rare clinical case of HH-IV. Materials and Methods: A 41-year-old woman with hyperferritinemia and normal TS. Causes of hyperferritinemia (inflammation, chronic alcohol consumption, metabolic syndrome, cell necrosis, non-alcoholic fatty liver disease and aceruloplasminemia) were assessed. Liver iron, evaluated by magnetic resonance imaging (MRI) was carried out. Screening for mutation in HFE and SCL40A1 genes were performed by Sanger sequencing. Baseline: Ferritin:708ng/ml; TS: 27%; MRI:85µmol/g; Hb:13,6g/dl. Therapy: weekly 450ml Therapeutic Phlebotomies (TP) until ferritin≤50ng/ml. Results: Hyperferritinemia comorbidities and common genetic mutations for haemochromatosis were negative. However, sequencing of the patient SLC40A1 gene has revealed the presence in heterozygosity of the variant c.238G>A; p.Gly80Ser. Due to low tolerance to TP, we adopted smaller phlebotomies every three weeks. Conclusion: This patient has a rare autosomal-dominant Ferroportin disease due to a mutated ferroportin which is predicted to be defective in iron cellular export. In agreement, she presents hyperferritinemia, with normal TS and liver iron overload. The genotype/phenotype association allowed to diagnosis this rare FD case. Although a mild form A, we decided to start TP. Her father also has been treated for iron overload.