Derived length and nilpotency class of zero entropy groups acting on compact Kahler manifolds

Let X be a compact Kahler manifold of dimension n and of Kodaira dimension kappa(X). Let G be a group of zero entropy automorphisms of X and G_0 the set of elements in G which are isotopic to the identity. We prove that replacing G by a suitable finite-index subgroup, G/G_0 is a unipotent group of derived length at most n-max(kappa(X),1) and the derived length of G is at most n-kappa(X). Up to taking a finite-index subgroup, we conjecture that the nilpotency class c(G/G_0) of G/G_0 is at most n-1. The conjecture is proved to be true for all complex tori. Assuming this conjecture for all compact Kahler manifolds, we show that c(G) is at most n-kappa(X). The algebro-geometric structure of X is studied when c(G)=n or c(G/G_0)=n-1. We also give an optimal upper bound of the size of the Jordan blocks of the unipotent automorphisms of H^2(X,C) induced by automorphisms of X.Comment: New version joined with Hsueh-Yung LIN. 38 pages. New results have been added and a mistake was fixe

A Retrospective Analysis to Validate the Alarm Signs Used in the CEDAP-Plus Study

Background and Study Aim. This study aimed to validate the alarm signs used in the 2007 German CEDAP-Plus study for indicating capsule endoscopy in patients who have idiopathic chronic abdominal pain. Patients and Methods. We retrospectively reviewed the cases of all patients who underwent capsule endoscopy at our institution between August 2007 and August 2009 for chronic hitherto undiagnosed abdominal pain, despite previous investigations. The demographic data, indications, findings, and diagnoses were recorded, as were the alarm signs (i.e., 10% loss of weight within 3 months, suspected small intestinal bleed or chronic anemia, and laboratory indications of inflammation). Results. Alarm signs were found in only 4 of the 62 included patients. Capsule endoscopy revealed findings that led to diagnoses of Crohn's disease (n = 4), tuberculosis (n = 1), gastrointestinal stromal tumors (n = 3), and hookworm (n = 1); these diagnoses included 100% (4/4) of the patients with alarm signs, but only 8.6% (5/58) of patients without them. However, 55.6% (5/9) of patients with clinically capsule endoscopy findings reported no alarm signs. Conclusions. Although selecting patients based on the alarm signs may increase the yield of capsule endoscopy, the alarm sign criteria appear to have low sensitivity

BTTB preconditioners for BTTB least squares problems

AbstractIn this paper, we consider solving the least squares problem minx‖b-Tx‖2 by using preconditioned conjugate gradient (PCG) methods, where T is a large rectangular matrix which consists of several square block-Toeplitz–Toeplitz-block (BTTB) matrices and b is a column vector. We propose a BTTB preconditioner to speed up the PCG method and prove that the BTTB preconditioner is a good preconditioner. We then discuss the construction of the BTTB preconditioner. Numerical examples, including image restoration problems, are given to illustrate the efficiency of our BTTB preconditioner. Numerical results show that our BTTB preconditioner is more efficient than the well-known Level-1 and Level-2 circulant preconditioners

Hemojuvelin-Neogenin Interaction Is Required for Bone Morphogenic Protein-4-induced Hepcidin Expression

Hemojuvelin (HJV) is a glycosylphosphatidylinositol-linked protein and binds both bone morphogenic proteins (BMPs) and neogenin. Cellular HJV acts as a BMP co-receptor to enhance the transcription of hepcidin, a key iron regulatory hormone secreted predominantly by liver hepatocytes. In this study we characterized the role of neogenin in HJV-regulated hepcidin expression. Both HJV and neogenin were expressed in liver hepatocytes. Knockdown of neogenin decreased BMP4-induced hepcidin mRNA levels by 16-fold in HJV-expressing HepG2 cells but only by about 2-fold in cells transfected with either empty vector or G99V mutant HJV that does not bind BMPs. Further studies indicated that disruption of the HJV-neogenin interaction is responsible for a marked suppression of hepcidin expression. Moreover, in vivo studies showed that hepatic hepcidin mRNA could be significantly suppressed by blocking the interaction of HJV with full-length neogenin with a soluble fragment of neogenin in mice. Together, these results suggest that the HJV-neogenin interaction is required for the BMP-mediated induction of hepcidin expression when HJV is expressed. Combined with our previous studies, our results support that hepatic neogenin possesses two functions, mediation of cellular HJV release, and stimulation of HJV-enhanced hepcidin expression

Edge modes in self-gravitating disc-planet interactions

We study the stability of gaps opened by a giant planet in a self-gravitating protoplanetary disc. We find a linear instability associated with both the self-gravity of the disc and local vortensity maxima which coincide with gap edges. For our models, these edge modes develop and extend to twice the orbital radius of a Saturn mass planet in discs with disc-to-star mass ratio >0.06, corresponding to a Toomre Q < 1.5 at the outer disc boundary. Unlike the local vortex-forming instabilities associated with gap edges in weakly or non-self-gravitating low viscosity discs, the edge modes are global and exist only in sufficiently massive discs, but for the typical viscosity values adopted for protoplanetary discs. Analytic modelling and linear calculations show edge modes may be interpreted as a localised disturbance associated with a gap edge inducing activity in the extended disc, through the launching of density waves excited at Lindblad resonances. Nonlinear hydrodynamic simulations are performed to investigate the evolution of edge modes in disc-planet systems. The form and growth rates of unstable modes are consistent with linear theory. Their dependence on viscosity and gravitational softening is also explored. We also performed a first study of the effect of edge modes on planetary migration. We found that if edge modes develop, then the average disc-on-planet torque becomes more positive with increasing disc mass. In simulations where the planet was allowed to migrate, although a fast type III migration could be seen that was similar to that seen in non-self-gravitating discs, we found that it was possible for the planet to interact gravitationally with the spiral arms associated with an edge mode and that this could result in the planet being scattered outwards. Thus orbital migration is likely to be complex and non monotonic in massive discs of the type we consider.Comment: 26 pages, 21 figures. Accepted by MNRAS. Abstract displayed is shortene

Hollow Gaussian Schell-model beam and its propagation

In this paper, we present a new model, hollow Gaussian-Schell model beams (HGSMBs), to describe the practical dark hollow beams. An analytical propagation formula for HGSMBs passing through a paraxial first-order optical system is derived based on the theory of coherence. Based on the derived formula, an application example showing the influence of spatial coherence on the propagation of beams is illustrated. It is found that the beam propagating properties of HGSMBs will be greatly affected by their spatial coherence. Our model provides a very convenient way for analyzing the propagation properties of partially coherent dark hollow beams.Comment: 13pages, 2 figure

Neogenin-mediated hemojuvelin shedding occurs after hemojuvelin traffics to the plamsa membrane

Hemochromatosis type 2 gene (HFE2) is highly expressed in skeletal muscle and liver hepatocytes. Its encoded protein, hemojuvelin (HJV), is a co-receptor for the bone morphogenetic proteins 2 and 4 (BMP2 and BMP4) and enhances the BMP-induced hepcidin expression. Hepcidin is a central iron regulatory hormone predominantly secreted from hepatocytes. HJV also binds neogenin, a membrane protein widely expressed in many tissues. Neogenin is required for the processing and release of HJV from cells. The role that neogenin plays in HJV trafficking was investigated, using HepG2 cells, a human hepatoma cell line. Knockdown of endogenous neogenin markedly suppresses HJV release, but has no evident effect on HJV trafficking to the plasma membrane. Addition of a soluble neogenin ectodomain to cells markedly inhibits HJV release, indicating that the HJV shedding is not processed before trafficking to the cell surface. At the plasma membrane it undergoes endocytosis in a dynamin-independent but cholesterol-dependent manner. The additional findings that HJV release is coupled to lysosomal degradation of neogenin, that HJV undergoes endocytosis, and that cholesterol depletion by filipin blocks both HJV endocytosis and HJV release, suggest that neogenin-mediated HJV release occurs after the HJV-neogenin complex is internalized from the cell surface