Stratifying quotient stacks and moduli stacks

Recent results in geometric invariant theory (GIT) for non-reductive linear algebraic group actions allow us to stratify quotient stacks of the form [X/H], where X is a projective scheme and H is a linear algebraic group with internally graded unipotent radical acting linearly on X, in such a way that each stratum [S/H] has a geometric quotient S/H. This leads to stratifications of moduli stacks (for example, sheaves over a projective scheme) such that each stratum has a coarse moduli space.Comment: 25 pages, submitted to the Proceedings of the Abel Symposium 201

Iron deficiency after kidney transplantation

Iron deficiency (ID) is highly prevalent in kidney transplant recipients (KTRs) and has been independently associated with an excess mortality risk in this population. Several causes lead to ID in KTRs, including inflammation, medication and an increased iron need after transplantation. Although many studies in other populations indicate a pivotal role for iron as a regulator of the immune system, little is known about the impact of ID on the immune system in KTRs. Moreover, clinical trials in patients with chronic kidney disease or heart failure have shown that correction of ID, with or without anaemia, improves exercise capacity and quality of life, and may improve survival. ID could therefore be a modifiable risk factor to improve graft and patient outcomes in KTRs; prospective studies are warranted to substantiate this hypothesis.</p

Effect of Cell Seeding Density and Inflammatory Cytokines on Adipose Tissue-Derived Stem Cells: an in Vitro Study

Adipose tissue-derived stem cells (ASCs) are known to be able to promote repair of injured tissue via paracrine factors. However, the effect of cell density and inflammatory cytokines on the paracrine ability of ASCs remains largely unknown. To investigate these effects, ASCs were cultured in 8000 cells/cm2, 20,000 cells/cm2, 50,000 cells/cm2, and 400,000 cells/cm2 with and without 10 or 20 ng/ml tumor necrosis factor alpha (TNFα) and 25 or 50 ng/ml interferon gamma (IFNγ). ASC-sheets formed at 400,000 cells/cm2 after 48 h of culture. With increasing concentrations of TNFα and IFNγ, ASC-sheets with 400,000 cells/cm2 had increased production of angiogenic factors Vascular Endothelial Growth Factor and Fibroblast Growth Factor and decreased expression of pro-inflammatory genes TNFA and Prostaglandin Synthase 2 (PTGS2) compared to lower density ASCs. Moreover, the conditioned medium of ASC-sheets with 400,000 cells/cm2 stimulated with the low concentration of TNFα and IFN

The orbit structure of Dynkin curves

Let G be a simple algebraic group over an algebraically closed field k; assume that Char k is zero or good for G. Let \cB be the variety of Borel subgroups of G and let e in Lie G be nilpotent. There is a natural action of the centralizer C_G(e) of e in G on the Springer fibre \cB_e = {B' in \cB | e in Lie B'} associated to e. In this paper we consider the case, where e lies in the subregular nilpotent orbit; in this case \cB_e is a Dynkin curve. We give a complete description of the C_G(e)-orbits in \cB_e. In particular, we classify the irreducible components of \cB_e on which C_G(e) acts with finitely many orbits. In an application we obtain a classification of all subregular orbital varieties admitting a finite number of B-orbits for B a fixed Borel subgroup of G.Comment: 12 pages, to appear in Math

Combined cardiological and neurological abnormalities due to filamin A gene mutation

Background: Cardiac defects can be the presenting symptom in patients with mutations in the X-linked gene FLNA. Dysfunction of this gene is associated with cardiac abnormalities, especially in the left ventricular outflow tract, but can also cause a congenital malformation of the cerebral cortex. We noticed that some patients diagnosed at the neurogenetics clinic had first presented to a cardiologist, suggesting that earlier recognition may be possible if the diagnosis is suspected. Methods and results: From the Erasmus MC cerebral malformations database 24 patients were identified with cerebral bilateral periventricular nodular heterotopia (PNH) without other cerebral cortical malformations. In six of these patients, a pathogenic mutation in FLNA was present. In five a cardiac defect was also found in the outflow tract. Four had presented to a cardiologist before the cerebral abnormalities were diagnosed. Conclusions: The cardiological phenotype typically consists of aortic or mitral regurgitation, coarctation of the aorta or other left-sided cardiac malformations. Most patients in this category will not have a FLNA mutation, but the presence of neurological complaints, hyperlaxity of the skin or joints and/or a family history with similar cardiac or neurological problems in a possibly X-linked pattern may alert the clinician to the possibility of a FLNA mutation