An Ecological Basis for Ecosystem Management

This report was prepared by the Southwestern Regional Ecosystem Management Study Team composed of management and research biologists. The USDA Forest Service Southwestern Regions Regional Forester, Larry Henson, and the Rocky Mountain Forest and Range Experiment Station Director, Denver Burns, chartered this team to recommend an ecological basis for ecosystem management. This report is not intended to provide details on all aspects of ecosystem management; it simply provides information and makes recommendations for an ecological basis for ecosystem management. The report is not a decision document. It does not allocate resources on public lands nor does it make recommendations to that effect. The report of this Study Team may be relied upon as input in processes initiated under the National Environmental Policy Act (NEPA), National Forest Management Act (NFMA), Endangered Species Act (ESA), Administrative Procedures Act (APA), and other applicable laws. The information contained in this report is general in nature, rather than site specific. Implementation of ecosystem management and allocation of resources on Forest Service administered lands is the responsibility of the National Forest System in partnership with Forest Service Research and State and Private Forestry. Implementation is done through Forest and project plans that are subject to the NEPA process of disclosing the effects of proposed actions and affording the opportunity for public comment. The Southwestern Region follows a planning process for projects called Integrated Resource Management (IRM). The opinions expressed by the authors do not necessarily represent the policy or position of the U.S. Department of Agriculture, the Forest Service, The Nature Conservancy, or the Arizona Game and Fish Department. The Study Team acknowledges the valuable input of more than 50 individuals from various agencies, universities, professional organizations, and other groups who provided thoughtful comments of an earlier draft of this document. Some of their comments are included in Appendix 3

One Loop Calculations in Gauge Theories Regulated on an x+x^+-p+p^+ Lattice

In earlier work, the planar diagrams of $SU(N_c)$ gauge theory have been regulated on the light-cone by a scheme involving both discrete $p^+$ and $\tau=ix^+$. The transverse coordinates remain continuous, but even so all diagrams are rendered finite by this procedure. In this scheme quartic interactions are represented as two cubics mediated by short lived fictitious particles whose detailed behavior could be adjusted to retain properties of the continuum theory, at least at one loop. Here we use this setup to calculate the one loop three gauge boson triangle diagram, and so complete the calculation of diagrams renormalizing the coupling to one loop. In particular, we find that the cubic vertex is correctly renormalized once the couplings to the fictitious particles are chosen to keep the gauge bosons massless.Comment: 26 pages, 36 figure

Discrete mode laser diodes with very narrow linewidth emission

Ex-facet, free-running low linewidth (~100 kHz), single mode laser emission is demonstrated using low cost, regrowth-free ridge waveguide Discrete Mode Fabry Pérot laser diode chips. These narrow linewidths are obtained from sub mW emission powers and above

Equivalence of Light-Front and Covariant Field Theory

In this paper we discuss the relation between the standard covariant quantum field theory and light-front field theory. We define covariant theory by its Feynman diagrams, whereas light-front field theory is defined in terms of light-cone time-ordered diagrams. A general algorithm is proposed that produces the latter from any Feynman diagram. The procedure is illustrated in several cases. Technical problems that occur in the light-front formulation and have no counterpart in the covariant formulation are identified and solved.Comment: 47 Pages, LaTeX with LaTeX figures included in the tex

Mitochondrial Release of Caspase-2 and -9 during the Apoptotic Process

The barrier function of mitochondrial membranes is perturbed early during the apoptotic process. Here we show that the mitochondria contain a caspase-like enzymatic activity cleaving the caspase substrate Z-VAD.afc, in addition to three biological activities previously suggested to participate in the apoptotic process: (a) cytochrome c; (b) an apoptosis-inducing factor (AIF) which causes isolated nuclei to undergo apoptosis in vitro; and (c) a DNAse activity. All of these factors, which are biochemically distinct, are released upon opening of the permeability transition (PT) pore in a coordinate, Bcl-2–inhibitable fashion. Caspase inhibitors fully neutralize the Z-VAD.afc–cleaving activity, have a limited effect on the AIF activity, and have no effect at all on the DNase activities. Purification of proteins reacting with the biotinylated caspase substrate Z-VAD, immunodetection, and immunodepletion experiments reveal the presence of procaspase-2 and -9 in mitochondria. Upon induction of PT pore opening, these procaspases are released from purified mitochondria and become activated. Similarly, upon induction of apoptosis, both procaspases redistribute from the mitochondrion to the cytosol and are processed to generate enzymatically active caspases. This redistribution is inhibited by Bcl-2. Recombinant caspase-2 and -9 suffice to provoke full-blown apoptosis upon microinjection into cells. Altogether, these data suggest that caspase-2 and -9 zymogens are essentially localized in mitochondria and that the disruption of the outer mitochondrial membrane occurring early during apoptosis may be critical for their subcellular redistribution and activation

Improving Genetic Prediction by Leveraging Genetic Correlations Among Human Diseases and Traits

Genomic prediction has the potential to contribute to precision medicine. However, to date, the utility of such predictors is limited due to low accuracy for most traits. Here theory and simulation study are used to demonstrate that widespread pleiotropy among phenotypes can be utilised to improve genomic risk prediction. We show how a genetic predictor can be created as a weighted index that combines published genome-wide association study (GWAS) summary statistics across many different traits. We apply this framework to predict risk of schizophrenia and bipolar disorder in the Psychiatric Genomics consortium data, finding substantial heterogeneity in prediction accuracy increases across cohorts. For six additional phenotypes in the UK Biobank data, we find increases in prediction accuracy ranging from 0.7 for height to 47 for type 2 diabetes, when using a multi-trait predictor that combines published summary statistics from multiple traits, as compared to a predictor based only on one trait. © 2018 The Author(s)

Genome-wide association study identifies 30 Loci Associated with Bipolar Disorder

This paper is dedicated to the memory of Psychiatric Genomics Consortium (PGC) founding member and Bipolar disorder working group co-chair Pamela Sklar. We thank the participants who donated their time, experiences and DNA to this research, and to the clinical and scientific teams that worked with them. We are deeply indebted to the investigators who comprise the PGC. The views expressed are those of the authors and not necessarily those of any funding or regulatory body. Analyses were carried out on the NL Genetic Cluster Computer (http://www.geneticcluster.org ) hosted by SURFsara, and the Mount Sinai high performance computing cluster (http://hpc.mssm.edu).Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P<1x10-4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (GWS, p < 5x10-8) in the discovery GWAS were not GWS in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis 30 loci were GWS including 20 novel loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene-sets including regulation of insulin secretion and endocannabinoid signaling. BDI is strongly genetically correlated with schizophrenia, driven by psychosis, whereas BDII is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential new biological mechanisms for BD.This work was funded in part by the Brain and Behavior Research Foundation, Stanley Medical Research Institute, University of Michigan, Pritzker Neuropsychiatric Disorders Research Fund L.L.C., Marriot Foundation and the Mayo Clinic Center for Individualized Medicine, the NIMH Intramural Research Program; Canadian Institutes of Health Research; the UK Maudsley NHS Foundation Trust, NIHR, NRS, MRC, Wellcome Trust; European Research Council; German Ministry for Education and Research, German Research Foundation IZKF of Münster, Deutsche Forschungsgemeinschaft, ImmunoSensation, the Dr. Lisa-Oehler Foundation, University of Bonn; the Swiss National Science Foundation; French Foundation FondaMental and ANR; Spanish Ministerio de Economía, CIBERSAM, Industria y Competitividad, European Regional Development Fund (ERDF), Generalitat de Catalunya, EU Horizon 2020 Research and Innovation Programme; BBMRI-NL; South-East Norway Regional Health Authority and Mrs. Throne-Holst; Swedish Research Council, Stockholm County Council, Söderström Foundation; Lundbeck Foundation, Aarhus University; Australia NHMRC, NSW Ministry of Health, Janette M O'Neil and Betty C Lynch