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Political attention has increasingly focused on limiting warming to 2êC. However, to date the only mitigation commitments accompanying this target are the so-called Copenhagen pledges, and these pledges appear to be inconsistent with the 2êC objective. Diverging opinions on whether this inconsistency can or should be resolved have been expressed. This paper clarifies the alternative assumptions underlying these diverging view points and explicits their implications. It first gives simple visualizations of the challenge posed by the 2êC target. It then proposes a decision tree, linking different beliefs on climate change, the achievability of different policies, and current international policy dynamics to various options to move forward on climate change.

This title is endorsed by Cambridge Assessment International Education to support the full syllabus for examination from 2020. Reinforce learning and deepen understanding of the key concepts covered in the latest syllabus; an ideal course companion or homework book for use throughout the course. - Develop and strengthen skills and knowledge with a wealth of additional exercises that perfectly supplement the Student's Book. - Build confidence with extra practice for each lesson to ensure that a topic is thoroughly understood before moving on. - Build a strong understanding of the main events of the course and the confidence to know how to use this knowledge. - Keep track of students' work with ready-to-go write-in exercises. - Save time with all answers available in the Online Teacher's Guide

Paper 1: San Francisco Peak: a plea to protect. This is a study done for the Plateau Sciences Society. It lists names of people (residing in the eastern part of Navajo-land) and their personal opinions. It gives an account on the importance the mountain ha

Semaphorin 3A (Sema3A) is a cell-secreted protein that participates in the axonal guidance pathways. Sema3A acts as a canonical repulsive axon guidance molecule, inhibiting CNS regenerative axonal growth and propagation. Therefore, interfering with Sema3A signaling is proposed as a therapeutic target for achieving functional recovery after CNS injuries. It has been shown that Sema3A adheres to the proteoglycan component of the extracellular matrix (ECM) and selectively binds to heparin and chondroitin sulfate-E (CS-E) glycosaminoglycans (GAGs). We hypothesize that the biologically relevant interaction between Sema3A and GAGs takes place at Sema3A C-terminal polybasic region (SCT). The aims of this study were to characterize the interaction of the whole Sema3A C-terminal polybasic region (Sema3A 725–771) with GAGs and to investigate the disruption of this interaction by small molecules. Recombinant Sema3A basic domain was produced and we used a combination of biophysical techniques (NMR, SPR, and heparin affinity chromatography) to gain insight into the interaction of the Sema3A C-terminal domain with GAGs. The results demonstrate that SCT is an intrinsically disordered region, which confirms that SCT binds to GAGs and helps to identify the specific residues involved in the interaction. NMR studies, supported by molecular dynamics simulations, show that a new peptoid molecule (CSIC02) may disrupt the interaction between SCT and heparin. Our structural study paves the way toward the design of new molecules targeting these protein–GAG interactions with potential therapeutic applications. ; This work was funded by the European Union Seventh Framework Programme (FP7/2007–2013) under Project VISION, grant No. 304884, the Spanish Ministry of Science and Innovation/Spanish Research Agency (MCI/AEI/FEDER, RTI2018–096182-B-I00) and AGAUR (2017 SGR 208). ; Peer reviewed

Tortajada, Agustín et alt. ; C3 glomerulopathies (C3G) are a group of severe renal diseases with distinct patterns of glomerular inflammation and C3 deposition caused by complement dysregulation. Here we report the identification of a familial C3G-associated genomic mutation in the gene complement factor H-related 1 (CFHR1), which encodes FHR1. The mutation resulted in the duplication of the N-terminal short consensus repeats (SCRs) that are conserved in FHR2 and FHR5. We determined that native FHR1, FHR2, and FHR5 circulate in plasma as homo- and hetero-oligomeric complexes, the formation of which is likely mediated by the conserved N-terminal domain. In mutant FHR1, duplication of the N-terminal domain resulted in the formation of unusually large multimeric FHR complexes that exhibited increased avidity for the FHR1 ligands C3b, iC3b, and C3dg and enhanced competition with complement factor H (FH) in surface plasmon resonance (SPR) studies and hemolytic assays. These data revealed that FHR1, FHR2, and FHR5 organize a combinatorial repertoire of oligomeric complexes and demonstrated that changes in FHR oligomerization influence the regulation of complement activation. In summary, our identification and characterization of a unique CFHR1 mutation provides insights into the biology of the FHRs and contributes to our understanding of the pathogenic mechanisms underlying C3G. Copyright © 2013, American Society for Clinical Investigation. ; Work in this report was funded by the Spanish Ministerio de Economía y Competitividad (SAF2011-26583), the Fundación Renal Iñigo Alvarez de Toledo and the 7FP European Union project EURenOmics to S. Rodríguez de Córdoba; the "Ramón Areces" Foundation, the Spanish Ministerio de Economía y Competitividad (SAF2011-22988), and the "Red Temática de Investigación Cooperativa en Cáncer(RTICC)" (RD06/0020/1001) to O. Llorca; the Spanish "Ministerio de Economía y Competitividad" (PI0900268) to P. Sánchez-Corral; the MRC UK (G0701298) to C.L. Harris; and the Spanish "Ministerio de Economía y Competitividad" (PS09/00122) to M. López Trascasa. In addition, this work was supported by a grant from the Autonomous Region of Madrid (S2010/BMD-2316) to S. Rodríguez de Córdoba, O. Llorca, M. López Trascasa, and P. Sánchez-Corral. M.C. Pickering is a Wellcome Trust Senior Fellow in Clinical Science (WT098476MA). H. Yébenes was supported by a postdoctoral contract by the RTICC, and C. Abarrategui-Garrido was supported by the "Fundación de Investigación Biomédica del Hospital Universitario La Paz." ; Peer reviewed

Volume III of National Accounts of OECD Countries comprises Volume IIIa - Financial Accounts - Flows and Volume IIIb - Financial Balance Sheets - Stocks . In both volumes, data, based on the System of National Accounts (SNA 1993), are expressed in national currency (in euros for euro area countries). Volume IIIa covers financial accounts of OECD countries and includes financial transactions (both net acquisition of financial assets and net incurrence of liabilities), by institutional sector (non-financial corporations, financial corporations, general government, households and non-profit insti

"11 December 1978." ; Shipping list no.: 89-483-P. ; "Reprint which includes current pages from changes 1 and 2." ; Cover title. ; Includes bibliographical references. ; Mode of access: Internet. ; 14

10 páginas.- 4 figuras.- referencias.-Data Availability Statement: All data underlying this article are available in the main publication and in its Supplementary Materials online. ; Unspecific peroxygenases (UPOs), the extracellular enzymes capable of oxygenating a potpourri of aliphatic and aromatic substrates with a peroxide as co-substrate, come out with a new reaction: carbon-chain shortening during the conversion of fatty acids with the well-known UPOs from Coprinopsis cinerea (rCciUPO) and Cyclocybe (Agrocybe) aegerita (AaeUPO). Although a pathway (Cα-oxidation) for shortening the hydrocarbon chain of saturated fatty acids has already been reported for the UPO from Marasmius rotula (MroUPO), it turned out that rCciUPO and AaeUPO shorten the chain length of both saturated and unsaturated fatty acids in a different way. Thus, the reaction sequence does not necessarily start at the Cα-carbon (adjacent to the carboxyl group), as in the case of MroUPO, but proceeds through the subterminal (ω-1 and ω-2) carbons of the chain via several oxygenations. This new type of shortening leads to the formation of a dicarboxylic fatty acid reduced in size by two carbon atoms in the first step, which can subsequently be further shortened, carbon by carbon, by the UPO Cα-oxidation mechanism. View Full-Text ; This research was funded by BioBased Industries Joint Undertaking under the European Union's Horizon 2020 Research and Innovation Programme, grant number 792063 (SusBind project; https://susbind.eu; to A.G., Á.T.M. and M.H.), the PID2020-118968RB-100 project by the Spanish MCIN/AEI/ 10.13039/501100011033 to A.G., and the CSIC projects PIE-202040E185 (to A.G.) and PIE-202120E019 (to Á.T.M.). ; Peer reviewed

33 p.-4 fig.-2 fig. supl. ; Complement is an essential component of innate immunity. Its activation results in the assembly of unstable protease complexes, denominated C3/C5 convertases, leading to inflammation and lysis. Regulatory proteins inactivate C3/C5 convertases on host surfaces to avoid collateral tissue damage. On pathogen surfaces, properdin stabilizes C3/C5 convertases to efficiently fight infection. How properdin performs this function is, however, unclear. Using electron microscopy we show that the N-and C-terminal ends of adjacent monomers in properdin oligomers conform a curly vertex that holds together the AP convertase, interacting with both the C345C and vWA domains of C3b and Bb, respectively. Properdin also promotes a large displacement of the TED (thioestercontaining domain) and CUB (complement protein subcomponents C1r/C1s, urchin embryonic growth factor and bone morphogenetic protein 1) domains of C3b, which likely impairs C3-convertase inactivation by regulatory proteins. The combined effect of molecular cross-linking and structural reorganization increases stability of the C3 convertase and facilitates recruitment of fluid-phase C3 convertase to the cell surfaces. Our model explains how properdin mediates the assembly of stabilized C3/C5-convertase clusters, which helps to localize complement amplification to pathogen surfaces. ; This work was funded by the Autonomous Region of Madrid (S2010/BMD-2316 to S.R.d.C. and O.L.), the Ramón Areces Foundation (O.L.), and the Spanish government (SAF2011-22988 to O.L. and SAF2011-26583 to S.R.d.C.). O.L. is additionally supported by Red Temática de Investigación Cooperativa en Cáncer (RD06/0020/1001), and S.R.d.C. is also supported by the Fundación Renal Iñigo Alvarez de Toledo and the Seventh Framework Programme European Union Project EURenOmics (European Consortium for High-Throughput Research in Rare Kidney Diseases-305608). ; Peer Reviewed

The Tweed Family Papers consists primarily of correspondence between Mrs. Richard Tweed and her children, relatives, and friends. Diaries, essays and poetry written by family members, newspaper clippings (photocopies), and financial and legal material are also included, as are a handful of photographs. All related primarily to the life of Mrs. Richard Tweed and her descendants. ; Mrs. Richard Tweed, upon whom the majority of the materials focus, was the sister-in-law of William Marcy ("Boss") Tweed, who controlled the Democratic political machine at New York City's Tammany Hall during the mid-19th century. He and his associates misappropriated public funds on a large scale, leading to his arrest and imprisonment in 1871. ; The Tweed Family Papers are organized by the following categories: Correspondence, Newspapers, Literary Production, Photographs, Financial Material, Printed Material, Scrapbook Material, Legal Material, and Artifacts. ; Tweed Family Papers, 1836-1932 and undated, Southwest Collection/Special Collections Library, Texas Tech University, Lubbock, Texas ; Box 1, File 14

Purpose Dysregulation of the complement cascade contributes to a variety of retinal dystrophies, including age-related macular degeneration (AMD). The central component of complement, C3, is expressed in abundance by macrophages in the outer retina, and its ablation suppresses photoreceptor death in experimental photo-oxidative damage. Whether this also influences macrophage reactivity in this model system, however, is unknown. We investigate the effect of C3 ablation on macrophage activity and phagocytosis by outer retinal macrophages during photo-oxidative damage. Methods Age-matched C3 knockout (KO) mice and wild-type (WT) C57/Bl6 mice were subjected to photo-oxidative damage. Measurements of the outer nuclear layer (ONL) thickness and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were used to assess pathology and photoreceptor apoptosis, respectively. Macrophage abundance and phagocytosis were assessed with immunolabeling for pan-macrophage and phagocytic markers, in conjunction with TUNEL staining in cohorts of C3 KO and WT mice. Results The C3 KO mice exhibited protection against photoreceptor cell death following photo-oxidative damage, which was associated with a reduction in immunoreactivity for the stress-related factor GFAP. In conjunction, there was a reduction in IBA1-positive macrophages in the outer retina compared to the WT mice and a decrease in the number of CD68-positive cells in the outer nuclear layer and the subretinal space. In addition, the engulfment of TUNEL-positive and -negative photoreceptors by macrophages was significantly lower in the C3 KO mice cohort following photo-oxidative damage compared to the WT cohort. Conclusions The results show that the absence of C3 mitigates the phagocytosis of photoreceptors by macrophages in the outer retina, and the net impact of C3 depletion is neuroprotective in the context of photo-oxidative damage. These data improve our understanding of the impact of C3 inhibition in subretinal inflammation and inform the development of treatments for targeting complement activation in diseases such as AMD. ; This study was supported by project grants from the National Health and Medical Research Council (APP1165599; APP1127705), Australian National University Translational Fellowship and Australian Government Research Training Program Scholarship.

5 p.-2 fig. ; [Background] Glomerulonephritis is one of the most severe complications of lupus, a systemic disease with multi-organ involvement, with tissue damage produced mainly by complement activation. As a result of this activation, patients with active lupus present hypocomplementemia during disease flares, but C3 and C4 levels are recovered between episodes. ; [Case presentation] We present a patient who suffered two lupus nephritis episodes in 5 years, achieving complete remission with treatment after both of them, but with C3 levels persistently below normal range. Genetic study revealed that the patient carried a mutation in heterozygosis in the C3 gene. Serial sera samples were analyzed, and autoantibodies to complement alternative pathway proteins (Factor I, Factor B, C3 and Properdin) were found. Functional assays showed that these autoantibodies cause alternative pathway activation. ; [Conclusion] This case is the first reported of a heterozygous C3 mutation associated with lupus nephritis and autoantibodies against complement alternative pathway proteins (Factor I, Factor B, C3 and Properdin).These autoantibodies cause activation of this pathway and this fact could explain that the tissue damage is restricted to the kidney. ; This work was funded by Spanish government, Ministerio de Economía y Competitividad (grant SAF2012-38636), Autonomous region of Madrid (S2010/BMD-2316 to SRdeC y MLT) and Sociedad Española de Nefrología Fundación Senefro to MLT. ; Peer reviewed

This biography examines the life of Helen Keller using easy-to-read, compelling text. Through striking historical and contemporary images and photographs and informative sidebars, readers will learn about Keller's family background, childhood, education, and time as a world-renowned activist and speaker. Informative sidebars enhance and support the text. Features include a table of contents, timeline, facts page, glossary, bibliography, and an index. Aligned to Common Core Standards and correlated to state standards. Essential Library is an imprint of Abdo Publishing, a division of ABDO

The Confederate Graves Survey Archive of the Texas Division, Sons of Confederate Veterans consists of surveys of cemeteries throughout Texas, and portions of Oklahoma and New Mexico. The surveys document the interment of Confederate States of America military veterans. United States of America (Union) veterans, as well as able-bodied men at the time of the Civil War, are also documented. 13 boxes entitled "Grave Surveys" contain grave surveys listed county-by-county, 3 boxes of "Unit Files" list surveyed individuals by their military unit. Finally, 17 boxes contain "Veteran Files" that document each veteran by name in "last name, first name, middle initial" format. An index that cross-references each of the collection series (Grave Surveys, Unit Files, and Veteran Files) is included, as are institutions to surveyors on how and what to document while conducting surveys. ; Pendleton Cemetery #678, Pendleton, Bell County, Texas | Veterans Interred: Brown, E. A. ; Abilene Cemetery #138, Abilene, Taylor County, Texas | Veterans Interred: Thomas, J. W. ; Abilene Cemetery #138, Abilene, Taylor County, Texas | Veterans Interred: Thomas, J. H. ; Weiland Cemetery #578, Weiland, Hunt County, Texas | Veterans Interred: Phillips, Robt Jackson. ; King Cemetery #685, Coryell County, Texas | Veterans Interred: Moseley, Elisha Alfred. ; Norton Cemetery #915, Runnels County, Texas | Veterans Interred: McDaniel, James M. ; Dickens Cemetery #340, Dickens, Dickens County, Texas | Veterans Interred: Sheilds, Thos. Jefferson. ; Shady Grove Cemetery #634, Wood County, Texas | Veterans Interred: Crone, Franklin M. ; Shady Grove Cemetery #634, Wood County, Texas | Veterans Interred: Jarred, James. ; Shady Grove Cemetery #634, Wood County, Texas | Veterans Interred: Brawning, Thomas. ; Moody Cemetery #28, Moody, McLennon County, Texas | Veterans Interred: Phillips, A. J. ; Weiland Cemetery #578, Weiland, Hunt County, Texas | Veterans Interred: Cummings, Henry. ; Weiland Cemetery #578, Weiland, Hunt County, Texas | Veterans Interred: Elledge, W. W. ; Forrest Park Cemetery #582, Hunt County, Texas | Veterans Interred: McMillan, Lee G. ; Abilene Cemetery #138, Abilene, Taylor County, Texas | Veterans Interred: Thomas, J. W. ; East Mt. Cemetery #572, Hunt County, Texas | Veterans Interred: Fountain E. P.

"This material appeared originally in Public documents . It was privately reprinted without change in 1935, was revised and published by the Library of Congress in 1939 and is here reissued with slight revision of the introductory section."--p. [2] ; At head of title: Library of Congress. Division of documents. ; Mode of access: Internet.