Changes in Wetland Vegetation in Regulated Lakes in Northern Minnesota, USA Ten Years after a New Regulation Plan Was Implemented

Lake-level regulation alters wetland plant communities and their role in providing faunal habitat. Regulation plans have sometimes been changed to restore ecosystem function; however, few studies have shown the effects of such changes. In 2000, a new plan was implemented for regulation of Rainy Lake and Namakan Reservoir in northern Minnesota, USA. We had studied wetland plant communities under the previous 1970 regulation plan in 1987 and used those data to evaluate changes during 2002–2006 and 2010 resampling efforts using the same methods. Ordinations showed that plant communities changed little on Rainy Lake, where regulation changes were minor. However, on Namakan Reservoir, substantial changes had occurred in both vegetation and faunal habitat within two years, as plants favored by dewatering were replaced by submersed aquatic plants favored by year-round flooding under the new 2000 regulation plan. After ten years, Namakan showed greater similarity to unregulated Lac La Croix but still differed overall. Longer-term studies may be needed to determine if the regulation-plan change continues to alter Namakan plant communities. The speed at which changes began suggests that studies on other regulated lakes should begin in the first growing season following implementation of a new regulation plan and should continue periodically for a decade or longer

Infrared Lightcurves of Near Earth Objects

We present lightcurves and derive periods and amplitudes for a subset of 38 near earth objects (NEOs) observed at 4.5 microns with the IRAC camera on the the Spitzer Space Telescope, many of them having no previously reported rotation periods. This subset was chosen from about 1800 IRAC NEO observations as having obvious periodicity and significant amplitude. For objects where the period observed did not sample the full rotational period, we derived lower limits to these parameters based on sinusoidal fits. Lightcurve durations ranged from 42 to 544 minutes, with derived periods from 16 to 400 minutes. We discuss the effects of lightcurve variations on the thermal modeling used to derive diameters and albedos from Spitzer photometry. We find that both diameters and albedos derived from the lightcurve maxima and minima agree with our previously published results, even for extreme objects, showing the conservative nature of the thermal model uncertainties. We also evaluate the NEO rotation rates, sizes, and their cohesive strengths.Comment: 16 pages, 4 figures, 3 tables, to appear in the Astrophysical Journal Supplement Serie

Enforced Bcl-2 Expression Inhibits Antigen-mediated Clonal Elimination of Peripheral B Cells in an Antigen Dose–dependent Manner and Promotes Receptor Editing in Autoreactive, Immature B Cells

The mechanisms that establish immune tolerance in immature and mature B cells appear to be distinct. Membrane-bound autoantigen is thought to induce developmental arrest and receptor editing in immature B cells, whereas mature B cells have shortened lifespans when exposed to the same stimulus. In this study, we used Eμ–bcl-2-22 transgenic (Tg) mice to test the prediction that enforced expression of the Bcl-2 apoptotic inhibitor in B cells would rescue mature, but not immature, B cells from tolerance induction. To monitor tolerance to the natural membrane autoantigen H-2Kb, we bred 3–83μδ (anti-Kk,b) Ig Tg mice to H-2b mice or to mice expressing transgene-driven Kb in the periphery. In 3–83μδ/bcl-2 Tg mice, deletion of autoreactive B cells induced by peripheral Kb antigen expression in the liver (MT-Kb Tg) or epithelia (KerIV-Kb Tg), was partly or completely inhibited, respectively. Furthermore, Bcl-2 protected peritoneal B-2 B cells from deletion mediated by acute antigen exposure, but this protection could be overcome by higher antigen dose. In contrast to its ability to block peripheral self-tolerance, Bcl-2 overexpression failed to inhibit central tolerance induced by bone marrow antigen expression, but instead, enhanced the receptor editing process. These studies indicate that apoptosis plays distinct roles in central and peripheral B cell tolerance

A history of deformation within Pietre Cotte rhyolite flow (Vulcano)

International audienc

Transcriptional dynamics of colorectal cancer risk associated variation at 11q23.1 correlate with tuft cell abundance and marker expression in silico

Colorectal cancer (CRC) is characterised by heritable risk that is not well understood. Heritable, genetic variation at 11q23.1 is associated with increased colorectal cancer (CRC) risk, demonstrating eQTL effects on 3 cis- and 23 trans-eQTL targets. We sought to determine the relationship between 11q23.1 cis- and trans-eQTL target expression and test for potential cell-specificity. scRNAseq from 32,361 healthy colonic epithelial cells was aggregated and subject to weighted gene co-expression network analysis (WGCNA). One module (blue) included 19 trans-eQTL targets and was correlated with POU2AF2 expression only. Following unsupervised clustering of single cells, the expression of 19 trans-eQTL targets was greatest and most variable in cluster number 11, which transcriptionally resembled tuft cells. 14 trans-eQTL targets were found to demarcate this cluster, 11 of which were corroborated in a second dataset. Intra-cluster WGCNA and module preservation analysis then identified twelve 11q23.1 trans-eQTL targets to comprise a network that was specific to cluster 11. Finally, linear modelling and differential abundance testing showed 11q23.1 trans-eQTL target expression was predictive of cluster 11 abundance. Our findings suggest 11q23.1 trans-eQTL targets comprise a POU2AF2-related network that is likely tuft cell-specific and reduced expression of these genes correlates with reduced tuft cell abundance in silico

Increased SK3 expression in DM1 lens cells leads to impaired growth through a greater calcium-induced fragility

Although cataract is a characteristic feature of myotonic dystrophy type 1 (DM1), little is known of the underlying mechanisms. We generated four lens epithelial cell lines derived from DM1 cataracts and two from age-matched, non-DM cataracts. Small-pool PCR revealed typical large triplet repeat expansions in the DM1 cells. Furthermore, real-time PCR analysis showed reduced SIX5 expression and increased expression of the Ca2+-activated K+ channel SK3 in the DM1 cells. These cells also exhibited longer population doubling times which did not arise through reduced proliferation, but rather increased cell death as shown by increased release of lactate dehydrogenase (LDH). Using 86Rb+ as a tracer for K+, we found no difference in the resting K+ influx or efflux kinetics. In all cases, the ouabain sensitive component of the influx contributed ~50% of the total. However, stimulating internal Ca2+ by exposure to ionomycin not only caused greater stimulation of K+ (86Rb) efflux in the DM1 cells but also induced a higher rate of cell death (LDH assay). Since both the hyper-stimulation of K+ efflux and cell death were reduced by the highly specific SK inhibitor apamin, we suggest that increased expression of SK3 has a critical role in the increased Ca2+-induced fragility in DM1 cells. The present data, therefore, both help explain the lower epithelial cell density previously observed in DM1 cataracts and provide general insights into mechanisms underlying the fragility of other DM1-affected tissues

Engineering Antigen-Specific T Cells from Genetically Modified Human Hematopoietic Stem Cells in Immunodeficient Mice

There is a desperate need for effective therapies to fight chronic viral infections. The immune response is normally fastidious at controlling the majority of viral infections and a therapeutic strategy aimed at reestablishing immune control represents a potentially powerful approach towards treating persistent viral infections. We examined the potential of genetically programming human hematopoietic stem cells to generate mature CD8+ cytotoxic T lymphocytes that express a molecularly cloned, “transgenic” human anti-HIV T cell receptor (TCR). Anti-HIV TCR transduction of human hematopoietic stem cells directed the maturation of a large population of polyfunctional, HIV-specific CD8+ cells capable of recognizing and killing viral antigen-presenting cells. Thus, through this proof-of-concept we propose that genetic engineering of human hematopoietic stem cells will allow the tailoring of effector T cell responses to fight HIV infection or other diseases that are characterized by the loss of immune control

Kapitalstrukturen börsennotierter Aktiengesellschaften - Deutschland und USA im Vergleich

Bisherige Evidenz über Kapitalstrukturunterschiede zwischen Deutschland und den USA deutet auf eine durchschnittlich höhere Verschuldung deutscher Unternehmen hin. Die vergangenen Jahre waren in Deutschland jedoch durch eine Förderung der Eigenkapitalfinanzierung seitens des deutschen Gesetzgebers und der Regulierungsbehörden geprägt. Die vorliegende Arbeit untersucht, inwieweit sich diese Änderungen tatsächlich auf den Verschuldungsgrad deutscher Unternehmen auswirken und ob es zu einer Annäherung an amerikanische Unternehmen kommt. Zu diesem Zweck werden durchschnittliche Verschuldungsgrade von US-amerikanischen und deutschen börsennotierten Gesellschaften über einen Zeitraum von 10 Jahren verglichen. Die Untersuchung zeigt, dass diese Änderungen vor allem den Verschuldungsgrad von Unternehmen beeinflusst haben, die erst in den letzten Jahren an einer deutschen Börse notiert wurden. Bei am deutschen Kapitalmarkt etablierten Unternehmen hingegen lässt sich keine aufgrund der neuen Rahmenbedingungen vorgenommene Anpassung der Verschuldungspolitik erkennen. Abstract Existing comparative evidence on corporate capital structure decisions in the U.S. and Germany traditionally reveals that German firms chose substantially higher levels of debt financing. Within the past years, however, Germany has experienced repeated initiatives by both legislative and regulatory bodies to promote equity finance. This paper tries to shed first light on how these initiatives affect the debt-equity-decision of German corporations and whether a convergence of German leverage levels to Anglo-American financing patterns can be observed. For this purpose we compare capital structures for a panel of U.S. and German public corporations over the past 10 years. The obtained evidence suggests that aggregate leverage ratios do indeed converge. Yet this development is primarily driven by recent German IPOs which seem to respond to the revamped institutional setting by choosing higher levels of equity. Established German corporations, by contrast, do not seem to have systematically adapted their financing patterns over the past decade